tinea pedis1

8/12/2019 Tinea Pedis1

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Background

Tinea pedis has afflicted humanity for centuries, so it is perhaps surprising that the condition was notdescribed 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 organismsthat producetinea capitis.

Tinea pedis is the term used for a dermatophyte infection of the soles of the feet and the interdigitalspaces. Tinea pedis is most commonly caused byTrichophyton rubrum,a dermatophyte initiallyendemic 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 wearocclusive footwear. The colonization of the T rubrumendemic regions by European nations helpedto spread the fungus throughout Europe. Wars with accompanying mass movements of troops andrefugees, the general increase in available means of travel, and the rise in the use of occlusivefootwear have all combined to make T rubrumthe world's most prevalent dermatophyte.[2]

The first reported case of tinea pedis in the United States was noted in Birmingham, Alabama, in the1920s. World War I troops returning from battle may have transported T rubrumto the United States.

Other Medscape Reference tinea articles includeTinea Barbae,Tinea Capitis,Tinea Corporis,Tinea

Cruris,Tinea Faciei,Tinea Nigra,andTinea Versicolor.

Pathophysiology

T rubrum, Trichophyton mentagrophytes,and Epidermophyton floccosummost commonly cause tineapedis, with T rubrumbeing the most common cause worldwide. Trichophyton tonsuranshas alsobeen implicated in children. Nondermatophyte causes include Scytalidium dimidiatum, Scytalidiumhyalinum, and, rarely, Candidaspecies.

Using enzymes called keratinases, dermatophyte fungi invade the superficial keratin of the skin, andthe infection remains limited to this layer. Dermatophyte cell walls also contain mannans, which caninhibit the body's immune response. T rubrumin 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 skinmay aid in dermatophyte invasion. The cutaneous presentation of tinea pedis is also dependent onthe host's immune system and the infecting dermatophyte.

Epidemiology

Frequency

InternationalTinea pedis is thought to be the world's most common dermatophytosis. Reportedly, 70% of thepopulation 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 tineapedis is rare.
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History

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

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

Interdigital tinea pediso 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 isoften accompanied by pruritus.

o The dorsal surface of the foot is usually clear, but some extension onto the plantar surface of thefoot may occur.

o This type can be associated with the dermatophytosis complex, which is an infection with fungifollowed by an infection with bacteria.

Chronic hyperkeratotic tinea pediso 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 pediso 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 symmetricalfashion, and it may mimic dyshidrosis (pompholyx). This is an allergy or hypersensitivity responseto the infection on the foot, and it contains no fungal elements. The specific explanation of thisphenomenon is still unclear. Distinguishing between a dermatophytid reaction and dyshidrosis canbe difficult. Dermatophytid reactions are associated with vesicular tinea pedis; therefore, a closeinspection of the feet is necessary in patients with vesicular hand dermatoses. The dermatophytidreaction resolves when the tinea pedis infection is treated, and treatment of the hands with topicalsteroids can hasten resolution.

Ulcerative tinea pediso 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 resultin 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, humidenvironments. Other possible causative organisms in tinea pedis include Tmentagrophytesvar interdigitaleand E floccosum.

Hyperhidrosis is a risk factor for infection.

Candida albicansand 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.
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Common culprits includePseudomonas, Proteus, and Staphylococcus aureus. Experts believe thatdermatophytes 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 possiblecausative organisms include T mentagrophytesvar interdigitale, E floccosum, and thenondermatophyte molds Scytalidium hyalinumandScytalidium 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 mentagrophytesvarmentagrophytes. 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. Certainactivities, 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 predispositionto the infection. A defect in cell-mediated immunity may predispose some individuals to develop tineapedis, 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 mayenhance the visibility of the hyaline hyphae found in dermatophyte infections. Examples include thechitin-specific stains chlorazol black E, which stains hyphae blue-black, and calcofluor, whichfluoresces 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 thepathogenic species.

Common media include dermatophyte test medium, Mycosel, or mycobiotic agar.

Use caution when choosing the correct culture medium because certain media (eg, dermatophytetest medium) contain cycloheximide, which inhibits the growth of nondermatophyte molds. Becausethese fungi can be a factor in tinea pedis, use agar without cycloheximide.

Histologic FindingsA 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 orGomori methenamine-silver stain but may be sparse or absent in inflammatory or interdigital tineapedis complicated by secondary bacterial infection. Neutrophils may be noted within the stratumcorneum, a finding that should prompt consideration of a dermatophyte infection. In vesicular tineapedis, spongiotic intraepidermal vesicles are present; in the chronic hyperkeratotic (moccasin) type,hyperkeratosis and epidermal acanthosis usually are present. Both types are associated with anacute or chronic dermatitis that may contain eosinophils.

Medical CareMedical therapy is the mainstay of tinea pedis treatment (see Medication).
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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 wheredermatophytes thrive. Therefore, patients should try to minimize foot moisture by limiting the use ofocclusive 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 agentsare used for 1-6 weeks, depending on manufacturers' recommendations. Luliconazole, an imidazoletopical 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 topicalagent 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 symptomsabate. A simple strategy to increase a patient's compliance is to prescribe a large quantity of topicalmedicine, 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 ofthe scale on the plantar surface. The concomitant use of topical urea or other keratolytics with topicalantifungals should improve the response to topical agents.[12] In addition, for moccasin tinea pediscaused byScytalidiumspecies, Whitfield solution, containing benzoic and salicylic acids, can bebeneficial. However, patients with extensive chronic hyperkeratotic tinea pedis orinflammatory/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 becausethey are effective against dermatophytes and Candida. Some of these drugs (eg, econazole) alsohave 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.


Ketoconazole topical (Nizoral)

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


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


Oxiconazole 1% cream (Oxistat)

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


Sertaconazole nitrate cream (Ertaczo)

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

for tinea pedis.


Luliconazole (Luzu)

Luliconazole is available as a 1% topical cream administered once daily for 1 week. It is an imidazoleantifungal 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 aretherefore 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 infungal cells.

Topical allylamines

Class Summary

Effective in treating all forms of tinea pedis. In vitro, these agents have demonstrated potent activityagainst 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 patientswith interdigital tinea pedis with only 1 wk of treatment. Patients with chronic hyperkeratotic tineapedis 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.


Terbinafine topical (Lamisil)

Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing death of fungal cells. Useuntil 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]

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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 tineapedis. Could also be used for patients with disabling disease, patients in whom topical treatmentshave failed, patients with diabetes or peripheral vascular disease, and patients withimmunocompromising conditions.


Itraconazole (Sporanox)

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


Terbinafine (Lamisil, Daskil)

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


Fluconazole (Diflucan)

Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450and 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.


Ammonium lactate lotion (Lac Hydrin)

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


Urea, topical (Carmol-40, Keralac)Used to decrease scaling in patients with hyperkeratotic soles. Promotes hydration and removal ofexcess 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. Furtheroutpatient visits may be indicated, depending on the extent and severity of the tinea pedis. Treatmentregimens may need to be switched or augmented.

Inpatient & Outpatient Medications

See Medication.
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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 patientswith conditions such as chronic edema, immunosuppression, hemiplegia and paraplegia,[17] anddiabetes.[18]

Also see the following clinical guideline summaries:

Wound, Ostomy, and Continence Nurses Society -Guideline for management of wounds in patientswith lower-extremity venous disease[19]

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

Prognosis

The type of tinea pedis infection and underlying conditions (eg, immunosuppression, diabetes) affectthe 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 todermatophytes. Old shoes are often sources of reinfection and should be disposed of or treated withantifungal powders.

Patients should be cautioned to wear protective footwear at communal pools and baths and shouldattempt 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 articlesAthlete'sFootandRingworm on Body.
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