Tinea Pedis



Tinea pedis has afflicted humanity for centuries, so it is perhaps surprising that the condition was not described until Pellizzari did so in 1888.[1] 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. Tinea pedis 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.[2]

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


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.




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.


Tinea pedis is not associated with significant mortality or morbidity.


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


Tinea pedis more commonly affects males compared with females.


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


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


Patients with tinea pedis have the clinical presentations described below.

Interdigital tinea pedis

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 tinea pedis

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 tinea pedis

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 tinea pedis

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.

Other associated dermatophyte infections

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 (2-feet–1-hand syndrome). One study suggests the scratching habits of the infected individual result in transmission of the dermatophytes from the feet to the hand.[3]


The interdigital type of tinea pedis is usually caused by T rubrum. It is more pruritic in hot, humid environments. Other possible causative organisms in tinea pedis 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.[4]

The chronic hyperkeratotic type of tinea pedis 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 of tinea pedis and the ulcerative type of tinea pedis 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.[5, 6]

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.

Laboratory Studies

In suspected tinea pedis, 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 of tinea pedis 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.

Medical Care

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

Surgical Care

Surgical care is usually not required for tinea pedis.


Tinea pedis 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.

Medication Summary

Tinea pedis can be treated with topical or oral antifungals or a combination of both.[7, 8, 9] Topical agents are used for 1-6 weeks, depending on manufacturers' recommendations. Luliconazole, an imidazole topical cream, is applied once daily for 2 weeks.[10, 11] 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.

Naftifine gel or cream 2% is indicated for interdigital tinea pedis in adults and adolescents. A study using 2% gel for interdigital-type tinea pedis demonstrated greater improvement from baseline for complete cure (P = .001), mycological cure (P < .0001), and treatment effectiveness (P < .0001) as early as 2 weeks when compared with vehicle; however the highest response rates were seen 4 weeks post treatment (P < .0001, for all endpoints). Statistically significant results for complete cure, mycological cure, and treatment effectiveness (P < .0001, for all endpoints) were also seen at week 6 among subjects with moccasin-type tinea pedis.[12]

Recurrence of tinea pedis 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.[13] 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,[14] diabetes,[15] peripheral vascular disease, or immunocompromising conditions.

Clotrimazole 1% (Mycelex, Lotrimin)

Clinical Context:  Clotrimazole is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell-membrane permeability, causing death of fungal cells. Reevaluate the diagnosis if no clinical improvement occurs after 4 weeks.

Econazole (Spectazole Topical)

Clinical Context:  Econazole is effective in cutaneous infections. It may interfere with RNA and protein synthesis and metabolism. Econazole disrupts cell membrane permeability, causing death of fungal cells.

Ketoconazole topical (Nizoral)

Clinical Context:  Ketoconazole is an imidazole broad-spectrum antifungal agent; it inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in death of fungal cells.

Miconazole topical (Monistat)

Clinical Context:  Miconazole damages the fungal cell wall membrane by inhibiting the 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.

Oxiconazole 1% cream (Oxistat)

Clinical Context:  Oxiconazole damages the fungal cell wall membrane by inhibiting the biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out, resulting in death of fungal cells.

Sertaconazole nitrate cream (Ertaczo)

Clinical Context:  Sertaconazole nitrate is a topical imidazole antifungal active against T rubrum, T mentagrophytes, and E floccosum. It is indicated for tinea pedis.

Luliconazole (Luzu)

Clinical Context:  Luliconazole is available as a 1% topical cream administered once daily for 1 week. It is an imidazole antifungal that alters the fungal cell membrane by interacting with 14-alpha demethylase (an enzyme necessary for conversion of lanosterol to ergosterol). It is indicated for tinea corporis.

Class Summary

Topical imidazoles are 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. An econazole foam is now available.[16]

Ciclopirox 1% cream (Loprox)

Clinical Context:  Ciclopirox interferes with the synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells.

Class Summary

Topical pyridones are 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.

Naftifine (Naftin)

Clinical Context:  Naftifine is a broad-spectrum antifungal agent and synthetic allylamine derivative. Naftifine interferes with sterol biosynthesis in the fungal cell wall by inhibiting squalene monooxygenase (squalene 2,3-epoxidase). It is indicated for tinea pedis caused by the organism Trichophyton rubrum. Use the 1% cream or gel in adults for tinea pedis (twice daily for 4 wk) or the 2% cream or gel in adolescents and adults with interdigital tinea pedis (once daily for 2 wk).

Terbinafine topical (Lamisil)

Clinical Context:  Terbinafine inhibits squalene epoxidase, which decreases ergosterol synthesis, causing death of fungal cells. Use it until symptoms significantly improve. The duration of treatment should be longer than 1 week but not longer than 4 weeks.

Class Summary

Topical allylamines are 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 week of treatment. Patients with chronic hyperkeratotic tinea pedis generally require 4 weeks of treatment.

Butenafine (Mentax)

Clinical Context:  Butenafine damages fungal cell membranes, arresting the growth of fungal cells.

Class Summary

Topical benzylamines are sometimes classified as a subset of allylamines. They are useful for treating patients with refractory tinea pedis (eg, chronic hyperkeratotic). They have been shown to be effective in some patients with interdigital tinea pedis with only 1 week of treatment.[17]

Itraconazole (Sporanox)

Clinical Context:  Itraconazole has fungistatic activity. It is a 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.

Terbinafine (Lamisil, Daskil)

Clinical Context:  Terbinafine inhibits squalene epoxidase, which decreases ergosterol synthesis, causing the death of fungal cells. Use it until symptoms significantly improve.

Fluconazole (Diflucan)

Clinical Context:  Fluconazole is a synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation.

Class Summary

Oral antimycotics should be considered in patients with extensive chronic hyperkeratotic or inflammatory/vesicular tinea pedis. They 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.

Aluminum acetate (Otic Domeboro, Burow's Solution)

Clinical Context:  Aluminum acetate is a drying agent for vesicular tinea pedis. Dissolve aluminum acetate tablets in water to produce a 1:10-40 solution.

Ammonium lactate lotion (Lac Hydrin)

Clinical Context:  Ammonium lactate lotion is used to decrease scaling in patients with hyperkeratotic soles. It contains lactic acid, an alpha hydroxy acid that has keratolytic action and thus facilitates release of comedones. It causes disadhesion of corneocytes. Ammonium lactate lotion is available in 12% and 5% strengths. Use 12% lotion.

Urea, topical (Carmol-40, Keralac)

Clinical Context:  Topical urea is esed to decrease scaling in patients with hyperkeratotic soles. It promotes hydration and removal of excess keratin by dissolving the intracellular matrix. It is available in 10-40% concentrations.

Class Summary

These dermatological agents may be used to supplement antimycotic agents in certain clinical situations.

Further Outpatient Care

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

Inpatient & Outpatient Medications

See Medication.


See Patient Education.


Secondary cellulitis, lymphangitis, pyoderma, and even osteomyelitis can result from mycotic infections of the feet, including tinea pedis. These complications are seen more frequently in patients with conditions such as chronic edema, immunosuppression, hemiplegia and paraplegia,[18] and diabetes.[19]


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


Courtney M Robbins, MD, Dermatologist, Associated Dermatologists, Birmingham, AL

Disclosure: Nothing to disclose.


Boni E Elewski, MD, Professor, Department of Dermatology, University of Alabama at Birmingham

Disclosure: Nothing to disclose.

Specialty Editors

Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Disclosure: Nothing to disclose.

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Disclosure: Nothing to disclose.

Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory

Disclosure: Nothing to disclose.

Catherine M Quirk, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Ackerman Academy of Dermatopathology, New York

Disclosure: Nothing to disclose.


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