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 and hair. Dermatophyte infections of the nails are discussed separately. (See "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 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 CAPITIS — Tinea capitis, dermatophyte infection of the scalp, almost always occurs in small children. A clinical diagnosis of tinea capitis in adults is often incorrect, and frequently turns out to be seborrheic dermatitis or another inflammatory condition. The major exception to this rule is the development of tinea capitis in immunocompromised or immunosuppressed adults.
Tinea capitis can occur in three distinctly different forms, "gray patch," "black dot" and favus. Black dot tinea capitis, most often caused by Trichophyton tonsurans, is the form predominantly seen in the United States. Favus, most often due to Trichophyton schoenleinii, is rarely seen in the United States and Europe, but may be seen in countries where Trichophyton schoenleinii infection is endemic, such as Iran, China, and Nigeria [9]. Immigration and travel may contribute to the occurrence of favus in patients who live in nonendemic areas.
Tinea capitis is most often an endothrix infection due to Trichophyton species; nonfluorescent arthroconidia are located within the hair shaft. Spores are identifiable by KOH examination of the hair shaft, not by KOH scraping of the scale, though hyphae may be seen on occasion. (See 'Black dot tinea capitis' below.)
Gray patch tinea capitis — Gray patch tinea capitis (GPTC) occurs in epidemic and endemic forms. Formerly common, the epidemic form has virtually disappeared from North America. The endemic form caused by Microsporum canis and contracted usually from cats and dogs, continues to be seen. Person to person spread is rare.
Clinical features — The infection begins with an erythematous, scaling, well-demarcated patch on the scalp that spreads centrifugally for a few weeks or months, ceases to spread, and persists indefinitely, sometimes for years. One or several lesions may be present (picture 1). The inflammation subsides, and the hairs within the patch break off a millimeter or two above the level of the scalp. The short, broken hairs take on a frosted appearance. Typical areas of tinea corporis may also be found on glabrous skin.
In a few cases the lesions change abruptly to become boggy, elevated, tender nodules (kerion). The surface of these lesions, largely devoid of hair, is covered with viscid exudate (picture 2). Kerion is a form of immune response to the fungus, but secondary staphylococcal infection with regional adenitis may also complicate the picture. Posterior cervical lymphadenopathy often occurs with kerion [10], but is also seen with more routine presentations.
Diagnosis — Spores in patients with GPTC are readily identifiable by KOH examination of manually epilated hair (picture 3). Infected hair fragments infected with Microsporum canis may also fluoresce bright green under a Wood's ultraviolet (UV) lamp. Culture of hairs on Sabouraud's medium can confirm the diagnosis in questionable cases, but is not usually necessary if either of the prior methods yields positive findings.
Black dot tinea capitis — Black dot tinea capitis (BDTC) is the most common form of tinea capitis in the United States. It is largely a disease of childhood, although adults, especially the elderly, are occasionally affected. All ethnic groups may be infected, but African-American children are particularly susceptible [11], possibly because of increased coiling of hair shafts. Spread is usually from child to child contact. Fomites (shared hats, combs, brushes, barrettes, rollers, etc) may play an important role. Asymptomatic carriers in the household may also be involved [12].
A case-control study compared the hair care practices of children with culture-proven Trichophyton tonsurans scalp infection and those without tinea capitis [13]. Exposure to Trichophyton tonsurans was associated with scalp infection, while hairstyling, frequency of washing, use of oils or grease, and other hair care practices did not appear to play a major role in the acquisition of the disease.
Clinical features — BDTC usually begins as an asymptomatic, erythematous, scaling patch on the scalp, which slowly enlarges. Lesions may be single or multiple. Early lesions are easily overlooked and the disease is not usually noticed until areas of alopecia become evident. Hairs within the patches break off flush with the scalp; detritus within the follicular opening formerly occupied by the hair appears as a black dot (picture 4). In some cases inflammation is prominent, and the lesions can resemble pyoderma or discoid lupus erythematosus. Painful lymphadenopathy can also occur in this setting [10]. Left untreated, scarring with permanent alopecia can occur and the disease can last indefinitely. Patches of tinea corporis may appear on glabrous skin, and the nails are sometimes involved. As in gray patch tinea capitis, a sudden transition to kerion may occur.
Diagnosis — Diagnosis of BDTC is made by performing KOH examination of spores on the hair shaft. Occasionally, hyphae may be seen in scale. In contrast to GPTC caused by Microsporum canis, the organisms that cause BDTC do not fluoresce green under Woods Light. Diagnosis can be confirmed by culture on Sabouraud's medium.
Favus — Favus (also known as tinea favosa) is a form of endothrix tinea capitis that has decreased in incidence worldwide, but remains endemic in China, Nigeria, and Iran [9]. Trichophyton schoenleinii is the most common cause of favus.
Clinical features — Patients initially develop perifollicular erythema on the scalp, which progresses to the characteristic finding of concave, cup-shaped yellow crusts called scutula. Scutula are composed of fungi, neutrophils, dried serum, and epidermal cells. As the disease advances, the scutula coalesce into confluent and adherent masses which overlay severe alopecia. Untreated infections may persist into adulthood.
Transmission usually does not occur with casual contact; rather, prolonged exposure appears to be required for acquisition. Familial cases are common.
Diagnosis — KOH examination of lesional hairs demonstrates fungal hyphae arranged in a longitudinal direction within the hair shafts. Culture can be performed on Sabouraud’s medium and Wood’s lamp examination of infected hairs reveals a characteristic sliver-blue fluorescence.
Treatment — Gray patch, black dot, and favus forms of tinea capitis all respond to the same medications [14].
Medications — Griseofulvin has a long history of safety and efficacy in tinea capitis in children. Oral terbinafine, itraconazole, and fluconazole are additional therapeutic options that allow shorter courses of treatment [15-22].
The comparative efficacy of terbinafine and griseofulvin for tinea capitis has been evaluated in multiple randomized trials [20-23]. In a meta-analysis of randomized trials (n = 2163), the drugs were similarly effective for the treatment of tinea capitis when all variants of the disease were considered [24]. However, subgroup analysis revealed that efficacy varied with the type of infection: terbinafine was less effective than griseofulvin for infections due to Microsporum species (odds ratio [OR] 0.41, 95% CI 0.25-0.66), and more effective for infections due to Trichophyton species (OR 1.62, 95% CI 1.27-2.05). The doses of griseofulvin used in the trials (<20 mg/kg per day) were lower than the doses used by many clinicians (including ourselves) for the treatment of tinea capitis, precluding conclusions about the relative efficacy of griseofulvin for Trichophyton infections when given at higher doses. There was only one serious adverse effect, reversible neutropenia, in a patient treated with terbinafine. There were no serious episodes of liver transaminitis in patients treated with terbinafine.
A few randomized trials have investigated the use of oral azole antifungals for tinea capitis [15,21]. The efficacy of itraconazole and fluconazole for tinea capitis appears to be similar to griseofulvin.
Griseofulvin is our first choice for the treatment of patients with Microsporum tinea capitis and patients in whom the inciting cause of tinea capitis is uncertain due to its long history of safety in children. Terbinafine is an alternative first line agent in patients with tinea capitis that is highly likely or known to be due to Trichophyton species, particularly when a shorter duration of therapy is desired. The release of a generic formulation of terbinafine has significantly reduced the cost of this agent in the United States.
Griseofulvin treatment schedules for children are as follows [25]:
- 20 to 25 mg/kg/day (microsize formulation) for 6 to 12 weeks
- 10 to 15 mg/kg/day (ultramicrosize formulation) for 6 to 12 weeks
Terbinafine tablet treatment schedules are based on weight [25]:
- 10 to 20 kg: 62.5 mg daily for two to four weeks
- 20 to 40 kg: 125 mg daily for two to four weeks
- Above 40 kg: 250 mg daily for two to four weeks
If terbinafine is used for the treatment of Microsporum tinea capitis, longer courses of treatment (8 to 10 weeks) may be necessary [15,26].
Terbinafine is also manufactured as a granule formulation, which can be sprinkled onto nonacidic foods (eg, pudding or mashed potatoes). The dose regimen for terbinafine granules is the following [22]:
- Less than 25 kg: 125 mg daily for six weeks
- 25 to 35 kg: 187.5 mg daily for six weeks
- Above 35 kg: 250 mg daily for six weeks
Itraconazole can be used in children as continuous therapy at a dose of 3 to 5 mg/kg daily for four to six weeks. Alternatively, pulse therapy with itraconazole capsules can be given at a dose of 5 mg/kg daily for one week each month for two to three months [14,25]. The suggested dose for pulse therapy with the oral solution of itraconazole is 3 mg/kg [25].
Tinea capitis may be treated with fluconazole 6 mg/kg/day for three to six weeks [19,27]. Intermittent dosing is another option for fluconazole therapy (6 mg/kg once weekly for 8 to 12 weeks) [25].
Follow-up visits should be scheduled to assess the response to treatment. Treatment may need to be extended if active disease remains at the end of a prescribed course of therapy.
Topical treatment of tinea capitis is futile and a common cause of treatment failure. Treatment or removal of an animal is important only when the diagnosis is gray patch tinea capitis caused by M canis.
Identification of asymptomatic carriers and household fomites is an important part of the management of BDTC [12]. Culture on Sabouraud's medium of hairs and scalp dander (collected by brushing the area with a tooth brush) facilitates carrier identification. Carriers should be treated with selenium sulfide shampoo or with oral therapy.
Household members — Cohabitants of patients with tinea capitis can be asymptomatic carriers of dermatophytes, and it has been speculated that these individuals may be sources of reinfection for some patients [12]. In one cross-sectional study in which scalp cultures were taken from 209 household contacts of patients with tinea capitis, 44 percent were found to be asymptomatic carriers [28]. Culture specimens were obtained via rubbing multiple areas of the scalp with a disposable toothbrush followed by inoculation onto agar.
Although high quality evidence regarding the impact of household members who are asymptomatic carriers on the development of recurrent or persistent disease is not available, some authors have suggested identifying and treating asymptomatic carriers with antifungal shampoo [12,28]. Routine treatment of all household contacts without performing preliminary cultures has also been recommended [29]. Selenium sulfide 2.5% or ketoconazole 2% shampoo applied for at least five minutes, three times weekly, can be prescribed.
Sharing of fomites, such as hats, combs, or brushes should be avoided in households with an affected patient. If transmission of Microsporum canis from a pet is suspected, the pet should be referred for treatment of the infection [29].
Kerion — Kerion is managed by treating the underlying fungal disorder. Some advocate the use of systemic glucocorticoid therapy in patients with a kerion, but randomized trials of oral or intralesional steroids plus oral antifungal agents versus oral antifungal agents alone showed no difference in cure rates [30,31]. However, glucocorticoid therapy may improve discomfort from kerion.
Inappropriate hospitalization sometimes occurs because clinicians mistakenly believe the patient with a kerion has severe secondary bacterial infection, conditions not borne out by diagnostic cultures [32]. Only limited evidence exists for combining antifungal treatment with oral administration of antibiotics active against staphylococci [33], and the majority of cases can be treated successfully without antibiotics.
In infants — Tinea capitis is rare in children younger than one year of age, but does occur. Most affected infants are immunologically normal, but the possibility of immunodeficiency should be kept in mind. Contacts of the infant with tinea capitis should be carefully examined to identify and treat the source of the infection [34,35].
Topical treatment is generally ineffective. Successful treatment of infants with tinea capitis has been reported with griseofulvin, terbinafine, ketoconazole, and fluconazole [34,35]. However, fluconazole is the only oral antifungal agent approved for children younger than two years.
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 5A-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 KOH examination of scrapings from the lesions (picture 6A-B). 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 7A-C). 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 8A-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 9). Mycotic nail dystrophy (onychomycosis) is also often present (picture 10).
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 6B), 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 11). (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 [36].
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) [36]. 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 [36]. 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) [25,37]. 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 [25]. 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 [38]. 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
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 12A-C). Multiple lesions may run together to produce "flower petal" configurations (picture 13).
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 [39], such as wrestlers (tinea corporis gladiatorum). Most cases of tinea gladiatorum appear to be caused by Trichophyton tonsurans [40].
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 14). 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 KOH preparation will show the segmented hyphae and arthrospores characteristic of all dermatophyte infections (picture 6B). 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 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 which classically presents with one or more erythematous or violaceous annular plaques on the extremities (picture 15A-B). Unlike tinea corporis, scale is absent. (See "Granuloma annulare", section on 'Clinical features'.)
Erythema annulare centrifugum, an inflammatory skin disorder of unknown etiology, also exhibits annular erythematous plaques (picture 16A-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) [41]. 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 [42-45]. Reasonable regimens in adults include: terbinafine 250 mg daily for one to two weeks; fluconazole 150 mg once weekly for two to four weeks; itraconazole 200 mg daily for one to two weeks; griseofulvin 250 mg three times daily for two weeks.
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 [40]. A randomized trial in 22 wrestlers compared topical clotrimazole cream (1 percent twice daily) with oral fluconazole (200 mg weekly) each for three weeks [46]. 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 [47].
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 [48]. 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 17A-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 18). 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 — KOH examination of scales scraped from the lesion will show the segmented hyphae and arthrospores characteristic of all dermatophyte infections. 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 19), erythrasma (picture 20A), seborrheic dermatitis (picture 21), 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 22A-B). Candidal pseudohyphae, hyphae, and/or yeast cells are visualized on KOH preparation (picture 23A-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 20A-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, pathophysiology, clinical manifestations, and diagnosis of psoriasis".)
Treatment — Topical antifungal treatment will suffice for the ordinary case (table 1). 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 [49,50].
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 [51].
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 [52,53]. 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 21). 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 [54-58]. 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 [51,54,59,60]. Rarely, systemic dissemination may occur [51,61].
In immunocompetent patients, topical corticosteroid use on a superficial dermatophyte infection can lead to local immunosuppression, and promote the development of Majocchi's granuloma [53,62,63].
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 [51]. Tissue culture can identify the causative organism. A KOH preparation, which identifies fungal forms only within the stratum corneum, may be negative [51,59,64,65].
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 [66,67]. 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 [68]. Treatment regimens with griseofulvin and daily itraconazole have also been suggested [64].
Immunocompromised patients have been successfully treated with oral antifungals. Treatment by local excision has been reported [57,58], 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 [69].
Dermatophytid reactions can occur in patients with tinea pedis, tinea manuum, tinea cruris, tinea corporis, or tinea capitis [69-75]. Patients typically present with pruritic, papulovesicular eruptions that can be quite distant from the site of infection (picture 22A, 22C). In one series of 213 patients with tinea pedis, 37 (17 percent) were diagnosed with dermatophytid reactions characterized by vesicular eruptions on the hands [70]. 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 [69].
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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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 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. 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 capitis most commonly occurs in children. Black dot tinea capitis is usually caused by Trichophyton tonsurans, and is the predominant form of tinea capitis seen in the United States. When performing a KOH for tinea capitis, hairs should be examined for the presence of fungal spores within or surrounding the hair shaft. Topical antifungals are ineffective for the treatment of tinea capitis. Patients should be treated with oral antifungals such as griseofulvin, terbinafine, or itraconazole. (See 'Tinea capitis' above.)
- Tinea capitis may evolve to form an inflammatory reaction called a kerion, which can be mistaken for a secondary bacterial infection. Posterior cervical lymphadenopathy is often seen with this variant, although lymphadenopathy may also occur in non-kerion tinea capitis. Kerion should respond to treatment with an oral antifungal alone. In some cases, systemic glucocorticoid therapy may help improve the patient's discomfort. (See 'Tinea capitis' 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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