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. 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.
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 Reference 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 following 4 possible clinical presentations:
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.
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 therapy is the mainstay of tinea pedis treatment (see Medication).
Surgical care is usually not required for tinea pedis.
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.
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. 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, diabetes, peripheral vascular disease, or immunocompromising conditions.
Clinical Context: 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.
Clinical Context: Effective in cutaneous infections. May interfere with RNA and protein synthesis and metabolism. Disrupts cell membrane permeability, causing death of fungal cells.
Clinical Context: Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in death of fungal cells.
Clinical Context: 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.
Clinical Context: 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.
Clinical Context: Topical imidazole antifungal active against T rubrum, T mentagrophytes, and E floccosum. Indicated for tinea pedis.
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.
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.
Clinical Context: Interferes with synthesis of DNA, RNA, and protein by inhibiting transport of essential elements in fungal cells.
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.
Clinical Context: Broad-spectrum antifungal agent and synthetic allylamine derivative; may decrease synthesis, which, in turn, inhibits growth of fungal cells.
Clinical Context: 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.
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.
Clinical Context: Damages fungal cell membranes, arresting growth of fungal cells.
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.
Clinical Context: 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.
Clinical Context: Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing death of fungal cells. Use until symptoms significantly improve.
Clinical Context: Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation.
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.
Clinical Context: Drying agent for vesicular tinea pedis. Dissolve aluminum acetate tablets in water to produce a 1:10-40 solution.
Clinical Context: 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.
Clinical Context: 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.
May use to supplement antimycotic agents in certain clinical situations.
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.
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, and diabetes.
Also see the following clinical guideline summaries:
The type of tinea pedis infection and underlying conditions (eg, immunosuppression, diabetes) affect the prognosis; however, with appropriate treatment, the prognosis is generally good.