eMedicine Specialties > Dermatology > Fungal Infections
Tinea Versicolor
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.
Differential Diagnoses
Erythrasma
Pityriasis Alba
Psoriasis, Guttate
Seborrheic Dermatitis
Tinea Corporis
Vitiligo
Other Problems to Be Considered
Confluent and reticulated papillomatosis of Gougerot and Carteaud
Workup
Laboratory 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. Contrast stain containing 1% Chicago sky blue 6B and 8% KOH (as the clearing agent) achieves the greatest sensitivity and specificity.12
- 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.13 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
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,14 as well as azole and allylamine antifungals.15,16,17 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.18,19,20 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.21 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.22 In the case of oral terbinafine, some subgroups of M furfur apparently are not clinically responsive, although in vitro studies suggest fungistatic activity.23 Also, a regimen of 1 tablet a month of ketoconazole, fluconazole, and itraconazole has been used successfully to prophylactically prevent recurrences.24
Surgical Care
Reports describe successful treatment of tinea versicolor with 5-aminolevulinic acid photodynamic therapy.25
Diet
Dietary alterations have not proved successful in the treatment of tinea versicolor.
Medication
Tinea versicolor responds well to both topical and oral antimycotic therapies. Many patients prefer oral therapy because of its convenience.
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.
Terbinafine (Lamisil)
Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing fungal cell death. Use medication until symptoms significantly improve. Duration of treatment should be >1 wk but not >4 wk.
Dosing
Adult
Apply bid 1-4 wk
Pediatric
<12 years: Not established
>12 years: Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Discontinue use if sensitivity or irritation occurs; for external use only; avoid contact with eyes
Clotrimazole (Mycelex, Lotrimin-AF)
Broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing fungal cell death. Reevaluate diagnosis if no clinical improvement after 4 wk.
Dosing
Adult
Gently massage into affected area and surrounding skin areas bid for 2-6 wk
Pediatric
Children: Not established
Adolescents: Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
For external use only; avoid contact with eyes; if irritation or sensitivity develops, discontinue use
Ketoconazole (Nizoral)
Both topical and systemic agent. Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. Achieves excellent skin levels with minimal oral dosing. M furfur is eradicated by the presence of ketoconazole in outer skin layers. Tinea versicolor is extremely rare in small children; thus, do not treat children aged <10 y with oral ketoconazole for tinea versicolor.
Dosing
Adult
Topical: Rub gently into affected area qd/bid for 2-4 wk
Oral: 400 mg PO once; alternatively, 200-mg dosing for 10 d
Pediatric
Topical: Apply as in adults
Oral: 3.3-6.6 mg/kg/d PO
Interactions
Isoniazid may decrease bioavailability; coadministration decreases effects of either rifampin or ketoconazole; may increase effect of anticoagulants; may increase toxicity of corticosteroids and cyclosporine (cyclosporine dosage can be adjusted); may decrease theophylline levels; inhibition of cytochrome P450 3A4–mediated metabolism of coadministered medications (associated with QT prolongation; therefore, caution with concurrent use of drugs that can prolong the QT interval)
As a CYP3A4 inhibitor (P450 metabolism), many drugs have interactions when coadministered with this medication; advise checking for possible interactions when considering adding this to other medications a patient may be starting or already taking
Contraindications
Documented hypersensitivity; fungal meningitis; concurrent use with astemizole, terfenadine, cisapride, or oral triazolam
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hepatotoxicity may occur; may reversibly decrease corticosteroid serum levels (adverse effects avoided with dose of 200-400 mg/d); administer antacid, anticholinergics, or H2 blockers at least 2 h after taking oral ketoconazole; if sensitivity or irritation develops with topical formulation, discontinue use; topical form is for external use only; avoid contact with eyes; caution in achlorhydria (reduces absorption); considered unsafe in persons with acute porphyrias (adrenal suppression, gynecomastia, hypocholesterolemia, and hypothyroidism have been cause by the administration of ketoconazole)
Ciclopirox (Loprox)
Interferes with synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells.
Dosing
Adult
Massage into affected areas bid; reevaluate the diagnosis if no improvement after 4 wk
Pediatric
<10 years: Not established
>10 years: Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Avoid contact with eyes and other internal routes
Butenafine (Mentax)
Damages fungal cell membranes causing fungal cell growth to arrest.
Dosing
Adult
Apply qd for 4 wk
Pediatric
<12 years: Not established
>12 years: Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Use topically (not for use in eyes, vagina, or other internal routes)
Naftifine (Naftin)
Broad-spectrum antifungal agent and synthetic allylamine derivative; may decrease the synthesis of ergosterol, which, in turn, inhibits fungal cell growth. If no clinical improvement after 4 wk, reevaluate the patient.
Dosing
Adult
Gently massage (cream/gel) sparingly into affected area and surrounding skin qd for 2-4 wk
Pediatric
Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Discontinue use if sensitivity or chemical irritation occurs; for external use only; avoid contact with eyes
Econazole (Spectazole)
Effective in cutaneous infections. Interferes with RNA and protein synthesis and metabolism. Disrupts fungal cell wall membrane permeability, causing fungal cell death.
Dosing
Adult
Apply sparingly over affected areas qd/bid
Pediatric
Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
If sensitivity or irritation develops, discontinue use; for external use only; avoid contact with eyes
Oxiconazole (Oxistat)
Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out and resulting in fungal cell death.
Dosing
Adult
Apply to affected area qid
Pediatric
Apply as in adults
Interactions
None reported
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
If sensitivity or chemical irritation occurs, discontinue use; for external use only; avoid contact with eyes
Follow-up
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.
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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, , Pityrosporon orbiculare, Pityrosporon ovale, Malassezia ovalis, Cushing disease
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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