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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.
[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 byTrichophyton 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 Reference 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.
Epidemiology
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
Tinea pedis 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.
History
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.
Physical
Patients with tinea pedis have the following 4 possible clinical presentations:
Interdigital tinea pedis
o 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.
o The dorsal surface of the foot is usually clear, but some extension onto the plantar surface of the
foot may occur.
o 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
o The hyperkeratotic type of tinea pedis is characterized by chronic plantar erythema with slight
scaling to diffuse hyperkeratosis.
o This type can be asymptomatic or pruritic.This type is also called moccasin tinea pedis, after its
moccasinlike distribution. Both feet are usually affected.
o 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
o Painful, pruritic vesicles or bullae, most often on the instep or anterior plantar surface, characterize
the inflammatory/vesicular type.
o The lesions can contain either clear or purulent fluid; after they rupture, scaling with erythema
persists.
o Cellulitis, lymphangitis, and adenopathy can complicate this type of tinea pedis.
o 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
o 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.
o Cellulitis, lymphangitis, pyrexia, and malaise can accompany this infection.
o Occasionally, large areas, even the entire sole, can be sloughed.
o This type is commonly seen in immunocompromised and diabetic patients.
Patients may have other associated dermatophyte infections, such asonychomycosis, tinea cruris,
and tinea manuum. Tinea manuum is often unilateral and associated with moccasin-type tinea pedis
(2-feet1-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]

Causes
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 includePseudomonas, 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 andScytalidium 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 varmentagrophytes.
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.

Differential Diagnoses
Candidiasis, Cutaneous
Contact Dermatitis, Allergic
Dyshidrotic Eczema
Erythema Multiforme
Erythrasma
Friction Blisters
Pityriasis Rubra Pilaris
Psoriasis, Plaque
Psoriasis, Pustular
Syphilis

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.
Activity
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.
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.
[12]
In addition, for moccasin tinea pedis
caused byScytalidium 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,
[13]
diabetes,
[14]
peripheral vascular disease, or immunocompromising conditions.
Topical imidazoles
Class Summary
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.
[15]

View full drug information
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.
Econazole (Spectazole Topical)

Effective in cutaneous infections. May interfere with RNA and protein synthesis and metabolism.
Disrupts cell membrane permeability, causing death of fungal cells.
View full drug information
Ketoconazole topical (Nizoral)

Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular
components to leak, resulting in death of fungal cells.
View full drug information
Miconazole topical (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.
View full drug information
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.
View full drug information
Sertaconazole nitrate cream (Ertaczo)

Topical imidazole antifungal active against T rubrum, T mentagrophytes, and E floccosum. Indicated
for tinea pedis.
View full drug information
Luliconazole (Luzu)

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.
Topical pyridones
Class Summary
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.
View full drug information
Ciclopirox 1% cream (Loprox)

Interferes with synthesis of DNA, RNA, and protein by inhibiting transport of essential elements in
fungal cells.
Topical allylamines
Class Summary
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.
View full drug information
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.
View full drug information
Terbinafine topical (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.
Topical benzylamines
Class Summary
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.
[16]

View full drug information
Butenafine (Mentax)

Damages fungal cell membranes, arresting growth of fungal cells.
Oral antimycotics
Class Summary
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.
View full drug information
Itraconazole (Sporanox)

Fungistatic activity. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting
cytochrome P-450dependent synthesis of ergosterol, a vital component of fungal cell membranes.
View full drug information
Terbinafine (Lamisil, Daskil)

Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing death of fungal cells. Use
until symptoms significantly improve.
View full drug information
Fluconazole (Diflucan)

Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450
and sterol C-14 alpha-demethylation.
Dermatological agents
Class Summary
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.
View full drug information
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.
View full drug information
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.

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.
Deterrence/Prevention
See Patient Education.
Complications
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,
[17]
and
diabetes.
[18]

Also see the following clinical guideline summaries:
Wound, Ostomy, and Continence Nurses Society - Guideline for management of wounds in patients
with lower-extremity venous disease
[19]

American College of Foot and Ankle Surgeons - Diabetic foot disorders: a clinical practice
guideline
[20]

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 with tinea pedis 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, see eMedicineHealth's patient education articles Athlete's
Foot and Ringworm on Body.