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Dermatophyte (tinea) infections
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Dermatophyte (tinea) infections

Disclosures: Adam O Goldstein, MD, MPH Nothing to disclose. Beth G Goldstein, MD Nothing to disclose. Robert P Dellavalle, MD, PhD, MSPH Nothing to disclose. Moise L Levy, MD Grant/Research/Clinical Trial Support: Anacor [atopic dermatitis (investigational drug)]; Stiefel/GlaxoSmithKline [psoriasis (calcipotriene foam)]. Consultant/Advisory Boards: Galderma [acne (adapalene/benzoyl peroxide)]; Anacor [atopic dermatitis (investigational drug)]; Promius [atopic dermatitis (investigational drug)]. Patent Holder: Incontinentia pigmenti (NEMO gene mutations). Ted Rosen, MD Consultant/Advisory Boards: Anacor [Onychmycosis (Tavaborole)]; Valeant [Onychmycosis (Efinaconazole)]; Leo [Actinic keratosis]. Abena O Ofori, MD Nothing to disclose.

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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2015. | This topic last updated: Apr 01, 2015.

INTRODUCTION — Dermatophyte infections are common disorders worldwide, and dermatophytes represent the prevailing type of fungi that cause infection of the skin and nails [1-3]. These infections lead to a variety of clinical manifestations, including tinea capitis, tinea pedis, tinea corporis, tinea cruris, and Majocchi’s granuloma.

This topic discusses the clinical features, diagnosis, and treatment of dermatophyte infections of the skin. Dermatophyte infections of the hair and nails are discussed separately. (See "Tinea capitis" and "Onychomycosis".)

OVERVIEW — Three types of dermatophytes account for the majority of infections: Epidermophyton, Trichophyton, and Microsporum. Dermatophytoses have varied presentations, are named by location, and have similar treatments.

Dermatophytes have acquired in the evolutionary process the ability to metabolize and subsist upon keratin, a protein resistant to most other organisms. The fungi attack skin, nails, and hair, where keratin is the major structural protein, leading to a wide variety of disease states.

The major types of dermatophyte infections include: involvement of the scalp (tinea capitis), feet (tinea pedis), groin (tinea cruris), and other body surfaces (tinea corporis). These are typically superficial, involving the epidermis. However, in some patients dermatophyte infections may penetrate the hair follicle and involve the dermis; this condition is termed Majocchi's granuloma. The diagnosis and management of the more common types of infestations are described here.

Dermatophyte infections routinely affect individuals who are otherwise healthy, but people with compromised immune systems are particularly susceptible. Bizarre presentations and failure to respond to treatment should alert care providers to the possibility of an underlying immunologic problem [4].

One of the most important considerations when evaluating superficial dermatophyte infections is confirming the diagnosis with a laboratory specimen, either a potassium hydroxide (KOH) preparation or culture. (See "Dermatologic procedures", section on 'Potassium hydroxide (KOH) prep'.)

A common mistake that many clinicians make is to prescribe combination antifungal corticosteroid products (eg, Lotrisone) for the treatment of common fungal skin infections without confirming the diagnosis. This course of action is not recommended for several reasons:

Topical corticosteroids can exacerbate tinea infections and may contribute to treatment failure, especially when infections are due to Microsporum species [5-7]. If the patient fails to improve, it is unclear why, and the use of a potent corticosteroid preparation in a combination product may alter the clinical appearance of a dermatophyte infection. This makes the diagnosis of the underlying disease more difficult. Lotrisone contains clotrimazole and betamethasone dipropionate, a high potency topical corticosteroid.

Some conditions, like tinea cruris, may require antifungal treatment for several weeks; using a combination product puts the patient at risk unnecessarily for side effects, such as skin atrophy, from topical corticosteroids.

Combination products are far more expensive than simple antifungal agents, or even generically available corticosteroid preparations. In one study, nondermatologists were more likely than dermatologists to prescribe combination products (34 versus 4 percent), leading to excess medical costs of $10 to 25 million [8].

In addition, clinicians should avoid the use of nystatin for the treatment of tinea infections. Nystatin is effective for cutaneous candidal infections, but not for the treatment of dermatophytes.

TINEA PEDIS — Tinea pedis (athlete's foot) is the most common dermatophyte infection encountered in practice. It is often accompanied by tinea manuum, onychomycosis (tinea unguium), or tinea cruris (dermatophyte infection of the hands, nails, or groin).

Tinea pedis presents in two readily distinguishable clinical forms, acute and chronic. Both are contagious, contracted by contact with arthrospores shed by infected individuals onto the floors of swimming pool facilities, locker rooms, etc. The acute form is usually caused by Trichophyton mentagrophytes, var. interdigitale, and the chronic form by Trichophyton rubrum.

Acute tinea pedis

Clinical features — Attacks of acute tinea pedis are self-limited, intermittent, and recurrent. They often follow activities that cause the feet to sweat. Acute tinea pedis begins with the appearance of intensely pruritic, sometimes painful, erythematous vesicles or bullae between the toes or on the soles, frequently extending up the instep (picture 1A-B). The disease may be unilateral or bilateral. Secondary staphylococcal infections with lymphangitis often complicate the picture.

Secondary eruptions at distant sites may occur simultaneously due to a presumed immunologic reaction to the fungus. This is a sterile vesicular eruption that often occurs on the palms and fingers, referred to as a dermatophytid reaction. This improves as the primary infection is treated. (See 'Dermatophytid (id) reactions' below.)

Diagnosis — The history and clinical picture combination is characteristic, but dyshidrotic eczema can resemble acute tinea pedis, and the diagnosis should be confirmed by potassium hydroxide (KOH) examination of scrapings from the lesions (picture 2A-C). The roof of a vesicle can provide an adequate specimen. Culture on Sabouraud's medium is also helpful in difficult cases.

Chronic tinea pedis

Clinical features — Chronic tinea pedis is the most common form of tinea pedis encountered in practice. Untreated it usually persists indefinitely. The disease begins with slowly progressive, pruritic, erythematous erosions and/or scales between the toes, especially in the third and fourth digital interspaces (picture 3A-B). Interdigital fissures are often present. Extension onto the sole, sides of the foot, and in some cases the top of the foot follows, presenting as chronic scaling ("moccasin ringworm") with variable degrees of underlying erythema (picture 4A-B). The border between involved and uninvolved skin is usually quite sharp, and the normal creases and markings of the skin (dermatoglyphics) tend to accumulate scale. In many cases the palms and flexor aspects of the fingers (tinea manuum) may be unilaterally involved (two feet, one hand) (picture 5). Mycotic nail dystrophy (onychomycosis) is also often present (picture 6).

The appearance of tinea pedis, cruris, and corporis can be modified in patients who have inappropriately been treated with topical steroids. This is referred to as tinea incognito. Patients can have diminished erythema without the typical scaling erythematous border, or can develop a deep-seated folliculitis (Majocchi granuloma) that may require oral antifungal therapy.

Diagnosis — The history and clinical picture combination is characteristic, but the diagnosis should be confirmed by KOH examination of scrapings from the lesions (picture 2B-C), as foot eczema and plantar psoriasis may be difficult to differentiate clinically from tinea pedis. Interdigital erythrasma may also resemble interdigital tinea pedis, but can be distinguished by the appearance of coral red fluorescence upon illumination with a Wood's lamp (picture 7). (See "Erythrasma".)

Treatment — Tinea pedis can usually be treated with a topical antifungal cream for four weeks; interdigital tinea pedis may only require one week of therapy. A review of the available evidence found strong evidence that topical treatments increase cure rates for tinea pedis compared with placebo [9].

A number of topical antifungal creams are available over the counter; some prescription agents have a broader spectrum of action and may be administered once instead of twice daily, but generally all of the creams that treat dermatophyte infections can be effective (table 1) [9]. A meta-analysis of 11 randomized trials concluded that treatment with allylamines (terbinafine or naftifine) produces a slightly higher cure rate than treatment with an azole [9]. Nystatin is not effective for the treatment of dermatophyte infections.

Patients with chronic or extensive disease may require oral antifungal therapy with terbinafine (250 mg daily for two weeks), itraconazole (200 mg twice daily for one week), or fluconazole (150 mg once weekly for two to six weeks) [10,11]. Griseofulvin (1000 mg/day of microsize, 660 or 750 mg/day of ultramicrosize) can also treat tinea pedis, but may be less effective than other oral antifungals, and requires four to eight weeks of therapy [10]. In a systematic review in which treatment regimens varied from the above, terbinafine was found to be more effective than griseofulvin, while the efficacy of terbinafine and itraconazole were similar [12]. Nail involvement is another indication for oral therapy; however, different treatment regimens are required to cure tinea infections of the nail. (See "Onychomycosis", section on 'Treatment'.)

Pediatric dosing options include:


10 to 20 kg: 62.5 mg daily

20 to 40 kg: 125 mg daily

Above 40 kg: 250 mg daily

Itraconazole 5 mg/kg daily

Fluconazole 6 mg/kg weekly

Griseofulvin 10 to 15 mg/kg daily or in divided doses

In addition to antifungal therapy, Burow's (1% aluminum acetate or 5% aluminum subacetate) wet dressings, applied for 20 minutes two to three times per day, may be helpful if vesiculation or maceration is present. Secondary infection should be treated with oral antibiotics. Other adjunctive therapies include use of foot powder to prevent maceration, treatment of shoes with antifungal powders, and avoidance of occlusive footwear.

TINEA CORPORIS — Tinea corporis, dermatophyte infection of the body, is an entity less amenable to strict categorization, because it can present as a part of the clinical picture of any of other forms of dermatophytosis described in this review.

Clinical features — Tinea corporis often begins as a pruritic, circular or oval, erythematous, scaling patch or plaque that spreads centrifugally. Central clearing follows, while the active advancing border, a few millimeters wide, retains its red color and with cross lighting can be seen to be slightly raised. The result is a lesion shaped like a ring (annular), from which the disease derives its common name (picture 8A-C). Multiple lesions may run together to produce "flower petal" configurations (picture 9). (See "Approach to the patient with annular skin lesions".)

Tinea corporis can be seen in adults caring for children with tinea capitis (most commonly seen in association with black dot tinea capitis caused by Trichophyton tonsurans). It is also often seen in association with Trichophyton rubrum infections. Extensive presentations should alert the examiner to the possibility of an underlying problem that has compromised the patient's immunologic system, for example, diabetes mellitus or HIV infection. Tinea corporis contracted from infected animals, particularly kittens and puppies, is often intensely inflammatory.

Tinea corporis can also occur in outbreaks among athletes who have skin-to-skin contact [13], such as wrestlers (tinea corporis gladiatorum). Most cases of tinea gladiatorum appear to be caused by Trichophyton tonsurans [14].

The appearance of tinea pedis, cruris, and corporis can be modified in patients who have inappropriately been treated with topical steroids. This is referred to as tinea incognito (picture 10). Patients can have diminished erythema without the typical scaling erythematous border, or can develop a folliculitis (Majocchi's granuloma) that may require oral antifungal therapy. (See 'Majocchi's granuloma' below.)

Diagnosis — A potassium hydroxide (KOH) preparation will show the segmented hyphae and arthrospores characteristic of all dermatophyte infections (picture 2B-C). Highest yields are obtained from material taken from the active border of the lesion. Cultures (on Sabouraud's medium) can also be used to confirm the diagnosis. (See "Dermatologic procedures", section on 'Potassium hydroxide (KOH) prep' and "Dermatologic procedures", section on 'Fungal culture'.)

Other cutaneous disorders may have clinical features that resemble tinea corporis. Localized granuloma annulare is a benign inflammatory condition that classically presents with one or more erythematous or violaceous annular plaques on the extremities (picture 11A-B). Unlike tinea corporis, scale is absent. (See "Approach to the patient with annular skin lesions" and "Granuloma annulare", section on 'Clinical features'.)

Erythema annulare centrifugum, an inflammatory skin disorder of unknown etiology, also exhibits annular erythematous plaques (picture 12A-B). A trailing rim of scale is often evident in the superficial variant of this disorder. Patients with nummular eczema, psoriasis, subacute cutaneous lupus erythematosus, and pityriasis rosea may also possess lesions that resemble the annular scaly plaques associated with tinea corporis.

Treatment — Tinea corporis usually responds well to the daily application of topical antifungals (table 1) [15,16]. Topical nystatin is ineffective due to its inactivity against dermatophytes. For individuals with extensive cases or patients who are severely immunocompromised, a systemic agent may be preferable. Systemic therapy is also appropriate in patients who have failed topical therapy.

Appropriate systemic agents include oral terbinafine, fluconazole, and itraconazole; all of these agents appear to have greater efficacy and fewer side effects than oral griseofulvin [17-20]. Reasonable regimens in adults include: terbinafine 250 mg daily for one week; fluconazole 150 to 200 mg once weekly for two to four weeks; itraconazole 200 mg daily for one week; griseofulvin 500 to 1000 mg per day (microsize) or 375 to 500 mg per day (ultramicrosize) for two to four weeks [21]. Children are treated for similar durations. Reasonable pediatric doses for these drugs are fluconazole 6 mg/kg once weekly, itraconazole 3 to 5 mg/kg per day (up to 200 mg per day), and griseofulvin microsize suspension 15 to 20 mg/kg per day [21]. Terbinafine granules are dosed by weight range: 125 mg per day for children <25 kg, 187.5 mg per day for children 25 to 35 kg, and 250 mg per day for children of higher weights. The duration of treatment in children and adults is similar.

Athletes with tinea (corporis) gladiatorum are generally not allowed to participate in matches or practice because of concerns about the spread of infection. The appropriate duration of treatment before returning to the sport is unknown [14]. A randomized trial in 22 wrestlers compared topical clotrimazole cream (1% twice daily) with oral fluconazole (200 mg weekly) each for three weeks [22]. Clinical response rates were similar. The time to when half of wrestlers had negative cultures was longer in the topical treatment group (23 versus 11 days); however, this result was not statistically significant in this small study. In a second study by the same authors, in which 21 wrestlers who developed tinea corporis gladiatorum were treated with open label fluconazole 200 mg weekly, all patients had negative cultures by the third week of therapy [23].

In the absence of more definitive information, we suggest that patients with tinea gladiatorum be treated with an oral agent. Ten to 15 days is probably a reasonable time period to restrict participation in sports [24]. It is possible that data on culture negativity may overestimate the time to resolution of infectivity.

TINEA CRURIS — Tinea cruris (jock itch) is a special form of tinea corporis involving the crural fold. In North America the most common cause is T rubrum. A few cases are caused by Epidermophyton floccosum and occasionally Trichophyton mentagrophytes.

Tinea cruris is far more common in men than women. The disease often begins after physical activity that results in copious sweating, and the source of the infecting fungus is usually the patient's own tinea pedis with or without onychomycosis. Obesity predisposes to tinea cruris, as do diabetes and immunodeficient states.

Clinical features — Tinea cruris begins with an erythematous patch high on the inner aspect of one or both thighs (opposite the scrotum in men). It spreads centrifugally, with partial central clearing and a slightly elevated, erythematous, sharply demarcated border that may show tiny vesicles that are visible only with a hand glass (picture 13A-B). When caused by Trichophyton rubrum, the disease may extend well down on the thighs and up into the pubic region. In some cases it is extremely chronic and progressive, extending onto the perineum and perianal areas, into the gluteal cleft, and onto the buttocks (picture 14). In males, the scrotum is typically spared. This is an important clinical distinction between tinea cruris and candidal intertrigo, as candidiasis in males often involves scrotal skin.

Tinea cruris caused by T. mentagrophytes is usually less extensive, but acutely inflammatory, and may clear spontaneously. Those that are caused by Epidermophyton floccosum are moderately inflammatory and sometimes occur in small case clusters that can be traced to fomites such as shared towels, contaminated exercise machines, etc.

The appearance of tinea pedis, cruris, and corporis can be modified in patients who have inappropriately been treated with topical steroids. This is referred to as tinea incognito. Patients can have diminished erythema without the typical scaling erythematous border, or can develop a folliculitis (Majocchi granuloma) that may require oral antifungal therapy. (See 'Majocchi's granuloma' below.)

Diagnosis — Potassium hydroxide (KOH) examination of scales scraped from the lesion will show the segmented hyphae and arthrospores characteristic of all dermatophyte infections (picture 2B). Highest yields are obtained from material taken from the active border of the lesion. Cultures (on Sabouraud's medium) can also be used to confirm the diagnosis.

Other common skin disorders that may present with erythematous patches or plaques in the inguinal region include inverse psoriasis (picture 15), erythrasma (picture 16A), seborrheic dermatitis (picture 17), and candidal intertrigo. A KOH preparation positive for hyphae rules out the first three disorders. Candidiasis is suggested by the presence of erythematous patches with satellite papules and pustules (picture 18A-B). Candidal pseudohyphae, hyphae, and/or yeast cells are visualized on KOH preparation (picture 19A-B). (See "Candidal intertrigo".)

A diagnosis of erythrasma is confirmed by the appearance of coral red fluorescence upon illumination with a Wood's lamp (picture 16A-B). Although not always present, the identification of lesions consistent with seborrheic dermatitis or psoriasis in other locations is useful for diagnosing these two conditions. (See "Erythrasma" and "Overview of dermatitis" and "Epidemiology, clinical manifestations, and diagnosis of psoriasis".)

Treatment — Topical antifungal treatment will suffice for the ordinary case (table 1) [15,16]. Nystatin is not effective for the treatment of tinea cruris. Lesions resistant to topical medications can be treated with griseofulvin by mouth, 250 mg three times daily for 14 days, or any of the other systemic agents.

Tinea pedis and onychomycosis are risk factors for tinea cruris, and failure to treat concomitant tinea pedis usually results in prompt recurrence. Subsequent episodes of tinea pedis should be treated promptly. Treatment of onychomycosis may also reduce the risk for recurrent disease.

Daily application of talcum or other desiccant powders to keep the area dry will help prevent recurrences. Itching can be alleviated by over the counter preparations such as Sarna or Prax, although these can be irritating if applied to inflamed or excoriated skin. Patients should also be advised to avoid hot baths and tight-fitting clothing; men should be advised to wear boxer shorts rather than briefs, and women to wear cotton underwear and avoid tight-fitting pants [25,26].

TINEA CAPITIS — Tinea capitis, dermatophyte infection of the scalp, almost always occurs in small children. The clinical manifestations, diagnosis, and management of tinea capitis is reviewed separately. (See "Tinea capitis".)

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 and subcutaneous tissue. Trichophyton rubrum is the most frequent etiologic agent, although other dermatophytes have been implicated [27].

The condition is thought to 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 [28,29]. Shaving the legs can be an inciting factor in women.

Clinical features — In immunocompetent patients, the clinical findings are typically characterized by a localized area with erythematous, perifollicular papules or small nodules (picture 20). Pustules may also be present.

Immunocompromised patients can also develop Majocchi's granuloma. They may present similarly to immunocompetent patients, or with subcutaneous nodules and abscesses [30-34]. Trauma is also thought to be an inciting factor in these cases. The depression of cell-mediated immunity and the inflammatory response, important for the inhibition of dermatophyte infections, may contribute to progression of the disorder [27,30,35,36]. Rarely, systemic dissemination may occur [27,37].

In immunocompetent patients, topical corticosteroid use on a superficial dermatophyte infection can lead to local immunosuppression, and promote the development of Majocchi's granuloma [29,38,39].

Diagnosis — A presumptive diagnosis is made based on the patient's history and clinical findings, and can be confirmed with a skin biopsy exhibiting fungal forms in the dermis [27]. Tissue culture can identify the causative organism. A potassium hydroxide (KOH) preparation, which identifies fungal forms only within the stratum corneum, may be negative [27,35,40,41].

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/day for two to four weeks has been used for the treatment of Majocchi's granuloma [42,43]. 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 1 week per month for 2 months [44]. Treatment regimens with griseofulvin and daily itraconazole have also been suggested [40].

Immunocompromised patients have been successfully treated with oral antifungals. Treatment by local excision has been reported [33,34], but may not be necessary.

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 [45].

Dermatophytid reactions can occur in patients with tinea pedis, tinea manuum, tinea cruris, tinea corporis, or tinea capitis [45-51]. Patients typically present with pruritic, papulovesicular eruptions that can be quite distant from the site of infection (picture 21A-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 [46]. 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 [45].

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. In rare cases, systemic glucocorticoids may be indicated.

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Basics topics (see "Patient information: Ringworm, athlete’s foot, and jock itch (The Basics)" and "Patient information: Fungal nail infections (The Basics)")

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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 capitis, tinea pedis, tinea corporis, tinea cruris, and Majocchi's granuloma. (See 'Overview' above.)

A potassium hydroxide (KOH) preparation should be used to confirm the diagnosis of a dermatophyte infection (picture 2B). Failing to accurately diagnose a dermatophyte infection may lead to inappropriate treatment with topical corticosteroids. The indiscriminate use of a combination antifungal and corticosteroid product, such as Lotrisone (clotrimazole/betamethasone dipropionate) should be avoided. Dermatophyte infections are not susceptible to nystatin. (See 'Overview' above.)

Tinea pedis is a common type of dermatophyte infection involving the feet. A vesicobullous form is occasionally seen. Topical antifungals are usually sufficient for treatment tinea pedis, although oral antifungals may be required in certain cases. (See 'Tinea pedis' above.)

Tinea corporis can usually be managed with topical antifungals. Extensive cases and patients who are severely immunocompromised may warrant treatment with an oral antifungal. Patients with a confirmed diagnosis who have failed topical therapy are also candidates for oral therapy. Patients with extensive cases of tinea corporis may suffer from underlying diseases such as diabetes mellitus or immunologic disorders, and may warrant further evaluation. (See 'Tinea corporis' above.)

Tinea cruris is a dermatophyte infection of the groin. Topical antifungal therapy is usually sufficient for resolving the local infection. Preventive behavioral changes and treatment of concomitant tinea pedis or onychomycosis reduce the risk for future recurrences. (See 'Tinea cruris' above.)

Majocchi's granuloma is a condition in which the dermatophyte invades the dermal and subcutaneous tissue via penetration of hair follicles. Inflammatory perifollicular papules, small nodules, or pustules are typically seen. A KOH preparation may be negative. Trauma, such as shaving legs, and topical corticosteroid use may be precipitating factors. Immunosuppressed patients may present with subcutaneous nodules and abscesses. Treatment requires the use of an oral antifungal. (See 'Majocchi's granuloma' above.)

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  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. Crissey JT, Lang H, Parish LC. Manual of Medical Mycology, Blackwell Science, Cambridge 1995. p.36.
  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. Smith ES, Fleischer AB Jr, Feldman SR. Nondermatologists are more likely than dermatologists to prescribe antifungal/corticosteroid products: an analysis of office visits for cutaneous fungal infections, 1990-1994. J Am Acad Dermatol 1998; 39:43.
  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. Gupta AK, Cooper EA. Update in antifungal therapy of dermatophytosis. Mycopathologia 2008; 166:353.
  11. Gupta AK, Doncker PD, Heremans A, et al. Itraconazole for the treatment of tinea pedis: a dosage of 400 mg/day given for 1 week is similar in efficacy to 100 or 200 mg/day given for 2 to 4 weeks. J Am Acad Dermatol 1997; 36:789.
  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. 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.
  14. Adams BB. Tinea corporis gladiatorum. J Am Acad Dermatol 2002; 47:286.
  15. El-Gohary M, van Zuuren EJ, Fedorowicz Z, et al. Topical antifungal treatments for tinea cruris and tinea corporis. Cochrane Database Syst Rev 2014; 8:CD009992.
  16. 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.
  17. 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.
  18. Cole GW, Stricklin G. A comparison of a new oral antifungal, terbinafine, with griseofulvin as therapy for tinea corporis. Arch Dermatol 1989; 125:1537.
  19. 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.
  20. 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.
  21. 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.
  22. Kohl TD, Martin DC, Berger MS. Comparison of topical and oral treatments for tinea gladiatorum. Clin J Sport Med 1999; 9:161.
  23. Kohl TD, Martin DC, Nemeth R, et al. Fluconazole for the prevention and treatment of tinea gladiatorum. Pediatr Infect Dis J 2000; 19:717.
  24. Beller M, Gessner BD. An outbreak of tinea corporis gladiatorum on a high school wrestling team. J Am Acad Dermatol 1994; 31:197.
  25. Akinwale SO. Personal hygiene as an alternative to griseofulvin in the treatment of tinea cruris. Afr J Med Med Sci 2000; 29:41.
  26. Pandey SS, Chandra S, Guha PK, et al. Dermatophyte infection of the penis. Association with a particular undergarment. Int J Dermatol 1981; 20:112.
  27. Smith KJ, Neafie RC, Skelton HG 3rd, et al. Majocchi's granuloma. J Cutan Pathol 1991; 18:28.
  28. Gill M, Sachdeva B, Gill PS, et al. Majocchi's granuloma of the face in an immunocompetent patient. J Dermatol 2007; 34:702.
  29. Cho HR, Lee MH, Haw CR. Majocchi's granuloma of the scrotum. Mycoses 2007; 50:520.
  30. 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.
  31. Elmets CA. Management of common superficial fungal infections in patients with AIDS. J Am Acad Dermatol 1994; 31:S60.
  32. Gupta S, Kumar B, Radotra BD, Rai R. Majocchi's granuloma trichophyticum in an immunocompromised patient. Int J Dermatol 2000; 39:140.
  33. Burg M, Jaekel D, Kiss E, Kliem V. Majocchi's granuloma after kidney transplantation. Exp Clin Transplant 2006; 4:518.
  34. 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.
  35. Kim ST, Baek JW, Kim TK, et al. Majocchi's granuloma in a woman with iatrogenic Cushing's syndrome. J Dermatol 2008; 35:789.
  36. 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.
  37. 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.
  38. Jacobs PH. Majocchi's granuloma (due to therapy with steroid and occlusion). Cutis 1986; 38:23.
  39. Elgart ML. Tinea incognito: an update on Majocchi granuloma. Dermatol Clin 1996; 14:51.
  40. Feng WW, Chen HC, Chen HC. Majocchi's granuloma in a 3-year-old boy. Pediatr Infect Dis J 2006; 25:658.
  41. 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.
  42. Gupta AK, Prussick R, Sibbald RG, Knowles SR. Terbinafine in the treatment of Majocchi's granuloma. Int J Dermatol 1995; 34:489.
  43. 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, 2008.
  44. 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.
  45. Cheng N, Rucker Wright D, Cohen BA. Dermatophytid in tinea capitis: rarely reported common phenomenon with clinical implications. Pediatrics 2011; 128:e453.
  46. Veien NK, Hattel T, Laurberg G. Plantar Trichophyton rubrum infections may cause dermatophytids on the hands. Acta Derm Venereol 1994; 74:403.
  47. 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.
  48. Al Aboud K, Al Hawsawi K, Alfadley A. Tinea incognito on the hand causing a facial dermatophytid reaction. Acta Derm Venereol 2003; 83:59.
  49. Gianni C, Betti R, Crosti C. Psoriasiform id reaction in tinea corporis. Mycoses 1996; 39:307.
  50. Derebery J, Berliner KI. Foot and ear disease--the dermatophytid reaction in otology. Laryngoscope 1996; 106:181.
  51. Iglesias ME, España A, Idoate MA, Quintanilla E. Generalized skin reaction following tinea pedis (dermatophytids). J Dermatol 1994; 21:31.
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