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Tinea Pedis Clinical Presentation

  • Author: Courtney M Robbins, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Nov 19, 2015
 

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.

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Physical

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]

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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 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.

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Contributor Information and Disclosures
Author

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

Courtney M Robbins, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, 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: Nothing to disclose.

Specialty Editor Board

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

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

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, Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

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

Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References
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  4. Leyden JJ. Progression of interdigital infections from simplex to complex. J Am Acad Dermatol. 1993 May. 28(5 Pt 1):S7-S11. [Medline].

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