Dermatophyte (tinea) infections

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Dermatophyte (tinea) infections

Author Adam O Goldstein, MD, MPHBeth G Goldstein, MDSection Editor Robert P Dellavalle, MD, PhD, MSPHMoise L Levy, MDDeputy Editor David M Rind, MD

Last literature review version 16.2:May 2008
This topic last updated: February 5, 2008 (More)

INTRODUCTION
Dermatophytes refer to the most common type of fungi that cause infection of the skin and nails. Patients commonly refer to dermatophyte infections of the body or scalp as "ringworm". Superficial dermatophyte infections account for over 5 million visits to physicians per year, at an average cost of over $200 million. The majority of all visits are to nondermatologists [1].

Three types of superficial fungi/dermatophytes account for the majority of infections: Epidermophyton, Trichophyton, and Microsporum. The infestations have varied presentations, are named by location, and have similar treatments. These organisms have acquired in the evolutionary process the ability to metabolize keratin, a protein resistant to most other organisms. The fungi attack skin, nails, and hair to produce a wide variety of disease states. 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 [2].

One of the most important considerations when evaluating superficial dermatophyte infections is confirming the diagnosis with a laboratory specimen, either a KOH test or culture. A common mistake that many clinicians make is to prescribe combination antifungal steroid products (eg, Mycolog, Lotrisone) for the treatment of common fungal skin infections without confirming the diagnosis. This course of action is wrong for several reasons:If the patient fails to improve, it is unclear why, and the use of more potent steroid preparations in the combination products may make the diagnosis of underlying disease more difficult.

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 from topical steroids. If the KOH is negative, the patient can be given the correct diagnosis, such as eczema, which can mimic fungal infection but tends to be more chronic. Combination products are far more expensive than simple antifungal agents, or even generically available steroid 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 [3] . This topic discusses the evaluation and treatment of dermatophyte infections of the skin. Dermatophyte infections of the nails are discussed separately. (See "Onychomycosis").

TINEA CAPITIS
Tinea capitis, dermatophyte infection of the scalp, occurs almost always 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.

Tinea capitis can occur in two distinctly different forms, "gray patch" and "black dot." Black dot tinea capitis, most often caused by Trichophyton tonsurans, is the form predominantly seen in the United States. Tinea capitis is most often an endothrix infection; 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.

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 (show picture 1). The inflammation subsides, and the hairs within the patch break off a millimeter or two above the level of the scalp. The hair stubs 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 (show 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 [4] , but is also seen with more routine presentations.

Diagnosis
Spores in patients with GPTC are readily identifiable by KOH examination of manually epilated stubs (show picture 3). Infected hair stubs of 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, 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 [5].

A case-control study compared the hair care practices of children with culture-proved Trichophyton tonsurans and those without scalp disease [6] . Exposure to Trichophyton tonsurans was associated with scalp infection, while hairstyling, frequency of washing, use of oils or grease, and other hair care practices were not.

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 (show 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 [4]. 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. In contrast to GPTC, the infected hairs of BDTC do not fluoresce green under Woods Light. Diagnosis can be confirmed by culture on Sabouraud's medium.

Treatment
Gray patch and black dot tinea capitis both respond to the same medications [7]. Griseofulvin remains the drug of choice, particularly when cost is a concern, although oral therapy with terbinafine, itraconazole, or fluconazole appears to have similar efficacy for the treatment of Trichophyton infections. These agents are typically more expensive than griseofulvin but allow a shorter course of treatment, and can be used for resistant cases or for patients who are allergic to griseofulvin [8-13]. Griseofulvin may be superior to terbinafine for treating tinea capitis due to Microsporum infections [12-14].

Griseofulvin treatment schedules are as follows:Adults: 250 mg ultramicrosize by mouth twice daily for 6 to 12 weeks. A few cases of the black dot type may require 250 mg three times daily for the same length of time. Children: 20 to 25 mg/kg of body weight for 6 to 12 weeks Terbinafine treatment schedules are based on weight:10 to 20 kg: 62.5 mg daily for four weeks 20 to 40 kg: 125 mg daily for four weeks Above 40 kg: 250 mg daily for four 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 or as pulse therapy at a dose of 5 mg/kg daily for one week each month for two to three months [7].

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 black dot tinea capitis [5]. 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 perhaps with oral therapy.

Kerion responds best by treating the underlying fungal disorder. Some advocate the use of corticosteroid 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 [15,16]. However, steroid 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 [17] . Only limited evidence exists for combining antifungal treatment with oral administration of antibiotics active against staphylococci [18], 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 [19,20] Topical treatment is generally ineffective. Successful treatment of infants with tinea capitis has been reported with griseofulvin, terbinafine, ketoconazole, and fluconazole [19,20]. 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 and on the soles, frequently extending up the instep (show picture 5). The disease may be unilateral or bilateral. Secondary staphylococcal infections with lymphangitis often complicate the picture.S econdary eruptions at distant sites may occur simultaneously due to an immunologic reaction to the fungus. This is a sterile vesicular eruption that often occurs on the palms and fingers, referred to as an "id" reaction. This improves as the primary infection is treated.

Diagnosis
The history and clinical picture combination is characteristic, but the diagnosis should be confirmed by KOH examination of scrapings from the lesions (show picture 6). The roof of a vesicle is a good place to look. 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 lesions (erosions, fissures, scales) between the toes, especially in the fourth digital interspace. Interdigital fissures are often present (show picture 7). Extension onto the sole follows and later onto the sides or even the top of the foot ("moccasin ringworm") as chronic scaling. The border between involved and uninvolved skin is usually quite sharp, and the normal creases and markings of the skin (dermatogliphs) 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). Mycotic nail dystrophy (onychomycosis) is also often present.

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.

Diagnosis
The history and clinical picture combination is characteristic, but the diagnosis should be confirmed by KOH examination of scrapings from the lesions (show picture 6), as foot eczema and tinea pedis may clinically be difficult to differentiate.

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 [21]. A number of topical antifungal creams are available over the counter (show table 1); some prescription agents have a broader spectrum of action and may be administered once instead of twice daily, but generally all of the creams are similarly effective [21] . 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 [22].

Patients with chronic disease or extensive disease may require oral antifungal therapy with griseofulvin (250 to 500 mg of microsize twice daily), terbinafine (250 mg daily), or itraconazole (200 mg daily). In a systematic review, terbinafine was found to be more effective than griseofulvin, while the efficacy of terbinafine and itraconazole were similar [23] . Nail involvement is another indication for oral therapy. Secondary infection should be treated with oral antibiotics.

Pediatric dosing options include:

• Griseofulvin 10 to 15 mg/kg daily or in divided doses
• Terbinafine: - 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 daily


In addition to antifungal therapy, Burow's (aluminum acetate) wet dressings, applied for 20 minutes two to three times per day, may be helpful if vesiculation or maceration is present. 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.

Tinea corporis begins as a pruritic circular or oval erythematous scaling patch/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 (show picture 8). Multiple lesions may run together to produce "flower petal" configurations.

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 is often intensely inflammatory.

Tinea corporis can also occur in outbreaks among athletes who have skin-to-skin contact [24] , such as wrestlers (tinea corporis gladiatorum). Most cases of tinea gladiatorum appear to be caused by Trichophyton tonsurans [25]. 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.

Treatment
Tinea corporis usually responds well to the daily application of topical antifungals (show table 1) [26] . For adults with extensive cases or with folliculitis, or in 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, however griseofulvin may be less expensive [27-30] .

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 [25]. A randomized trial in 22 wrestlers compared topical clotrimazole cream (1 percent twice daily) with oral fluconazole (200 mg weekly) each for three weeks [31]. 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 [32]. 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 [33] . 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 E floccosum and occasionally T 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. Obesity predisposes to tinea cruris.

Clinical picture
Tinea cruris begins with an erythematous patch high on the inner aspect of one or both thighs, opposite the scrotum. 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 (show picture 9).

When caused by T 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.

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.

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.

Treatment
Topical antifungal treatment will suffice for the ordinary case (show table 1). Failure to treat concomitant tinea pedis usually results in prompt recurrence. 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.

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, and to wear boxer shorts rather than briefs [34,35] .