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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 , 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 . 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
•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')
●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 non-fungal 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 . 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 0.42-0.94) . 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 .
●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 . In a systematic review, terbinafine was found more effective than griseofulvin, while the efficacy of terbinafine and itraconazole were similar . 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 .
Dosing for children is weight-based with durations of treatment similar to adults. Typical pediatric doses for oral therapy include:
•10 to 20 kg: 62.5 mg per day
•20 to 40 kg: 125 mg per day
•Above 40 kg: 250 mg per day
•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 , such as wrestlers (tinea corporis gladiatorum). T. tonsurans is a common cause of tinea corporis gladiatorum .
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 "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 "Mucocutaneous manifestations of systemic 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 . There are also data that suggest similar efficacy of topical allylamines and topical azoles . 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 :
●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:
•10 to 20 kg: 62.5 mg per day
•20 to 40 kg: 125 mg per day
•Above 40 kg: 250 mg per day
•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 tight-fitting 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 .
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.
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 . 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 . Treatment regimens with griseofulvin and daily itraconazole have also been suggested .
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) . 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 . 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 .
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 . 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 .
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 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.)
●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.)
- Havlickova B, Czaika VA, Friedrich M. Epidemiological trends in skin mycoses worldwide. Mycoses 2008; 51 Suppl 4:2.
- Seebacher C, Bouchara JP, Mignon B. Updates on the epidemiology of dermatophyte infections. Mycopathologia 2008; 166:335.
- Ameen M. Epidemiology of superficial fungal infections. Clin Dermatol 2010; 28:197.
- 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.
- Alston SJ, Cohen BA, Braun M. Persistent and recurrent tinea corporis in children treated with combination antifungal/ corticosteroid agents. Pediatrics 2003; 111:201.
- 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.
- Rosen T, Elewski BE. Failure of clotrimazole-betamethasone dipropionate cream in treatment of Microsporum canis infections. J Am Acad Dermatol 1995; 32:1050.
- Hawkins DM, Smidt AC. Superficial fungal infections in children. Pediatr Clin North Am 2014; 61:443.
- Crawford F, Hollis S. Topical treatments for fungal infections of the skin and nails of the foot. Cochrane Database Syst Rev 2007; :CD001434.
- 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.
- Gupta AK, Cooper EA. Update in antifungal therapy of dermatophytosis. Mycopathologia 2008; 166:353.
- 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.
- Shiraki Y, Hiruma M, Hirose N, et al. A nationwide survey of Trichophyton tonsurans infection among combat sport club members in Japan using a questionnaire form and the hairbrush method. J Am Acad Dermatol 2006; 54:622.
- Adams BB. Tinea corporis gladiatorum. J Am Acad Dermatol 2002; 47:286.
- 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.
- 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.
- Cole GW, Stricklin G. A comparison of a new oral antifungal, terbinafine, with griseofulvin as therapy for tinea corporis. Arch Dermatol 1989; 125:1537.
- 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.
- 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.
- Elewski BE, Hughey LC, Sobera JO. Fungal diseases. In: Dermatology, 3rd ed, Bolognia JL, Jorizzo JL, Schaffer JV (Eds), Elsevier Limited, Philadelphia; London 2012. Vol 2, p.1251.
- 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.
- Farag A, Taha M, Halim S. One-week therapy with oral terbinafine in cases of tinea cruris/corporis. Br J Dermatol 1994; 131:684.
- Smith KJ, Neafie RC, Skelton HG 3rd, et al. Majocchi's granuloma. J Cutan Pathol 1991; 18:28.
- Gill M, Sachdeva B, Gill PS, et al. Majocchi's granuloma of the face in an immunocompetent patient. J Dermatol 2007; 34:702.
- Cho HR, Lee MH, Haw CR. Majocchi's granuloma of the scrotum. Mycoses 2007; 50:520.
- 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.
- Kim ST, Baek JW, Kim TK, et al. Majocchi's granuloma in a woman with iatrogenic Cushing's syndrome. J Dermatol 2008; 35:789.
- 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.
- Jacobs PH. Majocchi's granuloma (due to therapy with steroid and occlusion). Cutis 1986; 38:23.
- Elgart ML. Tinea incognito: an update on Majocchi granuloma. Dermatol Clin 1996; 14:51.
- Elmets CA. Management of common superficial fungal infections in patients with AIDS. J Am Acad Dermatol 1994; 31:S60.
- Gupta S, Kumar B, Radotra BD, Rai R. Majocchi's granuloma trichophyticum in an immunocompromised patient. Int J Dermatol 2000; 39:140.
- Burg M, Jaekel D, Kiss E, Kliem V. Majocchi's granuloma after kidney transplantation. Exp Clin Transplant 2006; 4:518.
- Liao YH, Chu SH, Hsiao GH, et al. Majocchi's granuloma caused by Trichophyton tonsurans in a cardiac transplant recipient. Br J Dermatol 1999; 140:1194.
- 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.
- Feng WW, Chen HC, Chen HC. Majocchi's granuloma in a 3-year-old boy. Pediatr Infect Dis J 2006; 25:658.
- Sequeira M, Burdick AE, Elgart GW, Berman B. New-onset Majocchi's granuloma in two kidney transplant recipients under tacrolimus treatment. J Am Acad Dermatol 1998; 38:486.
- Gupta AK, Prussick R, Sibbald RG, Knowles SR. Terbinafine in the treatment of Majocchi's granuloma. Int J Dermatol 1995; 34:489.
- McMichael A, Sanchez DG, Kelly P. Folliculitis and the follicular occlusion tetrad. In: Dermatology, 2nd ed, Bolognia JL, Jorizzo JL, Rapini RP (Eds), Elsevier Limited, St. Louis 2008.
- Gupta AK, Groen K, Woestenborghs R, De Doncker P. Itraconazole pulse therapy is effective in the treatment of Majocchi's granuloma: a clinical and pharmacokinetic evaluation and implications for possible effectiveness in tinea capitis. Clin Exp Dermatol 1998; 23:103.
- Bonifaz A, Vázquez-González D. Tinea imbricata in the Americas. Curr Opin Infect Dis 2011; 24:106.
- Cheng N, Rucker Wright D, Cohen BA. Dermatophytid in tinea capitis: rarely reported common phenomenon with clinical implications. Pediatrics 2011; 128:e453.
- Veien NK, Hattel T, Laurberg G. Plantar Trichophyton rubrum infections may cause dermatophytids on the hands. Acta Derm Venereol 1994; 74:403.
- 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.
- Al Aboud K, Al Hawsawi K, Alfadley A. Tinea incognito on the hand causing a facial dermatophytid reaction. Acta Derm Venereol 2003; 83:59.
- Gianni C, Betti R, Crosti C. Psoriasiform id reaction in tinea corporis. Mycoses 1996; 39:307.
- Derebery J, Berliner KI. Foot and ear disease--the dermatophytid reaction in otology. Laryngoscope 1996; 106:181.
- Iglesias ME, España A, Idoate MA, Quintanilla E. Generalized skin reaction following tinea pedis (dermatophytids). J Dermatol 1994; 21:31.