Dermatophyte (tinea) infections

Authors
Adam O Goldstein, MD, MPH
Beth G Goldstein, MD
Section Editors
Robert P Dellavalle, MD, PhD, MSPH
Moise L Levy, MD
Ted Rosen, MD
Deputy Editor
Abena O Ofori, MD
Contributor disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Oct 2016. | This topic last updated: Nov 23, 2015.
INTRODUCTION Dermatophyte infections are common worldwide, and dermatophytes are the
prevailing causes of fungal infection of the skin, hair, and nails [1-3]. These infections lead to a
variety of clinical manifestations, such as tinea pedis, tinea corporis, tinea cruris, Majocchi's
granuloma, tinea capitis, and tinea unguium (dermatophyte onychomycosis).
The clinical features, diagnosis, and treatment of dermatophyte infections of the skin will be
reviewed here. Dermatophyte infections of scalp hair (tinea capitis) and nails (tinea unguium) are
discussed in detail separately. (See "Tinea capitis" and "Onychomycosis: Epidemiology, clinical
features, and diagnosis".)
GENERAL PRINCIPLES Dermatophytes are filamentous fungi in the
genera Trichophyton, Microsporum, and Epidermophyton. Dermatophytes metabolize and subsist
upon keratin in the skin, hair, and nails.
The major clinical subtypes of dermatophyte infections are:
Tinea corporis Infection of body surfaces other than the feet, groin, face, scalp hair, or
beard hair
Tinea pedis Infection of the foot
Tinea cruris Infection of the groin
Tinea capitis Infection of scalp hair
Tinea unguium (dermatophyte onychomycosis) Infection of the nail
Additional terms used to describe less common presentations are tinea faciei (infection of the face),
tinea manuum (infection of the hand), and tinea barbae (infection of beard hair). (See 'Other clinical
variants' below.)
Tinea corporis, tinea pedis, tinea cruris, tinea faciei, and tinea manuum infections are typically
superficial, involving only the epidermis. Occasionally, dermatophyte infections penetrate the hair
follicle and dermis causing a condition called Majocchi's granuloma. Tinea capitis and tinea barbae
are characterized by infection of terminal hairs.
A diagnosis of a cutaneous dermatophyte infection may be strongly suspected based upon the
clinical findings. However, testing to confirm the diagnosis is recommended because a variety of
cutaneous disorders may present with similar features. A potassium hydroxide (KOH) preparation is

a rapid method to confirm the diagnosis. A fungal culture may also confirm the diagnosis.
(See "Dermatologic procedures", section on 'Potassium hydroxide (KOH) prep'.)
If a cutaneous dermatophyte infection is misdiagnosed and initially treated with a topical
corticosteroid, the appearance of the infection may be altered, making diagnosis more difficult (ie,
tinea incognito). Patients can develop diminished erythema and scale, loss of a well-defined border,
exacerbation of disease, or a deep-seated folliculitis (Majocchi's granuloma). (See 'Majocchi's
granuloma' below.)
The simultaneous presence of more than one type of dermatophyte infection is common (eg, tinea
pedis and tinea cruris or tinea pedis and tinea unguium). Performance of a full skin examination
including the skin, hair, and nails aids in the detection of additional sites of infection. Occasionally,
patients develop a dermatophytid reaction, a secondary dermatitic reaction at a distant site that may
reflect an immunologic reaction to the infection. (See 'Dermatophytid (id) reactions'below.)
Topical or systemic antifungal drugs with anti-dermatophyte activity are effective therapies. Most
superficial cutaneous dermatophyte infections can be managed with topical therapy with agents
such as azoles, allylamines, butenafine, ciclopirox, and tolnaftate (table 1). Nystatin, an effective
treatment for Candida infections, is not effective for dermatophytes. Oral treatment with
agents such as terbinafine, itraconazole, fluconazole, and griseofulvin is used for extensive or
refractory cutaneous infections and infections extending into follicles or the dermis (eg, Majocchi's
granuloma) or involving nails. Patients should not be treated with oral ketoconazole because of risk
for severe liver injury, adrenal insufficiency, and drug interactions.
Although they can be effective and may accelerate resolution of the clinical manifestations of
superficial dermatophyte infections [4], use of combination antifungal and corticosteroid products
that include medium- or high-potency corticosteroids
(eg, clotrimazole 1%/betamethasone dipropionate 0.05%) is discouraged because corticosteroid
therapy is not necessary for achieving cure and use of a topical corticosteroid introduces risk for
topical corticosteroid-induced skin atrophy. Treatment failures have also been reported [5-7].
Immunosuppression may increase risk for dermatophyte infection and may contribute to the
development of extensive or persistent disease. The possibility of an underlying immune disorder
should be considered in patients with particularly severe or treatment-refractory disease.
TINEA PEDIS Tinea pedis (also known as athlete's foot) is the most common dermatophyte
infection. Tinea pedis may manifest as an interdigital, hyperkeratotic, or vesiculobullous eruption,
and rarely as an ulcerative skin disorder. Interdigital tinea pedis is most common. Tinea pedis
frequently is accompanied by tinea unguium, tinea cruris, or tinea manuum.
Etiology Tinea pedis usually occurs in adults and adolescents (particularly young men) and is
rare prior to puberty [8]. Common causes are T. rubrum, T. interdigitale (formerly T.
mentagrophytes), and E. floccosum. Infection is usually acquired by means of direct contact with
the causative organism, as may occur by walking barefoot in locker rooms or swimming pool
facilities.
Clinical features The three major clinical types of tinea pedis are:

Interdigital tinea pedis Interdigital tinea pedis manifests as pruritic, erythematous

erosions or scales between the toes, especially in the third and fourth digital interspaces
(picture 1). Associated interdigital fissures may cause pain.
Hyperkeratotic (moccasin-type) tinea pedis Hyperkeratotic tinea pedis is characterized
by a diffuse hyperkeratotic eruption involving the soles and medial and lateral surfaces of the
feet, resembling a "moccasin" distribution (picture 2). There is a variable degree of underlying
erythema.
Vesiculobullous (inflammatory) tinea pedis Vesiculobullous tinea pedis is characterized
by a pruritic, sometimes painful, vesicular or bullous eruption with underlying erythema (picture
3). The medial foot is often affected.
Infrequently, tinea pedis may manifest with interdigital erosions and ulcers (ulcerative tinea pedis)
(picture 4A-B). This presentation is usually associated with secondary bacterial infection.
Diagnosis The diagnosis is confirmed with the detection of segmented hyphae in skin scrapings
from an affected area with a potassium hydroxide (KOH) preparation (picture 5A-B). In
vesicobullous tinea pedis, the roof of a vesicle can provide an adequate specimen. A fungal culture
is an alternative diagnostic procedure. (See "Dermatologic procedures", section on 'Potassium
hydroxide (KOH) prep'.)
Patients who exhibit significant erosions, ulceration, or malodor in the affected area should have a
Gram stain and culture to evaluate for secondary bacterial infection.
Differential diagnosis The differential diagnosis varies according to the clinical subtype:
Interdigital tinea pedis
Erythrasma (picture 6)
Interdigital Candida infection (erosio interdigitalis blastomycetica) (picture 7)
Hyperkeratotic (moccasin-type) tinea pedis
Atopic dermatitis
Chronic contact dermatitis (picture 8)
Acute palmoplantar (dyshidrotic) eczema (picture 9)
Palmoplantar psoriasis (picture 10)
Pitted keratolysis (picture 11)
Juvenile plantar dermatosis (picture 12A-B)
Keratolysis exfoliativa (see "Peeling skin syndrome", section on 'Keratolysis exfoliativa')
Keratodermas
Vesiculobullous (inflammatory) tinea pedis
Acute palmoplantar (dyshidrotic) eczema (picture 13)
Acute contact dermatitis
Palmoplantar pustulosis (picture 14)
Scabies (picture 15)
A positive KOH preparation demonstrating segmented hyphae distinguishes tinea pedis from nonfungal diseases. Interdigital Candida infection will demonstrate budding yeasts, pseudohyphae, and
septate hyphae on a KOH preparation (picture 16A-B).

Treatment Treatment is recommended to alleviate symptoms (pruritus), reduce risk for

secondary bacterial infection, and limit spread of the infection to other body sites or other
individuals. Topical antifungal therapy is the treatment of choice for most patients. Systemic
antifungal agents are primarily reserved for patients who fail topical therapy.
Topical drugs effective for tinea pedis include azoles, allylamines, butenafine, ciclopirox, tolnaftate,
and amorolfine (table 1). Amorolfine is not available in the United States. A meta-analysis of
randomized trials published prior to February 2005 supports efficacy of topical therapy, finding
strong evidence of superiority of topical antifungal agents (azoles, allylamines, ciclopirox, tolnaftate,
butenafine, and undecanoate) over placebo [9]. Allylamines may be slightly more effective than
azoles; a meta-analysis of data from 11 trials that compared topical allylamines to topical azoles
found slightly higher cure rates with allylamines (risk ratio of treatment failure 0.63, 95% CI 0.420.94) [9]. Topical antifungal treatment is generally applied once or twice daily and continued for four
weeks. Shorter treatment courses may be effective; high cure rates have been obtained
with terbinafine 1% cream applied to interdigital tinea pedis for one week [10].
Patients requiring oral antifungal therapy are usually treated with terbinafine, itraconazole,
or fluconazole. Typical treatment regimens for adults include [11]:
Terbinafine: 250 mg per day for two weeks
Itraconazole: 200 mg twice daily for one week
Fluconazole: 150 mg once weekly for two to six weeks
Griseofulvin can also treat tinea pedis, but may be less effective than other oral antifungals and
requires a longer duration of therapy [11]. In a systematic review, terbinafine was found more
effective than griseofulvin, while the efficacy of terbinafine and itraconazole were similar [12].
Typical adult doses for griseofulvin for tinea pedis are: 1000 mg per day of griseofulvin microsize for
four to eight weeks or 660 or 750 mg per day of griseofulvin ultramicrosize for four to eight weeks
[11].
Dosing for children is weight-based with durations of treatment similar to adults. Typical pediatric
doses for oral therapy include:
Terbinafine tablets:
10 to 20 kg: 62.5 mg per day
20 to 40 kg: 125 mg per day
Above 40 kg: 250 mg per day
Terbinafine granules:
Less than 25 kg: 125 mg per day
25 to 35 kg: 187.5 mg per day
Above 35 kg: 250 mg per day
Itraconazole: 3 to 5 mg/kg per day
Fluconazole: 6 mg/kg once weekly
Griseofulvin microsize 10 to 20 mg/kg per day or griseofulvin ultramicrosize 5 to
15 mg/kg per day
In our experience, patients with hyperkeratotic tinea pedis can benefit from combining antifungal
treatment with a topical keratolytic, such as salicylic acid. Burow's (1% aluminum acetate or 5%

aluminum subacetate) wet dressings, applied for 20 minutes two to three times per day, or placing
gauze or cotton between toes may be helpful as an adjunctive measure for patients with
vesiculation or maceration. Interventions that may help to reduce recurrences include use of
desiccating foot powders, treatment of shoes with antifungal powder, and avoidance of occlusive
footwear.
TINEA CORPORIS Tinea corporis is a cutaneous dermatophyte infection occurring in sites other
than the feet, groin, face, or hand.
Etiology T. rubrum is the most common cause of tinea corporis. Other notable causes include T.
tonsurans, M. canis, T. interdigitale (formerly T. mentagrophytes), M. gypseum, T. violaceum,
and M. audouinii. Acquisition of infection may occur by direct skin contact with an infected individual
or animal, contact with fomites, or from secondary spread from other sites of dermatophyte infection
(eg, scalp, feet, etc).
In particular, T. tonsurans tinea corporis in adults may result from contact with a child with tinea
capitis, which is often caused by this organism. M. canis tinea corporis is often acquired by contact
with an infected cat or dog. Tinea corporis can also occur in outbreaks among athletes who have
skin-to-skin contact [13], such as wrestlers (tinea corporis gladiatorum). T. tonsurans is a common
cause of tinea corporis gladiatorum [14].
Clinical features Tinea corporis often begins as a pruritic, circular or oval, erythematous, scaling
patch or plaque that spreads centrifugally. Central clearing follows, while an active, advancing,
raised border remains. The result is an annular (ring-shaped) plaque from which the disease
derives its common name (ringworm) (picture 17A-C). Multiple plaques may coalesce (picture 18AB). Pustules occasionally appear (picture 19).
Tinea corporis contracted from infected animals, particularly kittens and puppies, is often intensely
inflammatory. Extensive tinea corporis should raise concern for an underlying immune disorder,
such as human immunodeficiency virus (HIV), or for diabetes.
Diagnosis A potassium hydroxide (KOH) preparation will show the segmented hyphae
characteristic of dermatophyte infections (picture 5A-B). The highest yield is obtained from skin
scrapings taken from the active border of a plaque. A fungal culture is an alternative, albeit slower
method for diagnosis. (See "Dermatologic procedures", section on 'Potassium hydroxide (KOH)
prep'.)
Differential diagnosis Tinea corporis may be confused with other annular skin eruptions,
especially subacute cutaneous lupus erythematosus (SCLE), granuloma annulare, and erythema
annulare centrifugum. SCLE can be idiopathic or occur in association with systemic lupus
erythematosus or drug exposure. SCLE often manifests as annular or polycyclic erythematous scaly
plaques on sun-exposed skin (picture 20). Granuloma annulare is a benign inflammatory condition
that classically presents with one or more erythematous or violaceous annular plaques on the
extremities (picture 21A-B). Unlike tinea corporis, scale is absent. Erythema annulare centrifugum,
an inflammatory skin disorder of unknown etiology, exhibits annular erythematous plaques (picture
22A-B). A trailing rim of scale is often evident in the superficial variant of this disorder.
(See "Overview of cutaneous lupus erythematosus" and "Granuloma annulare", section on 'Clinical
features'.)

Other disorders, such as nummular eczema (picture 23), psoriasis, subacute cutaneous lupus
erythematosus (picture 20), and pityriasis rosea (picture 24), may also exhibit scaling plaques that
resemble tinea corporis. (See "Approach to the patient with annular skin lesions".)
Treatment Tinea corporis usually responds well to topical antifungal drugs, such as azoles,
allylamines, butenafine, ciclopirox, and tolnaftate (table 1) [4,15]. Pooled data from randomized
trials supports the efficacy of two allylamines, terbinafine and naftifine, for tinea corporis and tinea
cruris [4]. There are also data that suggest similar efficacy of topical allylamines and topical azoles
[4]. Topical nystatin is not effective for dermatophyte infections.
Topical antifungal treatment is generally administered once or twice per day for one to three weeks
(table 1). The endpoint of treatment is clinical resolution.
Systemic treatment is an alternative for patients with extensive skin involvement and patients who
fail topical therapy. Terbinafine and itraconazole are common
treatments. Griseofulvin and fluconazole can also be effective, but may require longer courses of
therapy. Randomized trials support the efficacy of systemic therapy [16-19].
Reasonable regimens in adults include [20]:
Terbinafine 250 mg per day for one to two weeks [21,22]
Itraconazole 200 mg per day for one week
Fluconazole 150 to 200 mg once weekly for two to four weeks
Griseofulvin microsize 500 to 1000 mg per day or griseofulvin ultramicrosize 375 to 500 mg
per day for two to four weeks
Children are treated for similar durations. Reasonable pediatric doses for these drugs are:
Terbinafine tablets:
10 to 20 kg: 62.5 mg per day
20 to 40 kg: 125 mg per day
Above 40 kg: 250 mg per day
Terbinafine granules:
Less than 25 kg: 125 mg per day
25 to 35 kg: 187.5 mg per day
Above 35 kg: 250 mg per day
Itraconazole 3 to 5 mg/kg per day (up to 200 mg per day)
Fluconazole 6 mg/kg once weekly
Griseofulvin microsize 10 to 20 mg/kg per day or griseofulvin ultramicrosize 5 to
15 mg/kg per day
TINEA CRURIS Tinea cruris (also known as jock itch) is a dermatophyte infection involving the
crural fold.
Etiology The most common cause is T. rubrum. Other frequent causes include E.
floccosum and T. interdigitale (formerly T. mentagrophytes).

Tinea cruris is far more common in men than women. Often, infection results from the spread of the
dermatophyte infection from concomitant tinea pedis. Predisposing factors include copious
sweating, obesity, diabetes, and immunodeficiency.
Clinical features Tinea cruris begins with an erythematous patch on the proximal medial thigh.
The infection spreads centrifugally, with partial central clearing and a slightly elevated,
erythematous, sharply demarcated border that may have tiny vesicles (picture 25A-B). Infection
may spread to the perineum and perianal areas, into the gluteal cleft, or onto the buttocks. In males,
the scrotum is typically spared.
Diagnosis A potassium hydroxide (KOH) examination of scales scraped from tinea cruris will
show the segmented hyphae characteristic of dermatophyte infections (picture 5A-B). The highest
yield is obtained from skin scrapings taken from the active border. Fungal cultures can also confirm
the diagnosis. (See "Dermatologic procedures", section on 'Potassium hydroxide (KOH) prep'.)
Differential diagnosis Other common skin disorders that may present with erythematous
patches or plaques in the inguinal region include inverse psoriasis (picture 26), erythrasma (picture
27), seborrheic dermatitis (picture 28), and candidal intertrigo. A KOH preparation positive for
hyphae rules out the first three disorders.
A diagnosis of erythrasma is confirmed by the appearance of coral red fluorescence upon
illumination with a Wood's lamp (picture 29). Although not always present, the finding of seborrheic
dermatitis or psoriasis in other body locations is useful for identifying these conditions.
(See "Erythrasma" and "Overview of dermatitis" and "Epidemiology, clinical manifestations, and
diagnosis of psoriasis".)
Candidiasis is suggested by erythematous patches with satellite papules and pustules (picture 30).
Candidal pseudohyphae, hyphae, and yeast cells are seen on KOH preparation (picture 16A-B). In
contrast to tinea cruris, scrotal involvement is common in men with candidiasis of the crural folds.
(See "Candidal intertrigo".)
Treatment Treatment is similar to tinea corporis. Topical therapy with antifungal agents such as
azoles, allylamines, butenafine, ciclopirox, and tolnaftate is effective (table 1)
[4,15]. Nystatin is not effective for dermatophyte infections. Tinea cruris that is extensive or fails to
resolve with topical therapy can be treated with the oral antifungal regimens used for tinea corporis.
(See 'Tinea corporis' above.)
Recurrence of tinea cruris is common. Concomitant tinea pedis should be treated to reduce risk for
recurrence. Treatment of onychomycosis may also reduce recurrences. Other interventions that
may be helpful include daily use of desiccant powders in the inguinal area and avoidance of tightfitting clothing and non-cotton underwear.
MAJOCCHI'S GRANULOMA Dermatophyte infections are usually limited to the epidermis.
Majocchi's granuloma is an uncommon condition in which the dermatophyte invades the dermis or
subcutaneous tissue.
Etiology T. rubrum is the most frequent etiologic agent, although other dermatophytes have
been implicated [23].

Majocchi's granuloma may be precipitated by trauma to the skin or occlusion of hair follicles,
leading to the disruption of hair follicles and passage of the dermatophyte into the dermis [24,25].
Shaving the legs can be an inciting factor in women.
In immunosuppressed patients, the depression of cell-mediated immunity and the inflammatory
response may contribute to progression to Majocchi's granuloma [23,26-28]. In addition, topical
corticosteroid use on a superficial dermatophyte infection can lead to local immunosuppression and
the development of Majocchi's granuloma [25,29,30].
Clinical features In immunocompetent patients, the clinical findings are typically characterized
by a localized area with erythematous, perifollicular papules or small nodules (picture 31A-C).
Pustules may also be present.
Immunocompromised patients may present similarly to immunocompetent patients, or with
subcutaneous nodules and abscesses [26,31-34]. Rarely, systemic dissemination occurs [23,35].
Diagnosis A presumptive diagnosis is made based on the patient's history and clinical findings,
and is confirmed with a skin biopsy exhibiting fungal forms in the dermis [23]. Tissue culture can
identify the causative organism. A potassium hydroxide (KOH) preparation, which identifies fungal
forms only within the stratum corneum, may be negative [23,27,36,37].
Treatment Topical antifungals are unlikely to penetrate deeply enough to effectively treat
Majocchi's granuloma. Treatment with an oral antifungal is recommended, and multiple treatment
regimens have been proposed, although no randomized trials or large case series are available.
Terbinafine 250 mg per day for two to four weeks has been used for the treatment of Majocchi's
granuloma in adults [38,39]. A case series of seven successfully treated patients, including one
patient receiving systemic immunosuppressants for chronic lymphocytic leukemia, led to the
recommendation of pulse therapy with itraconazole 200 mg twice daily for one week per month for
two months [40]. Treatment regimens with griseofulvin and daily itraconazole have also been
suggested [36].
Immunocompromised patients have been successfully treated with oral antifungals. Treatment by
local excision has been reported [33,34], but may not be necessary.
OTHER CLINICAL VARIANTS Various other terms are used to describe additional clinical
subtypes of dermatophyte infection.
Tinea faciei Tinea faciei is a dermatophyte infection of facial skin devoid of terminal hairs. The
eruption may begin as small, scaly papules that evolve to form an annular plaque (picture 32) [8].
Tinea faciei is managed similarly to tinea corporis. (See 'Tinea corporis' above.)
Tinea manuum Tinea manuum is dermatophyte infection of the hand. Patients present with a
hyperkeratotic eruption on the palm or annular plaques similar to tinea corporis on the dorsal hand.
Tinea manuum commonly occurs in association with tinea pedis, and is often unilateral (picture 33).
This clinical presentation is often referred to "two-feet, one hand syndrome." The approach to
treatment is similar to tinea pedis. (See 'Tinea pedis' above.)

Tinea capitis Tinea capitis, dermatophyte infection of scalp hair, almost always occurs in small
children (picture 34). Oral antifungal therapy is the treatment of choice. Tinea capitis is reviewed in
detail separately. (See "Tinea capitis".)
Tinea barbae Tinea barbae is a dermatophyte infection involving beard hair in adolescent and
adult men (picture 35A-B). Oral antifungal therapy is necessary. Tinea barbae is reviewed
separately. (See "Infectious folliculitis", section on 'Fungal folliculitis'.)
Tinea imbricata Tinea imbricata (also known as Tokelau ringworm) is a variant of tinea corporis
caused by T. concentricum. The disorder primarily occurs in the South Pacific Islands, South Asia,
and South America. Tinea imbricata is characterized by concentric annular, scaly, erythematous
plaques (picture 36A-B). A potassium hydroxide (KOH) preparation demonstrates hyphae and
fungal culture confirms T. concentricum infection. The most effective treatments may be
oral terbinafine and griseofulvin [41]. Systemic therapy is often combined with a topical keratolytic
agent.
DERMATOPHYTID (ID) REACTIONS Autoeczematization reactions (also known as id reactions)
are secondary dermatitic eruptions that occur in association with primary, often inflammatory, skin
disorders. The term dermatophytid reaction describes this occurrence in relation to a dermatophyte
infection. The pathogenesis may involve an immunologic reaction to fungal antigens similar to a
delayed-type hypersensitivity response [42].
Dermatophytid reactions can occur in patients with tinea pedis, tinea manuum, tinea cruris, tinea
corporis, or tinea capitis [42-48]. Patients typically present with pruritic, papulovesicular eruptions
that can be quite distant from the site of infection (picture 37A-B). In one series of 213 patients with
tinea pedis, 37 (17 percent) were diagnosed with dermatophytid reactions characterized by
vesicular eruptions on the hands [43]. A separate series of five children with dermatophytid
reactions due to tinea capitis found that in addition to involvement on the head and neck, trunk and
extremity lesions were common [42].
The management of dermatophytid reactions involves the successful treatment of the dermatophyte
infection; this may be compromised if the reaction is mistaken for a drug eruption related to
antifungal therapy. Topical corticosteroids and antipruritic agents are typically used for acute
management. Rarely, systemic glucocorticoids are needed.
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The
Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language,
at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might
have about a given condition. These articles are best for patients who want a general overview and
who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer,
more sophisticated, and more detailed. These articles are written at the 10 th to 12th grade reading
level and are best for patients who want in-depth information and are comfortable with some
medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Ringworm, athlete's foot, and jock itch (The
Basics)" and "Patient education: Fungal nail infections (The Basics)")
Beyond the Basics topics (see "Patient education: Ringworm (including athlete's foot and
jock itch) (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
Superficial fungal infections are most commonly caused by dermatophytes in
the Epidermophyton, Trichophyton, and Microsporum genera. These organisms metabolize
keratin and cause a range of pathologic clinical presentations, including tinea pedis, tinea
corporis, tinea cruris, Majocchi's granuloma, tinea capitis, and tinea unguium. (See 'General
principles' above.)
A diagnosis of a cutaneous dermatophyte infection may be strongly suspected based upon
the clinical findings. A potassium hydroxide (KOH) preparation should be used to confirm the
diagnosis (picture 5A). Failing to accurately diagnose a dermatophyte infection may lead to
inappropriate treatment with topical corticosteroids. (See 'General principles' above.)
Most dermatophyte infections can be managed with topical treatments. For patients with
limited tinea pedis, tinea corporis, or tinea cruris, we suggest treatment with a topical
antifungal drug with anti-dermatophyte activity rather than systemic therapy (Grade 1A).
Examples of effective topical antifungal agents are azoles, allylamines, ciclopirox, butenafine,
and tolnaftate. Oral antifungal therapy is used for extensive infections or infections refractory
to topical therapy. Nystatin is not effective for dermatophyte infections. (See 'Tinea
pedis' above and 'Tinea corporis' above and 'Tinea cruris' above.)
Recurrences of tinea pedis and tinea cruris are common. For patients with tinea pedis, use of
desiccating foot powders, placement of antifungal powder in shoes, and avoidance of
occlusive footwear may help to reduce recurrences. Patients with tinea cruris may benefit from
treatment of concomitant tinea pedis or tinea unguium, use of desiccating powders in the
groin, and avoidance of occlusive clothing and non-cotton underwear. (See 'Tinea
pedis' above and 'Tinea cruris'above.)
Majocchi's granuloma is caused by dermatophyte invasion into the dermal or subcutaneous
tissue via penetration of hair follicles. Inflammatory perifollicular papules, small nodules, or
pustules are typically seen. A KOH preparation may be negative. Oral antifungal therapy is
indicated. (See 'Majocchi's granuloma'above.)
Dermatophytid reactions are secondary dermatitic eruptions that may be precipitated by an
immunologic response to dermatophyte infection. Management of dermatophytid reactions
involves treatment of the associated dermatophyte infection. Topical corticosteroids and
antipruritic agents may be beneficial for symptom relief. (See 'Dermatophytid (id)
reactions' above.)
Use of UpToDate is subject to the Subscription and License Agreement.

Tinea versicolor (Pityriasis versicolor)

Authors
Beth G Goldstein, MD
Adam O Goldstein, MD, MPH
Section Editors
Robert P Dellavalle, MD, PhD, MSPH
Moise L Levy, MD
Ted Rosen, MD
Deputy Editor
Abena O Ofori, MD

INTRODUCTION
Tinea versicolor (ie, pityriasis versicolor) is a common superficial fungal infection. Patients with this
disorder often present with hypopigmented, hyperpigmented, or erythematous macules on the trunk
and proximal upper extremities (picture 1A-E). Unlike other disorders utilizing the term tinea (eg,
tinea pedis, tinea capitis), tinea versicolor is not a dermatophyte infection. The causative organisms
are saprophytic, lipid-dependent yeasts in the genus Malassezia (formerly known as Pityrosporum)
[1].
Tinea versicolor responds well to medical therapy (table 1), but recurrence is common and longterm prophylactic therapy may be necessary. The clinical features, diagnosis, and management of
tinea versicolor will be reviewed here.

EPIDEMIOLOGY
Tinea versicolor occurs worldwide, but the highest incidence is found in tropical climates.
Prevalence of up to 50 percent has been reported in some tropical countries [2]. In Scandinavia, the
prevalence has been estimated to be approximately 1 percent [2].
Tinea versicolor most commonly affects adolescents and young adults, but can also occur in
children and has been reported in infants [3-6]. The disorder is not contagious, although successful
inoculation has occurred under experimental conditions utilizing topical oils and occlusion [7,8].

PATHOGENESIS AND RISK FACTORS

Malassezia is a lipid-dependent, dimorphic fungus that is a component of normal skin flora.
Transformation of Malassezia from yeast cells to a pathogenic mycelial form is associated with the
development of clinical disease. External factors suspected of contributing to this conversion
include exposure to hot and humid weather, hyperhidrosis, and the use of topical skin oils [9]. Tinea
versicolor is not related to poor hygiene.

REFERENCES
1.

Havlickova B, Czaika VA, Friedrich M. Epidemiological trends in skin mycoses worldwide.

Mycoses 2008; 51 Suppl 4:2.

2.

Seebacher C, Bouchara JP, Mignon B. Updates on the epidemiology of dermatophyte

infections. Mycopathologia 2008; 166:335.

3.

Ameen M. Epidemiology of superficial fungal infections. Clin Dermatol 2010; 28:197.

4.

El-Gohary M, van Zuuren EJ, Fedorowicz Z, et al. Topical antifungal treatments for tinea
cruris and tinea corporis. Cochrane Database Syst Rev 2014; :CD009992.

5.

Alston SJ, Cohen BA, Braun M. Persistent and recurrent tinea corporis in children treated
with combination antifungal/ corticosteroid agents. Pediatrics 2003; 111:201.

6.

Greenberg HL, Shwayder TA, Bieszk N, Fivenson DP. Clotrimazole/betamethasone

diproprionate: a review of costs and complications in the treatment of common cutaneous fungal
infections. Pediatr Dermatol 2002; 19:78.

7.

Rosen T, Elewski BE. Failure of clotrimazole-betamethasone dipropionate cream in

treatment of Microsporum canis infections. J Am Acad Dermatol 1995; 32:1050.

8.

Hawkins DM, Smidt AC. Superficial fungal infections in children. Pediatr Clin North Am
2014; 61:443.

9.

Crawford F, Hollis S. Topical treatments for fungal infections of the skin and nails of the foot.
Cochrane Database Syst Rev 2007; :CD001434.

10.

Korting HC, Tietz HJ, Brutigam M, et al. One week terbinafine 1% cream (Lamisil) once
daily is effective in the treatment of interdigital tinea pedis: a vehicle controlled study. LAS-INT-06
Study Group. Med Mycol 2001; 39:335.