Dermatophyte (tinea) infections

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 (picture 1A-C), tinea corporis (picture 2A-D), tinea cruris (picture 3A-E), tinea capitis (picture 4A-B), dermatophyte onychomycosis (tinea unguium (picture 5)), and Majocchi's granuloma (picture 6A-C).

The clinical features, diagnosis, and management of dermatophyte infections of the skin will be reviewed here (algorithm 1). Dermatophyte infections of scalp hair (tinea capitis), beard hair (tinea barbae), and nails (tinea unguium or dermatophyte onychomycosis) are discussed in detail separately.

●(See "Tinea capitis".)

●(See "Infectious folliculitis", section on 'Dermatophytic folliculitis'.)

●(See "Onychomycosis: Epidemiology, clinical features, and diagnosis".)

●(See "Onychomycosis: Management".)

The term "tinea" is also used in the names of some cutaneous fungal infections that are not caused by dermatophytes. These disorders are reviewed separately.

●(See "Tinea versicolor (pityriasis versicolor)".)

●(See "Tinea nigra".)

MICROBIOLOGY — Dermatophytes are filamentous fungi in the genera Trichophyton, Microsporum, and Epidermophyton. Dermatophytes metabolize and subsist upon keratin in the skin, hair, and nails.

CLINICAL SUBTYPES — The major clinical subtypes of dermatophyte infections include infections of the epidermis, hair, and nails.

●Epidermis

•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, proximal inner thighs, or buttocks

•Tinea faciei – Infection of the face

•Tinea manuum – Infection of the hand

●Hair

•Tinea capitis – Infection of scalp hair

•Tinea barbae – Infection of beard hair

●Nails

•Dermatophyte onychomycosis (tinea unguium)

Majocchi's granuloma is an additional subtype of dermatophyte infection characterized by the spread of epidermal infection into deep portions of the hair follicle and dermis. (See "Infectious folliculitis", section on 'Dermatophytic folliculitis'.)

DIAGNOSIS — Cutaneous dermatophyte infections may be strongly suspected based upon the physical examination. However, because the physical findings can overlap with other cutaneous disorders, we typically confirm the diagnosis with testing.

●Physical examination – A careful physical examination of the affected areas allows for recognition of findings consistent with or inconsistent with the suspected dermatophyte infection. (See 'Tinea pedis' below and 'Tinea corporis' below and 'Tinea cruris' below and 'Other clinical variants' below.)

Because the simultaneous presence of more than one type of dermatophyte infection is not uncommon (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.

●Diagnostic tests – The approach to diagnostic testing differs based upon the suspected type of infection.

•Epidermal infections (eg, tinea pedis, tinea corporis, tinea cruris) – A potassium hydroxide (KOH) preparation performed with skin scrapings from the affected areas is the primary method of confirming dermatophyte infections of the epidermis (eg, tinea corporis, tinea pedis, tinea cruris, tinea manuum, tinea faciei) (algorithm 1). A major advantage of the KOH preparation is the rapid availability of results, as the test can be performed by the evaluating clinician. Fungal culture is an alternative, albeit slower, method for diagnosis. (See "Office-based dermatologic diagnostic procedures", section on 'Potassium hydroxide preparation' and "Office-based dermatologic diagnostic procedures", section on 'Fungal culture'.)

The detection of segmented hyphae on a KOH preparation confirms a dermatophyte infection (picture 7A-B). This finding should be distinguished from the findings of budding yeasts, pseudohyphae, and septate hyphae on a KOH preparation from Candida infection (picture 8A-B) and the short hyphae and yeast cells found in a KOH preparation from tinea versicolor (picture 9). Clinician experience and proper technique influence the diagnostic accuracy of a KOH preparation [4]. The technique for performing a KOH preparation is reviewed separately. (See "Office-based dermatologic diagnostic procedures", section on 'Potassium hydroxide preparation'.)

Collection of an adequate specimen for a KOH preparation or fungal culture is important. In patients with tinea corporis or tinea cruris, the highest yield may be obtained from skin scrapings taken from the active border of a plaque or patch. In vesicobullous tinea pedis, the roof of a vesicle can provide an adequate specimen.

Polymerase chain reaction (PCR) tests have an emerging role in the diagnosis of dermatophytoses. (See "Onychomycosis: Epidemiology, clinical features, and diagnosis", section on 'Polymerase chain reaction'.)

•Hair or nail infections – The approach to the diagnosis of infections of the hair or nails is reviewed separately.

-(See "Tinea capitis", section on 'Diagnosis'.)

-(See "Infectious folliculitis", section on 'Diagnosis'.)

-(See "Onychomycosis: Epidemiology, clinical features, and diagnosis", section on 'Diagnosis'.)

COMPLICATIONS — Potential complications of dermatophyte infection include secondary bacterial infection, tinea incognito, Majocchi's granuloma, and id reactions.

Secondary infection — Secondary bacterial infection can occur in association with dermatophyte infections, particularly in moist or occluded skin areas (eg, the feet) [5]. Patients who exhibit significant erosions, ulceration, pain, or malodor in the affected area should have a Gram stain and culture to evaluate for secondary bacterial infection. (See 'Tinea pedis' below.)

Tinea incognito and Majocchi's granuloma — Misdiagnosis of a dermatophyte infection as a corticosteroid-responsive dermatosis (eg, eczema) may result in the inadvertent use of topical corticosteroids for treatment. The local immunosuppressive effects of topical corticosteroids can exacerbate dermatophyte infections and alter the clinical findings, making diagnosis more difficult (ie, tinea incognito) [6]. Alterations to the clinical presentation may include diminished erythema and scale or loss of a well-defined border.

Although the term "tinea incognito" is extensively used in the literature, it is grammatically incorrect according to Latin grammar rules [7,8]. The grammatically correct term, "tinea incognita," is also used.

In addition, topical corticosteroid use may promote extension of the infection into the hair follicle and dermis, resulting in Majocchi's granuloma, which requires oral antifungal treatment [9]. Similarly, in immunosuppressed patients, the depression of cell-mediated immunity and the inflammatory response may contribute to progression of epidermal dermatophyte infections to Majocchi's granuloma [10-13]. (See "Infectious folliculitis", section on 'Dermatophytic folliculitis'.)

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 [14].

Dermatophytid reactions can occur in patients with tinea pedis, tinea manuum, tinea cruris, tinea corporis, or tinea capitis [14-16]. Patients typically present with pruritic, papulovesicular eruptions that can be quite distant from the site of infection (picture 10A-B).

In one series of 213 patients with tinea pedis, 37 patients (17 percent) were diagnosed with dermatophytid reactions characterized by vesicular eruptions on the hands [17]. 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 [14].

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.

TREATMENT PRINCIPLES — Treatment of dermatophyte infections is generally indicated. Treatment is given to alleviate symptoms (eg, pruritus), reduce risk for secondary bacterial infection, and limit spread of the infection to other body sites or other individuals.

Treatment options — Treatment consists of topical or systemic antifungal drugs with antidermatophyte activity (algorithm 1).

Most cutaneous dermatophyte infections limited to the epidermis can be managed with topical antifungal therapy. Examples of agents effective for dermatophyte infections include azoles, allylamines, butenafine, ciclopirox, and tolnaftate (table 1).

Oral treatment with agents such as terbinafine, itraconazole, fluconazole, and griseofulvin is used for extensive infections, infections that are refractory to topical therapy, or infections extending into follicles or the dermis (eg, tinea capitis, tinea barbae, Majocchi's granuloma) or involving nails. Oral therapy is typically reserved for these presentations because of the broader side effect profile compared with topical therapy. Cutaneous adverse reactions, hepatotoxicity, and drug interactions are among the potential complications of oral antifungal therapy. (See "Terbinafine (systemic): Drug information" and "Itraconazole: Drug information" and "Fluconazole: Drug information" and "Griseofulvin: Drug information".)

Use of oral ketoconazole is no longer recommended because of risk for severe liver injury, adrenal insufficiency, and drug interactions. (See "Pharmacology of azoles", section on 'Ketoconazole'.)

Nystatin ineffective — Nystatin, an effective treatment for cutaneous Candida infections, is not effective for dermatophyte infections.

Adjunctive corticosteroid therapy — In general, we do not use topical corticosteroids in the treatment of dermatophyte infections. Although combination antifungal and low-potency corticosteroid products can be effective and may accelerate resolution of the clinical manifestations of superficial dermatophyte infections [18], combination therapy is not necessary for achieving cure. In particular, use of products that include medium- or high-potency corticosteroids (eg, betamethasone-clotrimazole) is discouraged because use of a topical corticosteroid introduces risk for topical corticosteroid-induced skin atrophy. Treatment failures have also been reported [19-21], and some authors postulate that overuse of topical corticosteroids may contribute to the emergence of resistant dermatophyte infections. (See 'Treatment failure' below.)

An infrequent exception to our avoidance of combination therapy is the addition of a low-potency topical corticosteroid (group 6 or 7) to antifungal therapy for patients with highly inflammatory lesions associated with severe pruritus (table 2). Some topical antifungal drugs (eg, allylamines and ciclopirox) have intrinsic anti-inflammatory properties that may also help to reduce inflammation [22,23].

Treatment failure — Dermatophyte infections usually respond well to a course of appropriate treatment.

●Patient assessment – Common reasons for failure to respond to antifungal therapy include inadequate administration of treatment (eg, stopping treatment as visible scale resolves) or an incorrect diagnosis (algorithm 1). Therefore, an evaluation of apparent treatment failure should include discussion of the use of the prescribed therapy and consideration of alternative diagnoses. The possibility of reinfection should also be reviewed.

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, treatment-refractory disease. (See "Initial evaluation of adults with HIV", section on 'Physical examination'.)

●Antifungal resistance – Emerging resistance of dermatophyte infections to antifungal therapy may account for some treatment failures. Terbinafine resistance secondary to single point mutations in the squalene oxidase gene has been reported most frequently [24]. Examples of other proposed mechanisms for resistance to antifungal therapies include upregulation of efflux pumps and mutations in the lanosterol-14-alpha demethylase gene [24]. Although not routinely performed in many locations, susceptibility testing may be of value for patients with confirmed dermatophyte infections that fail to respond to appropriate course of treatment [24].

•Trichophyton indotineae – Trichophyton indotineae is a highly transmissible species of dermatophyte that is often associated with resistance to antifungal therapy, particularly terbinafine [25,26]. Infections have been reported in Asia, Europe, North America, and the Middle East [27]. Infections most often present as annular, inflamed, scaly plaques on multiple body areas (tinea corporis, tinea cruris, and/or tinea faciei) [25,27].

T. indotineae cannot be identified through routine laboratory techniques due to morphologic similarities among T. indotineae, Trichophyton mentagrophytes, and Trichophyton interdigitale. Genomic sequencing is required for identification. Misuse and overuse of topical antifungal drugs and topical corticosteroids are proposed to contribute to the spread of resistant T. indotineae infections [25,26].

TINEA PEDIS

Overview — Tinea pedis (also known as athlete's foot) is a dermatophyte infection of the skin on the foot.

●Etiology and risk factors – Tinea pedis usually occurs in adults and adolescents and is rare prior to puberty [28]. Common causes are Trichophyton rubrum, T. mentagrophytes/interdigitale complex, 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. Other predisposing factors may include diabetes mellitus and the wearing of occlusive footwear [29-31].

●Clinical features – Tinea pedis may manifest in a variety of ways. The three major clinical types of tinea pedis are:

•Interdigital tinea pedis – Interdigital tinea pedis manifests as pruritic erosions or scales between the toes, especially in the third and fourth digital interspaces (picture 1A). 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 1B). 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 (picture 1C-D). Underlying erythema may be evident. The medial foot is often affected.

Infrequently, tinea pedis may manifest with interdigital erosions and ulcers (ulcerative tinea pedis) (picture 11A-B). This presentation is usually associated with secondary bacterial infection.

Tinea pedis can occur in association with onychomycosis, tinea cruris, or tinea manuum (picture 12A).

Differential diagnosis — The differential diagnosis of tinea pedis is broad and varies according to the clinical subtype.

●Interdigital tinea pedis

•Erythrasma (picture 13)

•Interdigital Candida infection (erosio interdigitalis blastomycetica (picture 14))

●Hyperkeratotic (moccasin-type) tinea pedis

•Atopic dermatitis

•Chronic contact dermatitis (picture 15)

•Chronic palmoplantar (dyshidrotic) eczema (picture 16)

•Palmoplantar psoriasis (picture 17)

•Pitted keratolysis (picture 18)

•Juvenile plantar dermatosis (picture 19A-B) (see "Overview of dermatitis (eczematous dermatoses)", section on 'Juvenile plantar dermatosis')

•Keratolysis exfoliativa (picture 20) (see "Peeling skin syndromes", section on 'Keratolysis exfoliativa')

•Keratodermas (see "Palmoplantar keratoderma")

●Vesiculobullous (inflammatory) tinea pedis

•Acute palmoplantar (dyshidrotic) eczema (picture 21)

•Acute contact dermatitis

•Palmoplantar pustulosis (picture 22)

•Scabies (picture 23)

A positive potassium hydroxide (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 8A-B). (See 'Diagnosis' above.)

Treatment — Topical antifungal therapy is the treatment of choice for most patients. Systemic antifungal agents are primarily reserved for patients who fail topical therapy (algorithm 1).

●Initial treatment – Examples of topical drugs effective for tinea pedis include azoles, allylamines, butenafine, ciclopirox, tolnaftate, and amorolfine (table 1). Topical nystatin is not effective for dermatophyte infections. Amorolfine is not available in the United States. (See 'Treatment principles' above.)

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 [32].

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 [33]. 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) [33].

●Refractory disease – Patients with confirmed tinea pedis who fail topical therapy may be treated with an oral antifungal drug. Potential causes of treatment failure should be reviewed. (See 'Treatment failure' above.)

•Adult dosing – Adults are usually treated with terbinafine, itraconazole, or fluconazole. Typical treatment regimens for adults are provide in a table (table 3) [34].

Griseofulvin, an oral antifungal agent frequently used for tinea capitis in children, can also treat tinea pedis but requires a longer duration of daily therapy [34]. Typical adult doses of griseofulvin are listed in a table (table 3).

Patient comorbidities, risk for drug interactions, and regimen preference influence the selection of an oral antifungal therapy. Differences in efficacy among most of the oral antifungal drugs used for tinea pedis have not been identified; however, many trials may have been underpowered to detect such differences [35,36]. Findings from a systematic review that identified two small, randomized trials that compared griseofulvin with terbinafine suggest greater efficacy of four- or six-week courses of terbinafine 250 mg per day compared with four- or six-week courses of griseofulvin 500 mg per day (risk ratio 2.26, 95% CI 1.49-3.44) [35]. However, these small trials assessed a longer duration of terbinafine treatment and a lower dose of griseofulvin than is often used for tinea pedis.

•Pediatric dosing – Dosing for children is weight based, with similar durations of treatment compared with adults. Typical pediatric doses are provided in a table (table 3).

●Adjunctive therapy for scale and maceration – In our experience, patients with hyperkeratotic tinea pedis may benefit from combining antifungal treatment with a topical keratolytic agent, such as salicylic acid, to accelerate resolution of scale. However, the addition of a keratolytic agent is not necessary for successful treatment of the infection.

Patients with significant vesiculation or maceration may benefit from Burow solution (at a dose of 1% aluminum acetate or 5% aluminum subacetate) wet dressings to reduce moisture and maceration. The wet dressings can be applied for 20 minutes two to three times per day. Placing gauze or cotton between toes may also be helpful.

●Prevention – Interventions that may help to reduce recurrences include use of socks with wick-away material, use of desiccating foot powders, treatment of hyperhidrosis if there is a history of moist feet, treatment of shoes with antifungal powder, and avoidance of occlusive footwear.

TINEA CORPORIS

Overview — The term "tinea corporis" refers to epidermal dermatophyte infections in sites other than the feet, groin, face, or hand.

●Etiology and risk factors – T. rubrum is the most common cause of tinea corporis. Other notable causes include Trichophyton tonsurans, Microsporum canis, T. mentagrophytes/interdigitale complex, T. indotineae, 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 [37].

●Clinical features – Tinea corporis often begins as a pruritic, circular or oval, erythematous or hyperpigmented, 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 2A-D)). Multiple plaques may coalesce (picture 24A-B). Pustules occasionally appear (picture 25).

Extensive tinea corporis should prompt consideration of an underlying immune disorder, such as HIV, or for diabetes.

Differential diagnosis — Examples of features that should prompt consideration of alternative diagnoses include extensive skin involvement and an absence of scale. A positive potassium hydroxide (KOH) preparation distinguishes tinea corporis.

Tinea corporis may be confused with other annular skin eruptions, particularly subacute cutaneous lupus erythematosus, granuloma annulare, and erythema annulare centrifugum.

●Subacute cutaneous lupus erythematosus – Subacute cutaneous lupus erythematosus is a subtype of cutaneous lupus erythematous that can manifest as annular or polycyclic, scaly plaques on sun-exposed skin (picture 26). Subacute cutaneous lupus erythematosus can be idiopathic or occur in association with systemic lupus erythematosus or drug exposure. (See "Overview of cutaneous lupus erythematosus", section on 'Subacute cutaneous lupus erythematosus'.)

●Granuloma annulare – Granuloma annulare is a benign, inflammatory condition that classically presents with one or more erythematous or violaceous, annular plaques on the extremities (picture 27A-C). Unlike tinea corporis, scale is absent. (See "Granuloma annulare: Epidemiology, clinical manifestations, and diagnosis".)

●Erythema annulare centrifugum – Erythema annulare centrifugum, an inflammatory skin disorder of unknown etiology, exhibits annular plaques (picture 28A-B). A trailing rim of scale is often evident in the superficial variant of this disorder. (See "Erythema annulare centrifugum".)

Other disorders, such as nummular eczema (picture 29A-B), psoriasis, pityriasis rosea (picture 30A-B), and disciform erythrasma (picture 31), may also exhibit scaling plaques that resemble tinea corporis. (See "Approach to the patient with annular skin lesions".)

Treatment — The extent of skin involvement with tinea corporis influences the approach to treatment (algorithm 1).

●Limited disease – Tinea corporis usually responds well to topical antifungal drugs, such as azoles, allylamines, butenafine, ciclopirox, tolnaftate, and amorolfine (table 1) [18,38]. Topical nystatin is not effective for dermatophyte infections. Amorolfine is not available in the United States.

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.

The topical antifungal agents listed above are all considered effective. Pooled data from randomized trials supports the efficacy of two allylamines, terbinafine and naftifine, for tinea corporis and tinea cruris [18]. There are also data that suggest similar efficacy of topical allylamines and topical azoles [18].

●Extensive or refractory disease – Oral treatment is an alternative for patients with extensive skin involvement and patients who fail topical therapy. Potential causes of treatment failure should be reviewed. (See 'Treatment failure' above.)

•Treatment options – Terbinafine and itraconazole are common treatments. Griseofulvin and fluconazole can also be effective but may require longer courses of therapy. Small, randomized trials support the efficacy of these oral antifungal therapies [39-43]. Patient comorbidities, risk for drug interactions, and regimen preference influence the selection of an initial oral therapy.

•Impact of antifungal resistance – Although historically all four major oral antifungal therapies used for tinea corporis and tinea cruris have been considered effective for tinea corporis and tinea cruris [43], local resistance patterns may impact treatment efficacy, particularly given the increasing prevalence of T. indotineae. Where available, susceptibility testing is helpful for treatment selection after treatment failure. (See 'Treatment failure' above.)

-In a trial performed in 2017 and 2018 in India, 200 adults and children with chronic (≥3 months) or chronically relapsing tinea corporis, tinea cruris, or tinea faciei were randomly assigned to treatment with fluconazole (approximately 5 mg/kg per day), griseofulvin microsize (approximately 10 mg/kg per day in two divided doses), itraconazole (approximately 5 mg/kg per day), or terbinafine (approximately 7.5 mg/kg per day) [44]. Doses were rounded to the nearest half-tablet or capsule dose, and treatment was given for up to eight weeks. At week 4, all four treatments were similarly ineffective for achieving complete clinical cure plus negative KOH microscopy, with cure rates ≤8 percent in all groups. At week 8, itraconazole was more effective than fluconazole, terbinafine, and griseofulvin (cure in 66, 42, 38, and 14 percent of patients, respectively). Fluconazole was also more effective than griseofulvin. (See 'Treatment failure' above.)

•Adult dosing – Reasonable regimens in adults are provided in a table (table 4).

Longer courses may be necessary in some cases [43,45].

•Pediatric dosing – Children are treated for similar durations as adults. Reasonable pediatric doses are provided in a table (table 4).

•Role of newer oral antifungal drugs – Use of newer antifungal agents, such as posaconazole, voriconazole, and fosravuconazole, for patients with tinea corporis or tinea cruris resistant to standard oral antifungal therapies has been reported [46-49]. These therapies are reserved for infections that cannot be treated with standard therapy. (See "Pharmacology of azoles".)

TINEA CRURIS

Overview — Tinea cruris (also known as jock itch) is a dermatophyte infection involving the crural fold.

●Etiology and risk factors – The most common cause is T. rubrum. Other frequent causes include E. floccosum, T. mentagrophytes/interdigitale complex, and T. indotineae.

Tinea cruris is far more common in males than females. 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 or hyperpigmented patch on the proximal medial thigh. The infection spreads centrifugally, with partial central clearing and a slightly elevated, erythematous or hyperpigmented, sharply demarcated border (picture 3A-E).

Infection may spread to the perineum and perianal areas, into the gluteal cleft, or onto the buttocks. In males, the scrotum is typically spared.

Differential diagnosis — Other common skin disorders that may present with erythematous patches or plaques in the inguinal region include:

●Candidal intertrigo – Candidiasis is suggested by inflamed patches with satellite papules and pustules (picture 32). Candidal pseudohyphae, hyphae, and yeast cells are seen on potassium hydroxide (KOH) preparation (picture 8A-B). In contrast to tinea cruris, scrotal involvement is common in males with candidiasis of the crural folds. (See "Intertrigo".)

●Seborrheic dermatitis – Intertriginous seborrheic dermatitis may present as moist, erythematous, or hyperpigmented patches in the genitocrural area (picture 33). Patients may also have findings of seborrheic dermatitis in other body areas. (See "Seborrheic dermatitis in adolescents and adults".)

●Inverse psoriasis – Inverse psoriasis typically presents as smooth, shiny plaques with absent or minimal scale in intertriginous areas (picture 34A-B). Patients may or may not have psoriasis in other body areas. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Inverse (intertriginous) psoriasis'.)

●Erythrasma – Erythrasma is a superficial bacterial infection of the skin caused by Corynebacterium minutissimum. Intertriginous involvement may present as erythematous to brown patches or thin plaques (picture 35A-B). The detection of coral red fluorescence during examination with a Wood's lamp can confirm the diagnosis (picture 36). (See "Erythrasma".)

A KOH preparation positive for hyphae rules out nonfungal disorders. (See 'Diagnosis' above.)

Treatment — Treatment is similar to treatment of tinea corporis (algorithm 1).

●Initial therapy – Topical therapy with antifungal agents, such as azoles, allylamines, butenafine, ciclopirox, tolnaftate, or amorolfine, is effective (table 1) [18,38]. Nystatin is not effective for dermatophyte infections. (See 'Tinea corporis' above.)

●Extensive or refractory to topical therapy – 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.)

Potential causes for treatment failure should be reviewed. (See 'Treatment failure' above.)

●Prevention – 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 or drying lotions in the inguinal area and avoidance of tight-fitting clothing and noncotton underwear.

OTHER CLINICAL VARIANTS — Various other terms are used to describe additional clinical subtypes of dermatophyte infection.

Onychomycosis — Dermatophyte infection is a common cause of onychomycosis (fungal infection of the nail). Clinical manifestations include nail discoloration, subungual hyperkeratosis, and other forms of nail dystrophy (picture 5). Onychomycosis is reviewed separately. (See "Onychomycosis: Epidemiology, clinical features, and diagnosis" and "Onychomycosis: Management".)

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 37) [28]. Tinea faciei is managed similarly to tinea corporis. (See 'Tinea corporis' above.)

Tinea manuum — Tinea manuum is a 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 12A-B). This clinical presentation is often referred to as "two feet-one hand syndrome." The approach to treatment is similar to tinea pedis. (See 'Tinea pedis' above.)

Tinea capitis — Tinea capitis, a dermatophyte infection of scalp hair, usually occurs in small children (picture 4A-B). 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 males (picture 38A-B). Oral antifungal therapy is necessary. Tinea barbae is reviewed separately. (See "Infectious folliculitis", section on 'Dermatophytic folliculitis' and "Infectious folliculitis", section on 'Management'.)

Majocchi's granuloma — Majocchi's granuloma is an uncommon subtype of dermatophyte infection in which the dermatophyte invades the deep follicle and dermis. The clinical findings are typically characterized by a localized area with erythematous or hyperpigmented, perifollicular papules or small nodules (picture 6A-C). Pustules may also be present.

Treatment consists of oral antifungal therapy. Majocchi's granuloma is reviewed separately. (See "Infectious folliculitis", section on 'Dermatophytic folliculitis' and "Infectious folliculitis", section on 'Management'.)

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 39A-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 [50]. Systemic therapy is often combined with a topical keratolytic agent.

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 5^th to 6^th 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 12^th 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

●Overview – 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 (picture 1A-C), tinea corporis (picture 2A-D), tinea cruris (picture 3A-E), tinea capitis, and onychomycosis. (See 'Microbiology' above and 'Tinea pedis' above and 'Tinea corporis' above and 'Tinea cruris' above and 'Other clinical variants' above.)

●Diagnosis – A diagnosis of a cutaneous dermatophyte infection may be strongly suspected based upon the clinical findings. A potassium hydroxide (KOH) preparation can be used to confirm the diagnosis (picture 7A). (See 'Diagnosis' above.)

●Treatment principles

•General approach – Treatment of tinea pedis, tinea corporis, and tinea cruris is indicated to alleviate symptoms (eg, pruritus), reduce risk for secondary bacterial infection, and limit spread of the infection to other body sites or other individuals.

Most dermatophyte infections can be managed with topical antifungal treatments. Oral therapy is typically reserved for refractory or extensive infections because of the broader adverse effect profile compared with topical therapy. (See 'Treatment options' above.)

•Inefficacy of nystatin – Nystatin is not effective for dermatophyte infections. (See 'Nystatin ineffective' above.)

•Adjunctive corticosteroids – Adjunctive topical corticosteroid therapy is not indicated for most patients. However, for patients with highly inflammatory lesions who require relief from severe pruritus, we suggest the addition of a low-potency topical corticosteroid (group 6 or 7 (table 2)) to antifungal therapy (Grade 2C). We avoid use of products containing medium-potency or high-potency topical corticosteroids (eg, betamethasone-clotrimazole).

Topical corticosteroid therapy is not necessary for cure and introduces risk for topical corticosteroid-induced skin atrophy. Overuse of topical corticosteroids is also postulated to contribute to the emergence of antifungal resistance. (See 'Adjunctive corticosteroid therapy' above.)

•Treatment failure – When topical therapy fails to resolve a dermatophyte infection, potential reasons for treatment failure should be reviewed. Common reasons for treatment failure include inadequate administration of treatment and an incorrect diagnosis (algorithm 1). The possibilities of reinfection and antifungal resistance should also be reviewed. (See 'Treatment failure' above.)

●Treatment of tinea pedis

•Initial therapy – For patients with tinea pedis, we suggest initial treatment with a topical antifungal drug with antidermatophyte activity rather than oral antifungal therapy (algorithm 1) (Grade 2C). Examples of effective topical antifungal agents are azoles, allylamines, ciclopirox, butenafine, and tolnaftate (table 1). Topical antifungal treatment is generally applied once or twice daily and continued for four weeks. Topical nystatin is not effective. (See 'Treatment' above.)

•Refractory infections – For patients with tinea pedis refractory to topical therapy, we suggest treatment with oral terbinafine, oral itraconazole, or oral fluconazole rather than oral griseofulvin (table 3) (Grade 2C). Griseofulvin is a reasonable alternative but may require a longer duration of daily treatment compared with terbinafine and itraconazole. Selection among these therapies is based upon consideration of patient comorbidities, risk for drug interactions, and regimen preference. (See 'Treatment' above.)

●Treatment of tinea corporis or tinea cruris

•Initial therapy – For most patients with tinea corporis or tinea cruris, we suggest initial treatment with a topical antifungal drug with antidermatophyte activity rather than oral antifungal therapy (algorithm 1) (Grade 2C). Examples of effective topical antifungal agents are azoles, allylamines, ciclopirox, butenafine, and tolnaftate (table 1). Topical antifungal treatment is generally administered once or twice per day for one to three weeks. Topical nystatin is not effective. (See 'Treatment' above.)

•Extensive infections or refractory infections – For patients with extensive tinea corporis or tinea cruris or patients with infections refractory to topical therapy, we suggest oral antifungal therapy rather than topical antifungal therapy (algorithm 1) (Grade 2C). Options include oral terbinafine, itraconazole, fluconazole, and griseofulvin (table 4).

In the absence of known resistance to specific oral antifungal therapies, we treat most patients with terbinafine, itraconazole, or fluconazole because of the longer course of daily treatment associated with griseofulvin compared with terbinafine and itraconazole. Selection among these therapies is based upon consideration of patient comorbidities, risk for drug interactions, and regimen preference.

In the event of oral antifungal treatment failure, susceptibility testing (where available) is helpful for selecting subsequent therapy. (See 'Treatment' above and 'Treatment failure' above.)