Official reprint from UpToDate®

www.uptodate.com ©2020 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

The content on the UpToDate website is not intended nor recommended as a substitute for
medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other
qualified health care professional regarding any medical questions or conditions. The use of
UpToDate content is governed by the UpToDate Terms of Use. ©2020 UpToDate, Inc. All rights
reserved.

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

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jan 2020. | This topic last updated: Aug 30, 2019.

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), beard hair (tinea barbae), and
nails (tinea unguium) are discussed in detail separately. (See "Tinea capitis" and "Infectious
folliculitis", section on 'Fungal folliculitis' 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. Dermatophyte test medium or a fungal culture may
also be used to confirm the diagnosis. (See "Office-based dermatologic diagnostic procedures",
section on 'Potassium hydroxide preparation'.)

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 antidermatophyte 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, betamethasone-clotrimazole) 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 Trichophyton rubrum, Trichophyton interdigitale
(formerly Trichophyton mentagrophytes), and Epidermophyton 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. Dermatophyte
test medium and fungal culture are alternative diagnostic procedures. (See "Office-based
dermatologic diagnostic procedures", section on 'Potassium hydroxide preparation'.)

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)
• Chronic palmoplantar (dyshidrotic) eczema (picture 9)
• Palmoplantar psoriasis (picture 10)
• Pitted keratolysis (picture 11)
• Juvenile plantar dermatosis (picture 12A-B)
• Keratolysis exfoliativa (see "Peeling skin syndromes", 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). The cost of these agents varies widely. 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 with topical azoles found slightly higher cure rates with allylamines
(risk ratio of treatment failure 0.63, 95% CI 0.42-0.94) [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 of 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
Trichophyton tonsurans, Microsporum canis, T. interdigitale (formerly T. mentagrophytes),
Microsporum gypseum, Trichophyton violaceum, and Microsporum 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, such as wrestlers (tinea corporis gladiatorum). T. tonsurans is a
common cause of tinea corporis gladiatorum [13].

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
18A-B). 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 "Office-based dermatologic diagnostic procedures", section on
'Potassium hydroxide preparation'.)

Differential diagnosis — A wide variety of cutaneous disorders are included in the differential
diagnosis for tinea corporis. Examples of features that should raise consideration for alternative
diagnoses include extensive skin involvement, absence of scale, failure to respond to antifungal
therapy, and a negative KOH preparation.

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, SCLE (picture 20), pityriasis
rosea (picture 24), and disciform erythrasma (picture 25), 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) [4,14]. 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 [15-18].

Reasonable regimens in adults include [19]:

● Terbinafine 250 mg per day for one to two weeks [20,21]

● 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 often 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 26A-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. Dermatophyte test medium and
fungal cultures can also be used to confirm the diagnosis. (See "Office-based dermatologic
diagnostic procedures", section on 'Potassium hydroxide preparation'.)

Differential diagnosis — Other common skin disorders that may present with erythematous
patches or plaques in the inguinal region include inverse psoriasis (picture 27), erythrasma (picture
28), seborrheic dermatitis (picture 29), 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 30). Although not always present, the finding of
seborrheic dermatitis or psoriasis in other body locations is useful for identifying these conditions.
(See "Erythrasma" and "Seborrheic dermatitis in adolescents and adults" and "Psoriasis:
Epidemiology, clinical manifestations, and diagnosis".)

Candidiasis is suggested by erythematous patches with satellite papules and pustules (picture
31). 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 "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) [4,14]. 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
tight-fitting clothing and noncotton 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. (See
"Infectious folliculitis", section on 'Fungal folliculitis'.)

Etiology — T. rubrum is the most frequent etiologic agent, although other dermatophytes have
been implicated [22].

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 [23,24].
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 [22,25-27]. In addition, topical
corticosteroid use on a superficial dermatophyte infection can lead to local immunosuppression
and the development of Majocchi's granuloma [28].

Clinical features — In immunocompetent patients, the clinical findings are typically characterized
by a localized area with erythematous, perifollicular papules or small nodules (picture 32A-C).
Pustules may also be present.

Immunocompromised patients may present similarly to immunocompetent patients or with

subcutaneous nodules and abscesses [28]. Rarely, systemic dissemination occurs [22,29].

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 [22]. Tissue culture can
identify the causative organism. A potassium hydroxide (KOH) preparation, which identifies fungal
forms only within the stratum corneum, may be negative [30].

Treatment — Topical antifungals are unlikely to penetrate deeply enough to effectively treat

Majocchi's granuloma. Treatment with an oral antifungal is recommended. (See "Infectious
folliculitis", section on 'Fungal folliculitis'.)

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 33) [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
34). 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, usually occurs in small children
(picture 35). 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 36A-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 Trichophyton 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 37A-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 [31]. 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 [32].

Dermatophytid reactions can occur in patients with tinea pedis, tinea manuum, tinea cruris, tinea
corporis, or tinea capitis [32-34]. Patients typically present with pruritic, papulovesicular eruptions
that can be quite distant from the site of infection (picture 38A-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 [35]. 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 [32].

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.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Dermatophyte infections".)

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 10th 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

Trichophyton, Epidermophyton, 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 recommend treatment with a topical
antifungal drug with antidermatophyte 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 noncotton 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.)

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, Bräutigam 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.

11. Gupta AK, Cooper EA. Update in antifungal therapy of dermatophytosis. Mycopathologia
2008; 166:353.

12. Bell-Syer SE, Khan SM, Torgerson DJ. Oral treatments for fungal infections of the skin of the
foot. Cochrane Database Syst Rev 2012; 10:CD003584.

13. Adams BB. Tinea corporis gladiatorum. J Am Acad Dermatol 2002; 47:286.

14. van Zuuren EJ, Fedorowicz Z, El-Gohary M. Evidence-based topical treatments for tinea cruris
and tinea corporis: a summary of a Cochrane systematic review. Br J Dermatol 2015;
172:616.

15. Bourlond A, Lachapelle JM, Aussems J, et al. Double-blind comparison of itraconazole with
griseofulvin in the treatment of tinea corporis and tinea cruris. Int J Dermatol 1989; 28:410.

16. Cole GW, Stricklin G. A comparison of a new oral antifungal, terbinafine, with griseofulvin as
therapy for tinea corporis. Arch Dermatol 1989; 125:1537.

17. Panagiotidou D, Kousidou T, Chaidemenos G, et al. A comparison of itraconazole and

griseofulvin in the treatment of tinea corporis and tinea cruris: a double-blind study. J Int Med
Res 1992; 20:392.

18. Faergemann J, Mörk NJ, Haglund A, Odegård T. A multicentre (double-blind) comparative

study to assess the safety and efficacy of fluconazole and griseofulvin in the treatment of
tinea corporis and tinea cruris. Br J Dermatol 1997; 136:575.

19. Elewski BE, Hughey LC, Sobera JO. Fungal diseases. In: Dermatology, 3rd ed, Bolognia JL, Jor
izzo JL, Schaffer JV (Eds), Elsevier Limited, Philadelphia; London 2012. Vol 2, p.1251.

20. Voravutinon V. Oral treatment of tinea corporis and tinea cruris with terbinafine and
griseofulvin: a randomized double blind comparative study. J Med Assoc Thai 1993; 76:388.

21. Farag A, Taha M, Halim S. One-week therapy with oral terbinafine in cases of tinea
cruris/corporis. Br J Dermatol 1994; 131:684.

22. Smith KJ, Neafie RC, Skelton HG 3rd, et al. Majocchi's granuloma. J Cutan Pathol 1991;
18:28.

23. Gill M, Sachdeva B, Gill PS, et al. Majocchi's granuloma of the face in an immunocompetent
patient. J Dermatol 2007; 34:702.
 24. Cho HR, Lee MH, Haw CR. Majocchi's granuloma of the scrotum. Mycoses 2007; 50:520.

25. Tse KC, Yeung CK, Tang S, et al. Majocchi's granuloma and posttransplant
lymphoproliferative disease in a renal transplant recipient. Am J Kidney Dis 2001; 38:E38.

26. Kim ST, Baek JW, Kim TK, et al. Majocchi's granuloma in a woman with iatrogenic Cushing's
syndrome. J Dermatol 2008; 35:789.

27. Akiba H, Motoki Y, Satoh M, et al. Recalcitrant trichophytic granuloma associated with NK-cell
deficiency in a SLE patient treated with corticosteroid. Eur J Dermatol 2001; 11:58.

28. Ilkit M, Durdu M, Karakaş M. Majocchi's granuloma: a symptom complex caused by fungal
pathogens. Med Mycol 2012; 50:449.

29. Novick NL, Tapia L, Bottone EJ. Invasive trichophyton rubrum infection in an
immunocompromised host. Case report and review of the literature. Am J Med 1987; 82:321.

30. Feng WW, Chen HC, Chen HC. Majocchi's granuloma in a 3-year-old boy. Pediatr Infect Dis J
2006; 25:658.

31. Bonifaz A, Vázquez-González D. Tinea imbricata in the Americas. Curr Opin Infect Dis 2011;
24:106.

32. Cheng N, Rucker Wright D, Cohen BA. Dermatophytid in tinea capitis: rarely reported common
phenomenon with clinical implications. Pediatrics 2011; 128:e453.

33. Romano C, Rubegni P, Ghilardi A, Fimiani M. A case of bullous tinea pedis with dermatophytid
reaction caused by Trichophyton violaceum. Mycoses 2006; 49:249.

34. Al Aboud K, Al Hawsawi K, Alfadley A. Tinea incognito on the hand causing a facial
dermatophytid reaction. Acta Derm Venereol 2003; 83:59.

35. Veien NK, Hattel T, Laurberg G. Plantar Trichophyton rubrum infections may cause
dermatophytids on the hands. Acta Derm Venereol 1994; 74:403.

Topic 4030 Version 36.0

Contributor Disclosures
Adam O Goldstein, MD, MPH Nothing to disclose Beth G Goldstein, MD Nothing to disclose Robert P
Dellavalle, MD, PhD, MSPH Grant/Research/Clinical Trial Support: Pfizer [Development of patient decision
aids]; Pfizer [Inflammatory and Immune-mediated Skin Disease Fellowship grant to the University of Colorado
[The fellowship will train a fellow in inflammatory and immune-mediated skin disease outcomes research].
Consultant/Advisory Boards: Altus Labs [Itch (Cannabidiol)]. Equity Ownership/Stock Options: Altus Labs
[Itch (Cannabidiol)]. Other Financial Interest: Stipends from the Journal of Investigative Dermatology (Podcast
editor), Journal of the American Academy of Dermatology (Dermatology section editor); expense
reimbursement for attending Cochrane Council meetings (Coordinating Editors Representative). Moise L
Levy, MD Grant/Research/Clinical Trial Support: Galderma [Atopic dermatitis (Investigational drug)]; Janssen
Pharmaceutica [Psoriasis (Investigational drug)]; Pfizer [Atopic dermatitis (Investigational drug)].
Consultant/Advisory Boards: Cassiopea [Pediatric and adolescent acne]; Regeneron Pharmaceuticals [Atopic
dermatitis (Dupilumab)]; UCB [Psoriasis (Certolizumab pegol)]. Patent Holder: Incontinentia pigmenti (NEMO
gene mutations). Other Financial Interest: Novan [Data safety monitoring board for molluscum contagiosum
trial (Investigational drug)]. Ted Rosen, MD Consultant/Advisory Boards: Medimetriks; Cutanea [Impetigo
(Ozenoxacin)]; Menlo [Prurigo nodularis (Serlopitant)]; Foamix [Acne (Minocycline foam)]. Abena O Ofori,
MD Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.

Conflict of interest policy