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Tinea Pedis

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

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 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.

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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.

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Epidemiology

Frequency

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.

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.

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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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  17. Savin R, De Villez RL, Elewski B, et al. One-week therapy with twice-daily butenafine 1% cream versus vehicle in the treatment of tinea pedis: a multicenter, double-blind trial. J Am Acad Dermatol. 1997 Feb. 36(2 Pt 1):S15-9. [Medline].

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