eMedicine Specialties > Dermatology > Fungal Infections

Tinea Pedis

Courtney M Robbins, MD, Resident Physician, Department of Dermatology, University of Alabama at Birmingham School of Medicine
Boni E Elewski, MD, Professor, Department of Dermatology, University of Alabama at Birmingham

Updated: Nov 13, 2008

Introduction

Background

Tinea pedis has afflicted humanity for centuries, so it is perhaps surprising that the condition was not described until Pellizzari did so in 1888. The first report of tinea pedis was in 1908 by Whitfield, who, with Sabouraud, believed that tinea pedis was a very rare infection caused by the same organisms that produce tinea capitis.

Tinea pedis is the term used for a dermatophyte infection of the soles of the feet and the interdigital spaces. It is most commonly caused by Trichophyton rubrum, a dermatophyte initially endemic only to a small region of Southeast Asia and in parts of Africa and Australia. Interestingly, tinea pedis was not noted in these areas then, possibly because these populations did not wear occlusive footwear. The colonization of the T rubrum –endemic regions by European nations helped to spread the fungus throughout Europe. Wars with accompanying mass movements of troops and refugees, the general increase in available means of travel, and the rise in the use of occlusive footwear have all combined to make T rubrum the world's most prevalent dermatophyte.

The first reported case of tinea pedis in the United States was noted in Birmingham, Alabama, in the 1920s. World War I troops returning from battle may have transported T rubrum to the United States.

Other eMedicine tinea articles include Tinea Barbae, Tinea Capitis, Tinea Corporis, Tinea Cruris, Tinea Faciei, Tinea Nigra, and Tinea Versicolor.

Pathophysiology

T rubrum, Trichophyton mentagrophytes, and Epidermophyton floccosum most commonly cause tinea pedis, with T rubrum being the most common cause worldwide. Trichophyton tonsurans has also been implicated in children. Nondermatophyte causes include Scytalidium dimidiatum, Scytalidium hyalinum, and, rarely, Candida species.

Using enzymes called keratinases, dermatophyte fungi invade the superficial keratin of the skin, and the infection remains limited to this layer. Dermatophyte cell walls also contain mannans, which can inhibit the body's immune response. T rubrum in particular contains mannans that may reduce keratinocyte proliferation, resulting in a decreased rate of sloughing and a chronic state of infection.

Temperature and serum factors, such as beta globulins and ferritin, appear to have a growth-inhibitory effect on dermatophytes; however, this pathophysiology is not completely understood. Sebum also is inhibitory, thus partly explaining the propensity for dermatophyte infection of the feet, which have no sebaceous glands.  Host factors such as breaks in the skin and maceration of the skin may aid in dermatophyte invasion. The cutaneous presentation of tinea pedis is also dependent on the host's immune system and the infecting dermatophyte.

Frequency

International

Tinea pedis is thought to be the world's most common dermatophytosis. Reportedly, 70% of the population will be infected with tinea pedis at some time.

Mortality/Morbidity

Tinea pedis is not associated with significant mortality or morbidity.

Race

Tinea pedis has no predilection for any racial or ethnic group.

Sex

The disease more commonly affects males compared with females.

Age

The prevalence of tinea pedis increases with age. Most cases occur after puberty. Childhood tinea pedis is rare.

Clinical

History

Commonly, patients describe pruritic, scaly soles and, often, painful fissures between the toes. Less often, patients describe vesicular or ulcerative lesions. Some patients, especially elderly persons, may simply attribute their scaling feet to dry skin.

Physical

Patients with tinea pedis have the following 4 possible clinical presentations:

• Interdigital
  • The interdigital presentation is the most characteristic type of tinea pedis, with erythema, maceration, fissuring, and scaling, most often seen between the fourth and fifth toes. This type is often accompanied by pruritus.
  • The dorsal surface of the foot is usually clear, but some extension onto the plantar surface of the foot may occur.
  • This type can be associated with the dermatophytosis complex, which is an infection with fungi followed by an infection with bacteria.
• Chronic hyperkeratotic
  • The hyperkeratotic type of tinea pedis is characterized by chronic plantar erythema with slight scaling to diffuse hyperkeratosis. This type can be asymptomatic or pruritic.
  • This type is also called moccasin tinea pedis, after its moccasinlike distribution. Both feet are usually affected.
  • Typically, the dorsal surface of the foot is clear, but, in severe cases, the condition may extend onto the sides of the foot.
• Inflammatory/vesicular
  • Painful, pruritic vesicles or bullae, most often on the instep or anterior plantar surface, characterize the inflammatory/vesicular type.
  • The lesions can contain either clear or purulent fluid; after they rupture, scaling with erythema persists.
  • Cellulitis, lymphangitis, and adenopathy can complicate this type of tinea pedis.
  • The inflammatory/vesicular type can be associated with an eruption called the dermatophytid reaction, which develops on the palmar surface of one or both hands and/or the sides of the fingers. Papules, vesicles, and occasionally bullae or pustules may occur, often in a symmetrical fashion, and it may mimic dyshidrosis (pompholyx). This is an allergy or hypersensitivity response to the infection on the foot, and it contains no fungal elements. The specific explanation of this phenomenon is still unclear. Distinguishing between a dermatophytid reaction and dyshidrosis can be difficult. Dermatophytid reactions are associated with vesicular tinea pedis; therefore, a close inspection of the feet is necessary in patients with vesicular hand dermatoses. The dermatophytid reaction resolves when the tinea pedis infection is treated, and treatment of the hands with topical steroids can hasten resolution.
• Ulcerative
  • The ulcerative variety is characterized by rapidly spreading vesiculopustular lesions, ulcers, and erosions, typically in the web spaces, and is often accompanied by a secondary bacterial infection.
  • Cellulitis, lymphangitis, pyrexia, and malaise can accompany this infection.
  • Occasionally, large areas, even the entire sole, can be sloughed.
  • This type is commonly seen in immunocompromised and diabetic patients.

Patients may have other associated dermatophyte infections, such as onychomycosis, tinea cruris, and tinea manuum. Tinea manuum is often unilateral and associated with moccasin-type tinea pedis (two feet – one hand syndrome).

Causes

• The interdigital type is usually caused by T rubrum. It is more pruritic in hot, humid environments. Other possible causative organisms include T mentagrophytes var interdigitale and E floccosum.
  • Hyperhidrosis is a risk factor for infection.
  • Candida albicans and bacteria can complicate the process as secondary pathogens.
  • In 1993, the term dermatophytosis complex was coined to describe the manifestation of moist, oozing, pruritic toe-web spaces from which bacteria, but not dermatophytes, have been isolated. Common culprits include Pseudomonas, Proteus, and Staphylococcus aureus. Experts believe that dermatophytes invade the stratum corneum, paving the way for secondary bacterial infection.
• The chronic hyperkeratotic type is usually caused by T rubrum. Other possible causative organisms include T mentagrophytes var interdigitale, E floccosum, and the nondermatophyte molds Scytalidium hyalinum and Scytalidium dimidiatum.
• Both the inflammatory/vesicular type and the ulcerative type are most commonly caused by the zoophilic fungus T mentagrophytes var mentagrophytes.
• A hot, humid, tropical environment and prolonged use of occlusive footwear, with the resulting complications of hyperhidrosis and maceration, are risk factors for all types of tinea pedis. Certain activities, such as swimming and communal bathing, may also increase the risk of infection.^1,2
• Tinea pedis is more common in some families, and certain people may have a genetic predisposition to the infection. A defect in cell-mediated immunity may predispose some individuals to develop tinea pedis, but this is not certain.

Differential Diagnoses

Other Problems to Be Considered

Autoimmune blistering disorders
Bacterial infection
Eczematous dermatitis
Xerosis

Workup

Laboratory Studies

• Order direct potassium hydroxide (KOH) staining for fungal elements. Usually, the fungal elements are easily identified from scaly lesions. Using counterstains may enhance the visibility of the hyaline hyphae found in dermatophyte infections. Examples include the chitin-specific stains chlorazol black E, which stains hyphae blue-black, and calcofluor, which fluoresces hyphae under a fluorescent microscope.
  • A sample from skin scrapings may be obtained using a No. 15 blade.
  • When blisters are present, the highest fungal yield is obtained by scraping the roof of the vesicle.
• A fungal culture may be performed to confirm the diagnosis and to identify the pathogenic species.
  • Common media include dermatophyte test medium, Mycosel, or mycobiotic agar.
  • Use caution when choosing the correct culture medium because certain media (eg, dermatophyte test medium) contain cycloheximide, which inhibits the growth of nondermatophyte molds. Because these fungi can be a factor in tinea pedis, use agar without cycloheximide.

Histologic Findings

A skin biopsy and histopathological study are rarely needed to confirm a diagnosis of tinea pedis. Fungal elements within the stratum corneum can usually be identified using periodic acid-Schiff or Gomori methenamine-silver stain but may be sparse or absent in inflammatory or interdigital tinea pedis complicated by secondary bacterial infection. Neutrophils may be noted within the stratum corneum, a finding that should prompt consideration of a dermatophyte infection. In vesicular tinea pedis, spongiotic intraepidermal vesicles are present; in the chronic hyperkeratotic (moccasin) type, hyperkeratosis and epidermal acanthosis usually are present. Both types are associated with an acute or chronic dermatitis that may contain eosinophils.

Treatment

Medical Care

Medical therapy is the mainstay of tinea pedis treatment (see Medication).

Surgical Care

Surgical care is usually not required.

Activity

• Infection can occur through contact with infected scales on bath or pool floors, so wearing protective footwear in communal areas may help decrease the likelihood of infection.
• Because infected scales can be present on clothing, frequent laundering is a good idea.
• Occlusive footwear promotes infection by creating warm, humid, macerating environments where dermatophytes thrive. Therefore, patients should try to minimize foot moisture by limiting the use of occlusive footwear and should discard shoes that may be contributing to recurrence of the infection.
• The Medscape Exercise and Sports Medicine Resource Center may be of interest.

Medication

Tinea pedis can be treated with topical or oral antifungals or a combination of both. Topical agents are used for 1-6 weeks, depending on manufacturers' recommendations. A patient with chronic hyperkeratotic (moccasin) tinea pedis should be instructed to apply medication to the bottoms and sides of his or her feet. For interdigital tinea pedis, even though symptoms may not be present, a patient should apply the topical agent to the interdigital areas and to the soles because of the likelihood of plantar-surface infection.

Recurrence of the infection is often due to a patient's discontinuance of medication after symptoms abate. A simple strategy to increase a patient's compliance is to prescribe a large quantity of topical medicine, which may motivate a patient to continue use until the entire tube is empty.

Moccasin-type tinea pedis is often recalcitrant to topical antifungals alone, owing to the thickness of the scale on the plantar surface. The concomitant use of topical urea or other keratolytics with topical antifungals should improve the response to topical agents. In addition, for moccasin tinea pedis caused by Scytalidium species, Whitfield solution, containing benzoic and salicylic acids, can be beneficial. However, patients with extensive chronic hyperkeratotic tinea pedis or inflammatory/vesicular tinea pedis usually require oral therapy, as do patients with concomitant onychomycosis,³ diabetes, peripheral vascular disease, or immunocompromising conditions.

Topical imidazoles

Effective in all forms of tinea pedis but are excellent treatments for interdigital tinea pedis because they are effective against dermatophytes and Candida. Some of these drugs (eg, econazole) also have antibacterial activity.

Clotrimazole 1% (Mycelex, Lotrimin)

Broad-spectrum antifungal agent that inhibits yeast growth by altering cell-membrane permeability, causing death of fungal cells. Reevaluate diagnosis if no clinical improvement after 4 wk.

Dosing

Adult

Gently massage into affected area and surrounding skin areas bid for 2-6 wk

Pediatric

Children: Not established
Adolescents: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

For external use only; avoid contact with eyes; discontinue if irritation or sensitivity develops

Econazole 1% cream (Spectazole Topical)

Effective in cutaneous infections. May interfere with RNA and protein synthesis and metabolism. Disrupts cell membrane permeability, causing death of fungal cells.

Dosing

Adult

Apply sparingly over affected areas qd/bid for 4 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue if sensitivity or irritation develops; for external use only; avoid contact with eyes

Ketoconazole 1% cream (Nizoral)

Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in death of fungal cells.

Dosing

Adult

Rub gently into affected area bid/qid for 2-4 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; fungal meningitis

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue if sensitivity or irritation develops; for external use only; avoid contact with eyes

Miconazole (Monistat)

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out, resulting in fungal cell death. The 2% lotion is preferred in intertriginous areas. If the 2% cream is used, apply sparingly to avoid maceration effects.

Dosing

Adult

Cream and lotion: Cover affected areas bid for 2-6 wk
Powder: Spray or sprinkle liberally over affected area bid for 2-4 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue if sensitivity or chemical irritation occurs; for external use only; avoid contact with eyes

Oxiconazole 1% cream (Oxistat)

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out, resulting in death of fungal cells.

Dosing

Adult

Apply to affected area bid for 4 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Discontinue if sensitivity or chemical irritation occurs; for external use only; avoid contact with eyes

Sertaconazole nitrate cream (Ertaczo)

Topical imidazole antifungal active against T rubrum, T mentagrophytes, and E floccosum. Indicated for tinea pedis.

Dosing

Adult

Apply topically bid to clean, dry skin between toes and immediate surrounding healthy skin for 4 wk

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

For topical use only; may cause dermatitis, dry skin, burning sensation, pruritus, hyperpigmentation, desquamation, or skin tenderness

Topical pyridones

Broad-spectrum agents with antidermatophytic, antibacterial, and anticandidal activity and are therefore useful in all forms of tinea pedis but especially effective in interdigital tinea pedis.

Ciclopirox 1% cream (Loprox)

Interferes with synthesis of DNA, RNA, and protein by inhibiting transport of essential elements in fungal cells.

Dosing

Adult

Massage into affected area bid; reevaluate diagnosis if no improvement after 4 wk

Pediatric

<10 years: Not established
>10 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Avoid contact with eyes and other internal routes; discontinue if irritation or sensitivity develops

Topical allylamines

Effective in treating all forms of tinea pedis. In vitro, these agents have demonstrated potent activity against dermatophyte fungi, so they are useful in treating patients with refractory tinea pedis (eg, chronic hyperkeratotic). Terbinafine 1% (Lamisil) has been shown to be effective in some patients with interdigital tinea pedis with only 1 wk of treatment. Patients with chronic hyperkeratotic tinea pedis generally require 4 wk of treatment.

Naftifine 1% cream and gel (Naftin)

Broad-spectrum antifungal agent and synthetic allylamine derivative; may decrease synthesis, which, in turn, inhibits growth of fungal cells.

Dosing

Adult

Cream: Apply to affected area qd for 4 wk
Gel: Apply to affected areas bid for 4 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Discontinue if sensitivity or irritation occurs; for external use only; avoid contact with eyes

Terbinafine (Lamisil)

Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing death of fungal cells. Use until symptoms significantly improve. Duration of treatment should be >1 wk but not >4 wk.

Dosing

Adult

Cream: Apply bid 1-4 wk
Spray: Apply bid (morning and night) for 1 wk

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Discontinue if sensitivity or irritation occurs; for external use only; avoid contact with eyes

Topical benzylamines

Sometimes classified as a subset of allylamines. Useful for treating patients with refractory tinea pedis (eg, chronic hyperkeratotic). Have been shown to be effective in some patients with interdigital tinea pedis with only 1 wk of treatment.⁴

Butenafine 1% cream (Mentax)

Damages fungal cell membranes, arresting growth of fungal cells.

Dosing

Adult

Apply bid for 1 wk or apply topically to affected area qd for 4 wk

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

For external use only; discontinue if irritation or sensitivity develops

Oral antimycotics

Should be considered in patients with extensive chronic hyperkeratotic or inflammatory/vesicular tinea pedis. Could also be used for patients with disabling disease, patients in whom topical treatments have failed, patients with diabetes or peripheral vascular disease, and patients with immunocompromising conditions.

Itraconazole (Sporanox)

Fungistatic activity. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Dosing

Adult

200 mg PO qd for 1 wk; not to exceed 400 mg/d; increase in 100-mg increments if no improvement (administer >200 mg/d in divided doses)

Pediatric

Not established; suggested dose of 100 mg/d for systemic fungal infections

Interactions

Antacids may reduce absorption; edema may occur with coadministration of calcium channel blockers (eg, amlodipine, nifedipine); hypoglycemia may occur with sulfonylureas; may increase tacrolimus and cyclosporine plasma concentrations when high doses are used; rhabdomyolysis may occur with coadministration of HMG-CoA reductase inhibitors (eg, lovastatin, simvastatin); coadministration with cisapride can cause cardiac rhythm abnormalities and death; may increase digoxin levels; coadministration may increase plasma levels of midazolam or triazolam; phenytoin and rifampin may reduce levels (phenytoin metabolism may be altered)

Contraindications

Documented hypersensitivity; coadministration with terfenadine (withdrawn from US market), astemizole (withdrawn from US market), triazolam, simvastatin, cisapride, quinidine, pimozide (withdrawn from US market), and HMG-CoA reductase inhibitors may cause adverse cardiovascular effects (possibly death)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor hepatic function in patients taking itraconazole for >1 mo and in patients who develop any sign of hepatic insufficiency

Terbinafine (Lamisil, Daskil)

Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing death of fungal cells. Use until symptoms significantly improve.

Dosing

Adult

250 mg PO qd for 1-2 wk

Pediatric

Weight-based dosing
12-20 kg: 62.5 mg/d PO
20-40 kg: 125 mg/d PO
>40 kg: 250 mg/d PO
Treatment duration as in adults

Interactions

May decrease cyclosporine effects; toxicity may increase with rifampin and cimetidine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Perform hepatic function tests and CBC counts when taking for >6 wk, if signs of hepatic dysfunction develop, or if immunocompromised; not recommended for patients with preexisting liver disease or renal impairment

Fluconazole (Diflucan)

Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation.

Dosing

Adult

150 mg PO qwk for up to 4 wk

Pediatric

6 mg/kg/d PO for 2-3 wk

Interactions

Levels may increase with coadministration of hydrochlorothiazide; levels may decrease with long-term coadministration of rifampin; coadministration of fluconazole may decrease phenytoin clearance; may increase concentrations of theophylline, tolbutamide, glyburide, and glipizide; effects of anticoagulants may increase with coadministration of fluconazole; increases in cyclosporine concentrations may occur when administered concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor closely if rash develops and discontinue drug if lesions progress; may cause clinical hepatitis, cholestasis, and fulminant hepatic failure (including death) with underlying medical conditions (eg, AIDS, malignancy) and while taking multiple concomitant medications; not recommended in breastfeeding

Dermatological agents

May use to supplement antimycotic agents in certain clinical situations.

Aluminum acetate (Otic Domeboro, Burow's Solution)

Drying agent for vesicular tinea pedis. Dissolve aluminum acetate tablets in water to produce a 1:10-40 solution.

Dosing

Adult

Soak feet bid; apply as a compress for 20-30 min 4-6 times/d until condition resolves

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

For external use only

Ammonium lactate lotion (Lac Hydrin)

Used to decrease scaling in patients with hyperkeratotic soles. Contains lactic acid, an alpha hydroxy acid that has keratolytic action and thus facilitates release of comedones. Causes disadhesion of corneocytes. Available in 12% and 5% strengths. Use 12% lotion.

Dosing

Adult

Apply liberally to all affected areas bid until condition resolves

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause pain if applied on broken skin; may cause irritation with erythema, burning, and peeling if applied to face in 12% concentration

Urea, topical (Carmol-40, Keralac)

Used to decrease scaling in patients with hyperkeratotic soles. Promotes hydration and removal of excess keratin by dissolving the intracellular matrix. Available in 10-40% concentration.

Dosing

Adult

Apply to all affected areas bid

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

For external use only

Follow-up

Further Outpatient Care

The need for follow-up care should be assessed on a case-by-case basis. Further outpatient visits may be indicated, depending on the extent and severity of the infection. Treatment regimens may need to be switched or augmented.

Inpatient & Outpatient Medications

See Medication.

Deterrence/Prevention

See Patient Education.

Complications

Secondary cellulitis, lymphangitis, pyoderma, and even osteomyelitis can result from mycotic infections of the feet. These complications are seen more frequently in patients with conditions such as chronic edema, immunosuppression, and diabetes.

Prognosis

The type of tinea pedis infection and underlying conditions (eg, immunosuppression, diabetes) affect the prognosis; however, with appropriate treatment, the prognosis is generally good.

Patient Education

Patients should be educated that reinfection can occur if they are reexposed to dermatophytes. Old shoes are often sources of reinfection and should be disposed of or treated with antifungal powders.

Patients should be cautioned to wear protective footwear at communal pools and baths and should attempt to keep their feet dry by limiting occlusive footwear. When occlusive footwear is worn, wearing cotton socks and adding a drying powder with antifungal action in the shoes may be helpful.

For excellent patient education resources, visit eMedicine's Foot Care Center. In addition, see eMedicine's patient education articles Athlete's Foot and Ringworm on Body.

Miscellaneous

Medicolegal Pitfalls

Because tinea pedis is not associated with significant mortality or morbidity, the risk of medicolegal liability is slight. Secondary cellulitis, lymphangitis, and pyoderma can result from complications of mycotic infections of the feet, and practitioners must provide appropriate treatment in such cases.

References

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Keywords

athlete's foot, ringworm of the feet, dermatophytosis, dermatophytid, Trichophyton rubrum, T rubrum, Trichophyton mentagrophytes, T mentagrophytes, Epidermophyton floccosum, E floccosum, Scytalidium hyalinum, S hyalinum, Scytalidium dimidiatum, S dimidiatum

Contributor Information and Disclosures

Author

Courtney M Robbins, MD, Resident Physician, Department of Dermatology, University of Alabama at Birmingham School of Medicine
Courtney M Robbins, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Coauthor(s)

Boni E Elewski, MD, Professor, Department of Dermatology, University of Alabama at Birmingham
Boni E Elewski, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Abbott #1 Grant/research funds Investigator; Amgen Honoraria Consulting; Amgen #1 Grant/research funds Investigator; Amgen #2 Stock Stockholder; Barrier #1 Grant/research funds Investigator; Centocor #1 Grant/research funds Investigator; Intendis  Consulting; Mediquest #1 Grant/research funds Investigator; NanoBio Honoraria Consulting; Novartis #1 Grant/research funds Investigator

Medical Editor

Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle
Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other; american college of physicians Honoraria Other

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