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emedicine.medscape.com

Pediatric Tinea Versicolor 

Updated: Jan 27, 2020
Author: Lyubomir A Dourmishev, MD, PhD; Chief Editor: Dirk M Elston, MD 

Overview

Background
Tinea versicolor or pityriasis versicolor is a common superficial cutaneous fungal infection characterized by pityriasiform
desquamation and hypopigmented or hyperpigmented macules formation, primarily located on the chest and back with tendency
to spread. The condition is frequently asymptomatic; however, some patients occasionally report pruritus. Tinea versicolor
results from an overgrowth of Malassezia furfur, which is part of normal skin flora and produces pigmentation changes when it
flourishes beyond normal levels.

Historical data

The first clinical observation of pityriasis versicolor was by Willan in 1801.[1] The causative agent was isolated by Eichsted in
1846; 7 years later, the German surgeon Robin named it Microsporon furfur. Billon proposed a new family name Malassezia and
subsequently proposed a new species name: Malassezia furfur. Clatelani and Chambers and, later, Gordon proposed the name
Pityrosporon ovale or orbiculare and confirmed it role as a causative agent.[1]

M furfur is a dimorphic lipophilic organism that is able to exist in both yeast and mycelial forms and does not attack the hair
shaft, nails, or mucous membranes. The infection is localized to the stratum corneum and chronically recurs in predisposed
patients. It is more common during warmer months and in warmer climates. Sun exposure frequently makes the lesions more
apparent because affected areas become hypopigmented. In temperate climates, patients develop the disease in the spring and
summer. In the tropics, patients are more likely to have tinea versicolor throughout the year.[2]

Although M furfur is a component of normal flora, it is also an opportunistic pathogen.[3] The organism is considered a possible
factor in other cutaneous diseases, including Pityrosporum folliculitis, confluent and reticulate papillomatosis, seborrheic
dermatitis, the provocation of psoriatic lesions, and some forms of atopic dermatitis.[4]

Studies also show that tinea versicolor occurs with malnutrition and various diseases, including Cushing syndrome. Pregnancy
and oral contraceptives may influence susceptibility, but firm data are lacking. Patients with AIDS may present with severe
seborrhea but do not have a higher incidence of tinea versicolor. Systemic infections are attributed to Pityrosporum in extremely
rare cases.

Different rare clinical forms have been described as follows:

Papulous variant

Erythematous and papulous variant in children

Tinea versicolor with atypical localization on face

Tinea versicolor with atypical localization on wrists

Pityriasis versicolor alba

Pathophysiology
The nutritional requirement of M furfur is one of the most important factors that affect the growth of the organism on the skin.
Studies show that lesion sites have a decrease in sebaceous gland secretions and water content, along with an increase in pH

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value compared with normal skin. M furfur is lipophilic, and the mycelial stage of M furfur can be induced in vitro by the addition
of cholesterol and cholesterol esters to the appropriate medium. However, significantly more amino acids are extracted from the
skin of infected patients, suggesting that amino acids, rather than lipids, are critical for the development of the disease. In vitro,
the amino acid asparagine stimulates the growth of the organism, while glycine induces hyphal formation.

Patient immune response also affects infection. Studies suggest a reduced body response to the specific fungal elements that
produce tinea versicolor. In various studies, defects in lymphokine production and natural killer T cells were found;
phytohemagglutinin (PHA) and concanavalin A (Con A) stimulation was decreased; and interleukin (IL)–2, IL-10, and interferon
(IFN)–g production by lymphocytes was decreased in affected patients. The exact pathophysiology of this disorder remains
undefined, and additional studies are needed.

In patients with hypopigmentation, tyrosinase inhibitors competitively inhibit an enzyme necessary for melanocyte pigment
formation. In hyperpigmented macules, the organism induces enlargement of melanosomes made by melanocytes in the basal
layer of the epidermis.

Etiology
M furfur is now the most commonly accepted name for the etiologic agent of tinea versicolor. Thus, P orbiculare, P ovale, and
Malassezia ovalis are synonyms .

M furfur is a dimorphic lipophilic organism that is cultured only in media enriched with C12-sized or C14-sized fatty acids.
Malassezia is able to exist in both yeast and mycelial forms, with yeast most commonly associated with saprofital form (P
ovale). Historically, the name M furfur was used to designate the fungal pathogen of tinea versicolor before it is grown in culture.
M furfur is not a dermatophyte, does not grow on dermatophyte test media (DTM), and does not respond to griseofulvin therapy.

With the advent of DNA sequencing, numerous pathogenic and nonpathogenic species were found. Some of them appear to be
more common in certain areas of the world, and some are more likely to be pathogenic in one area and not in another. Much of
the confusion was resolved with the taxonomic revision in 1996, based on sequencing of the large-subunit rRNA and nuclear
DNA of more than 100 isolates of Malassezia species.[3] The genus Malassezia was revised to include 7 species: Malassezia
globosa, Malassezia sympodialis, M furfur, Malassezia slooffiae, Malassezia pachydermatis, Malassezia restricta, and
Malassezia obtusa. The clinical significance of each of these species is under investigation. A study of the epidemiology of
Malassezia yeasts associated with pityriasis (tinea) versicolor in Canada revealed the most frequently isolated species included
M sympodialis, M globosa, and M furfur.

One study found M globosa in 97% of patients with tinea versicolor; it was found alone in 60% of cases, was associated with M
sympodialis in 29% of cases, and was associated with M slooffiae in 7% of cases.[3]  M sympodialis and M slooffiae were found
in similar percentages on clinically uninvolved skin of the trunk, whereas M globosa was not isolated at other sites. Thus, some
authors suggest that M globosa in its mycelial phase is the causative agent of tinea versicolor.[3, 4]

Epidemiology
Frequency

United States

Depending on the method and sensitivity of sampling methods, Malassezia species may be found in as many as 18% of infants
and 90-100% of adults. Clinical tinea versicolor is more common in areas with higher temperatures and higher relative
humidities. The incidence of this condition is approximately 2-8% of the population. The exact incidence is difficult to assess
because many affected individuals may not seek medical attention.

International

Tinea versicolor occurs worldwide, with an incidence rate of 50% in the humid, hot environment of Western Samoa and 1.1% in
the colder environment of Sweden. In temperate zones, the onset occurs during the warmer months of the year, and the lesions
generally fade in the cooler and drier months. In tropical countries, where heat and high humidity are more continuous, people
develop more extensive and persistent disease.

Race

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Although tinea versicolor is usually more apparent in darker-skinned individuals, the incidence of tinea versicolor appears to be
the same in all races.

Sex

Females and males are equally affected.

Age

In temperate zones (including most of the United States), tinea versicolor is rare in children. Affected infants or children often
have an atypical presentation. In temperate areas, the disorder is common in young adults aged 17-24 years. In tropical
climates, tinea versicolor is more common in individuals aged about 20-30 years. Beyond age 40 years, lipid levels in the skin
gradually decrease, and tinea versicolor becomes uncommon.

Prognosis
Prognosis is excellent. Although tinea versicolor is recurrent in some patients, the condition remains treatable.

Morbidity primarily results from the discoloration. The adverse cosmetic effect of lesions may lead to significant emotional
distress, particularly in adolescents. Tinea versicolor frequently recurs despite adequate initial therapy. Even with adequate
therapy, residual pigmentary changes may take several weeks to resolve.

The yeasts of the genus Malassezia have been associated with numerous other diseases that affect the human skin, such as
Malassezia (Pityrosporum) folliculitis, seborrheic dermatitis, atopic dermatitis, psoriasis, confluent and reticulated papillomatosis,
onychomycosis, and transient acantholytic dermatosis.

Patient Education
Tinea versicolor is caused by a fungus that is normally present on the skin surface and, therefore, is not considered a
contagious disease. The disease causes no permanent sequelae, and any pigmentary alterations resolve entirely within a few
months of adequate treatment. Effective therapy is available. Recurrences are common, and prophylactic therapy may be
required.

Presentation

History
Questioning the patient with tinea versicolor about skin or systemic diseases, current therapy, and drug allergies provides
guidance in selecting an appropriate therapy. The following are factors that may be used to guide therapy:

Other diseases, including renal disease, hepatic disease, and endocrine disease (eg, diabetes mellitus)

History of HIV or other immunocompromising disorder, which can increase the severity of tinea versicolor

Other skin disorders, including personal or family history of atopy or other eczematous conditions

Current or recent topical or systemic therapy

Drug allergies

Seasonal variations in skin color

Use of some body oils, which may supply additional nutrients to the M furfur

Sweat associated with exercise, which may contribute to disease development and recurrence

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Physical Examination
Lesion characteristics

Skin lesions are either hypopigmented or hyperpigmented maculae in various shapes. Hyperpigmented maculae become
hypopigmented after solar irradiation and subsequent tanning, as the name implies.

Lesions are either macules or very superficial plaques with fine scale that may not be evident except upon close examination.
Even when scale is not apparent, when the skin is wiped with a wet cloth and scraped for examination, it yields a surprising
amount of dirty-brown keratin. In some cases, lesions may appear atrophic (atrophying pityriasis versicolor).[5]

If not, the areas of dyschromia may represent residual effects of previously treated tinea versicolor. Occasionally, determining
whether the lighter or darker skin is affected is difficult.

Lesions have relatively sharp margins and may be lighter or darker than the normal skin color. The lesions are frequently a light
tan color in light-skinned individuals. The color of lesions varies from individual to individual, but each individual's lesions are
approximately the same color. Lesions are evenly pigmented. The inflammatory border, relative central clearing, and erythema
seen in most fungal infections are lacking.

Small lesions are usually circular or oval. Confluent patches with scattered circular or oval macules around the edges are
common. Other lesions may be large enough to cover most of the trunk.

Lesions are usually asymptomatic but may be mildly pruritic. The pruritus is more intense when the patient is excessively warm.

Residual hypopigmentation, without overlying scale, may remain for many months following effective treatment. These areas
may become more apparent following sun exposure, causing the patient to incorrectly suspect that the infection has recurred.

Examples of findings in tinea versicolor are shown in the images below.

In patients with lighter skin color, lesions frequently are a light tan or salmon color.

Scale is frequently difficult to appreciate upon clinical examination.

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This individual developed skin discoloration and mild itching every summer for the past few years. These patients should be
instructed on the prophylactic use of topical therapy.

This superficial plaque of tinea versicolor is located in the right antecubital fossa of an adult. This appearance and distribution
is uncommon but not rare. A potassium hydroxide (KOH) preparation confirmed the diagnosis.

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Although tinea versicolor is uncommon in children in temperate climates, when it does occur, it is more likely to be atypical in
distribution. This 7-year-old boy had areas of tinea versicolor across the forehead and both temples. He was in good health
and lived in Washington state when he was diagnosed.

In some patients, the areas affected by tinea versicolor are not always obvious. In this patient, the abnormal areas are
hypopigmented.

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Some patients present with extensive tinea versicolor. This patient related that his discoloration had been present for more
than 20 years. The light-colored areas on the abdomen are the normal areas of skin. Although topical therapy alone is usually
effective, this patient may benefit from initial therapy with oral ketoconazole, followed by selenium sulfide applications in the
shower 2-3 times a month.

Significant hyperpigmentation caused by a tinea versicolor infection.

Lesion distribution

The upper trunk is most commonly affected, but the lesions often spread to the upper arms, antecubital fossae, neck, abdomen,
and popliteal fossae. Lesions in the axillae, groin, thighs, and genitalia are less common.[6] Facial, scalp, and palmar lesions
occur in the tropics but are rare in temperate zones

In some patients, tinea versicolor primarily affects the flexural regions, the face or isolated areas of the extremities. This unusual
pattern of tinea versicolor is seen more often in immunocompromised hosts and can be confused with candidiasis, seborrheic
dermatitis, psoriasis, erythrasma, and dermatophyte infections.

Lesions that are imperceptible or doubtful are more visible using a Wood lamp in a darkened room.

Complications
The disease has benign course; however, it tends to have recurrences that must be properly treated. Some patients report for
itching, burning and irritation of lesions. Severe depigmentation may cause significant psychological discomfort.

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DDx

Diagnostic Considerations
Also consider the following:

Acanthosis nigricans

Confluent and reticulated papillomatosis of Gougerot and Carteaud

Erythrasma: Erythrasma may closely mimic tinea versicolor with pigmentary change and scaling, but satellite lesions are
less common, and erythrasma fluoresces pink under a Wood lamp.

Psoriasis (guttate form or psoriatic leucoderma)

Seborrheic dermatitis, pityriasis rosea, secondary syphilis, pinta, and tinea corporis: These all show more inflammatory
change than tinea versicolor.

Differential Diagnoses
Confluent and Reticulated Papillomatosis

Cutaneous T-Cell Lymphoma

Leprosy

Nummular Dermatitis (Nummular Eczema)

Parapsoriasis

Pityriasis Alba

Pityriasis Rosea

Syphilis

Vitiligo

Workup
 

Workup

Laboratory Studies
The diagnosis of tinea versicolor is usually made based on clinical examination findings; however, the diagnosis is easily
confirmed with microscopic examination of scales soaked in 10-15% potassium hydroxide (KOH). See the images below.

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Upon potassium hydroxide (KOH) examination, hyphae are visible and grow into strands within clumps of keratinocytes.
Thick-walled spores frequently occur in grapelike clumps. Individual spores and short stubby hyphae float in the clear areas
between clumps of keratinocytes. Many of the short hyphae are dystrophic.

Mycelium strands and numerous spores observed on a potassium hydroxide (KOH) preparation of tinea versicolor. This
combination is commonly referred to as "spaghetti and meatballs."

Microscopic examination

Microscopic examination demonstrates the characteristic thick-walled spherical or oval yeast forms and coarse septate
mycelium, often broken up into short filaments. This combination of mycelium strands and numerous spores is commonly
referred to as "spaghetti and meatballs."

Liquid blue ink, methylene blue, or Swartz-Medrik stain can be added to the KOH preparation for better visualization of the
causative organism.

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Scales may also be removed using clear adhesive tape; they are then directly examined. The tape must be clear and is pressed
several times over involved areas of skin. The tape is then lightly pressed, sticky side down, onto a microscope slide. A small
drop of methylene blue or other appropriate stain is placed at the edge of the tape and allowed to run between the tape and the
glass slide. Spores, often in grapelike clumps, and mycelium are easily seen. See the image below.

Clear adhesive tape can be pressed onto areas of tinea versicolor to collect hyphae and spores. The tape is then lightly
pressed onto a glass slide, and a drop of methylene blue is placed at the edge of the tape. The methylene blue is allowed to
run under the tape staining Malassezia furfur. The spores and hyphae easily are seen against a background clutter of
keratinocytes and glue.

A few reports in literature have recently stated that 1% Chicago Sky Blue 6B (CSB) staining with 10% KOH is a new promising
contrast diagnostic method for pityriasis versicolor, with 100% of sensitivity compared with 60.9% in culture.[7]

Cultures

M furfur is a dimorphic lipophilic organism, which is cultured only in media enriched with C12-sized to C14-sized fatty acids. It is
not a dermatophyte, does not grow on DTM, and does not respond to griseofulvin therapy.

If inoculated into lipid-rich media, the scales of tinea versicolor show spherical yeasts that produce the mycelial phase of the
normal flora yeast P orbiculare. Scales that show mycelium and clusters of oval yeasts on direct microscopy grow P ovale on
culture.

Colonization by M furfur is especially dense in the scalp, the upper trunk, and the flexures. In patients with clinical disease, the
organism occurs in both the filamentous (hyphal) and the yeast (spore) stage forms.

Imaging Studies
The disease does not require any imaging studies.

Other Tests
Wood lamp evaluation

Pityriasis versicolor showe blue-green fluorescence of macular dyschromic lesions if irradiated by ultraviolet light with
wavelength of approximately 365 nm (black light). However, the test findings may be negative in individuals on antimycotic
therapy of those who have recently showered because the fluorescent is water soluble.[8]

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Histologic Findings
The characteristic histological changes include hyperkeratosis, parakeratosis, and slight acanthosis with a mild perivascular
inflammatory infiltrate in the upper dermis. The organism is usually present in the upper layers of the stratum corneum, and
electron microscopy reveals invasion between and within the keratinized cells.

M furfur is detected by hematoxylin and eosin (H and E) stain alone, although periodic acid-Schiff (PAS) or methenamine-silver
staining facilitates detection.

Treatment

Medical Care
Tinea versicolor can be treated with various agents, and skin color alterations usually resolve within a few months of treatment.
[9] It does not leave any permanent scars or pigment changes.

Topical therapy alone is indicated for most patients. Systemic treatment is indicated for extensive involvement, for recurrent
infections, or when topical therapy has failed. Because treatment is relatively easy and recurrence is common, therapy must be
as safe, inexpensive, and convenient as possible. A plan for prophylactic therapy should be discussed with all patients to reduce
the high recurrence rate.

Various regimens involve both topical and oral therapies.[10, 11] The most common is varying regimens of selenium sulfide
lotion, topical zinc pyrithione, topical benzoyl peroxide, and topical therapy with imidazoles. Oral imidazole therapy is used in
adults but less commonly in children.[12, 13, 14]

Surgical Care
The disease does not require any surgical care.

Diet
Because studies indicate that tinea versicolor may associate with malnutrition the diet of patients have to be rational and not
restrictive.

Activity
Activity limitations are not necessary. However, active patients who excessively perspire are more likely to develop recurrences.

Prevention
Tinea versicolor has a high recurrence rate and may require frequent prophylactic treatment with intermittent topical or oral
therapy.

Good personal hygiene may help limit recurrences. Specifically, patients should shower as soon as possible after participating in
activities or exercise that produce significant perspiration.

Some authors recommend prophylaxsis with varying regimens of selenium sulfide shampoo or lotion.

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Long-Term Monitoring
Tinea versicolor tends to be associated with recurrences that must be properly treated.

Medication

Medication Summary
Tinea versicolor responds well to both topical and oral antimycotic therapies. Some patients prefer oral therapy because of
convenience, while others prefer the safety of topical therapies. Many effective topical therapies are available without
prescription and can be used for suppressive therapy or for treating recurrences without the need for a follow-up visit. Traditional
topical herbal therapies are still used in many parts of the world.[15]

Topical therapy alone is indicated for most patients. Systemic treatment may be indicated for patients with extensive
involvement, those with recurrent infections, or those in whom topical therapy has failed.

Systemic azoles are highly effective against M furfur and are usually combined with topical antimycotics in severe cases, and
new agents are being investigated.[16]  While oral fluconazole has been used in tinea versicolor, the results may be no better
than with topical agents.[17, 18]

Antifungal Agent, Topical

Class Summary
Selenium sulfide is effective against M furfur; it also has cytostatic effects on the epidermis and follicular epithelium, thus
reducing corneocyte production. Azole, allylamine and other antifungal creams are also highly effective mycocides against M
furfur.

Selenium sulfide topical (Selsun Blue, Exsel, Head & Shoulders)

Selenium sulfide is available as a shampoo or lotion in 1% or 2.5% concentrations. It is a safe and effective therapy that has
been used for years. The principle advantages of selenium sulfide are its low cost, over-the-counter availability, and convenient
application. However, it is an irritant, and some patients report itching or eczema after overnight applications. It may also stain
clothes and bedding. Lotion is preferred in children and patients with sensitive skin.

Clotrimazole topical (Lotrimin-AF, Canesten)

Clotrimazole is an imidazole broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular
components to leak, resulting in fungal cell death.

Econazole topical (Ecoza)

Econazole is an antifungal agent that is a water-miscible base consisting of pegoxol 7 stearate, peglicol 5 oleate, mineral oil,
benzoic acid, butylated hydroxyanisole, and purified water. The color of the soft cream is white to off-white and is for topical use
only. It interferes with RNA and protein synthesis and metabolism. It disrupts fungal cell wall permeability, causing fungal cell
death. Econazole exhibits broad-spectrum antifungal activity against many gram-negative organisms. It is effective in cutaneous
infections.

Ketoconazole topical (Nizoral)

Ketoconazole is an imidazole broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular
components to leak, resulting in fungal cell death.
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Oxiconazole (Oxistat)
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.

Sertaconazole (Ertaczo)
Sertaconazole is an imidazole broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular
components to leak, resulting in fungal cell death.

Ciclopirox (Batrafen, Loprox)

Ciclopirox interferes with the synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells.

Naftifine (Exoderil, Naftin)

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.

Terbinafine topical (Lamisil)

Terbinafine inhibits squalene epoxidase, which decreases ergosterol synthesis, causing fungal cell death. Use the medication
until symptoms significantly improve. The duration of treatment should be greater than 1 week, but not greater than 4 weeks.

Butenafine (Mentax)
Butenafine inhibits squalene epoxidation, which, in turn, causes blockage of ergosterol biosynthesis (an essential component of
fungal cell membranes). It is used topically for tinea (pityriasis) versicolor due to M furfur, tinea pedis (ie, athlete's foot), tinea
corporis (ie, ringworm), and tinea cruris (ie, jock itch) due to Epidermophyton floccosum, Trichophyton mentagrophytes,
Trichophyton rubrum, and Trichophyton tonsurans.

Antifungal Agent, Systemic

Class Summary
Systemic azoles are highly effective against M furfur and are usually combined with topical antimycotics in severe cases, and
new agents are being investigated.

Ketoconazole oral (Nizoral)

Ketoconazole is an imidazole broad-spectrum antifungal agent; it inhibits the synthesis of ergosterol, causing cellular
components to leak, resulting in fungal cell death.  While available as both a topical and systemic agent, systemic use of the
drug carries a black box warning and is inappropriate for conditions that are not severe or life-threatening. M furfur is eradicated
by the presence of ketoconazole in outer skin layers.

Fluconazole (Diflucan)
Fluconazole is a synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and
sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes. It
has little affinity for mammalian cytochromes, which is believed to explain its low toxicity. Fluconazole is available as tablets for
oral administration, as a powder for oral suspension, and as a sterile solution for intravenous use. It has fewer adverse effects
and better tissue distribution than older systemic imidazoles. It is most commonly used in the treatment of candidiasis. While it
has been used in tinea versicolor, the results may be no better than with topical agents.
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Itraconazole (Sporanox, Orungal)

Itraconazole is a synthetic triazole antifungal agent that inhibits fungal cell growth by inhibiting the cytochrome P-450–dependent
synthesis of ergosterol, a vital component of fungal cell membranes.

Questions & Answers

Overview

What is pediatric tinea versicolor?

When was pediatric tinea versicolor first identified?

What is the causative agent of pediatric tinea versicolor?

What are the risk factors for pediatric tinea versicolor?

What are the clinical variants of pediatric tinea versicolor?

What is the pathophysiology of pediatric tinea versicolor?

What causes pediatric tinea versicolor?

What is the prevalence of pediatric tinea versicolor in the US?

What is the global prevalence of pediatric tinea versicolor?

What are the racial predilections of pediatric tinea versicolor?

What are the sexual predilections of pediatric tinea versicolor?

Which age groups have the highest prevalence of pediatric tinea versicolor?

What is the prognosis of pediatric tinea versicolor?

What is included in patient education about pediatric tinea versicolor?

Presentation

Which clinical history findings are used to guide therapy for pediatric tinea versicolor?

How are pediatric tinea versicolor lesions characterized?

What is the distribution of lesions in pediatric tinea versicolor?

What are the possible complications of pediatric tinea versicolor?

DDX

Which conditions are included in the differential diagnoses of pediatric tinea versicolor?

What are the differential diagnoses for Pediatric Tinea Versicolor?

Workup

What is the role of lab testing in the workup of pediatric tinea versicolor?

What is the role of microscopy in the diagnosis of pediatric tinea versicolor?

What is the role of cultures in the diagnosis of pediatric tinea versicolor?

What is the role of imaging studies in the workup of pediatric tinea versicolor?

What is the role of a Wood lamp exam in the diagnosis of pediatric tinea versicolor?

Which histologic findings are characteristic of pediatric tinea versicolor?

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Treatment

How is pediatric tinea versicolor treated?

What is the role of surgery in the treatment of pediatric tinea versicolor?

Which dietary modifications are used in the treatment of pediatric tinea versicolor?

Which activity modifications are used in the treatment of pediatric tinea versicolor?

How is pediatric tinea versicolor prevented?

What is included in the long-term monitoring of pediatric tinea versicolor?

Medications

Which medications are indicated in the treatment of pediatric tinea versicolor?

Which medications in the drug class Antifungal Agent, Systemic are used in the treatment of Pediatric Tinea Versicolor?

Which medications in the drug class Antifungal Agent, Topical are used in the treatment of Pediatric Tinea Versicolor?

Contributor Information and Disclosures

Author

Lyubomir A Dourmishev, MD, PhD Associate Professor, Department of Dermatology and Venereology, Medical University of
Sofia, Bulgaria

Lyubomir A Dourmishev, MD, PhD is a member of the following medical societies: European Academy of Dermatology and
Venereology

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-
Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor
of Medicine, Rutgers New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of
Dermatology, New York Academy of Medicine, Royal College of Physicians of Edinburgh, Sigma Xi, The Scientific Research
Honor Society

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of
South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Additional Contributors

Kevin P Connelly, DO Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency
Care, Virginia Commonwealth University School of Medicine; Medical Director, Paws for Health Pet Visitation Program of the
Richmond SPCA; Pediatric Emergency Physician, Emergency Consultants Inc, Chippenham Medical Center

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Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of
Osteopathic Pediatricians, American Osteopathic Association

Disclosure: Nothing to disclose.

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