Introduction
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. 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. It 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 eMedicine 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.
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
The disease 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.
Clinical
History
Commonly, patients describe pruritic, scaly soles and, often, painful fissures between the toes. Less often, patients describe vesicular or ulcerative lesions. Some 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
- 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
- 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
- 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
- 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.
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 (two feet – one hand syndrome).
Causes
- The interdigital type is usually caused by T rubrum. It is more pruritic in hot, humid environments. Other possible causative organisms 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.
- The chronic hyperkeratotic type 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 and the ulcerative type 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.1,2
- 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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| Follow-up: Tinea Pedis |
| References |
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References
Gentles JC. The isolation of dermatophytes from the floors of communal bathing places. J Clin Pathol. Nov 1956;9(4):374-7. [Medline].
Gentles JC, Evans EG. Foot infections in swimming baths. Br Med J. Aug 4 1973;3(5874):260-2. [Medline].
Gupta AK, Baran R, Summerbell R. Onychomycosis: strategies to improve efficacy and reduce recurrence. J Eur Acad Dermatol Venereol. Nov 2002;16(6):579-86. [Medline].
Savin R, De Villez RL, Elewski B, Hong S, Jones T, Lowe N, 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. Feb 1997;36(2 Pt 1):S15-9. [Medline].
Bolognia JL, Jorizzo JL, Rapini RP, et al. Dermatology. New York, NY: Mosby; 2003:1174-85.
Brodell RT, Elewski B. Antifungal drug interactions. Avoidance requires more than memorization. Postgrad Med. Jan 2000;107(1):41-3. [Medline].
Brodell RT, Elewski BE. Clinical pearl: systemic antifungal drugs and drug interactions. J Am Acad Dermatol. Aug 1995;33(2 Pt 1):259-60. [Medline].
Drake LA, Dinehart SM, Farmer ER, Goltz RW, Graham GF, Hardinsky MK, et al. Guidelines of care for superficial mycotic infections of the skin: tinea corporis, tinea cruris, tinea faciei, tinea manuum, and tinea pedis. Guidelines/Outcomes Committee. American Academy of Dermatology. J Am Acad Dermatol. Feb 1996;34(2 Pt 1):282-6. [Medline].
Elewski B, Hay RJ. International summit on cutaneous antifungal therapy. Boston, Massachusetts, Nov. 11-13, 1994. J Am Acad Dermatol. Nov 1995;33(5 Pt 1):816-22. [Medline].
Elewski BE. Tinea pedis and tinea manuum. In: Demis DJ. Clinical Dermatology. Vol 3. Philadelphia, Pa: Lippincott; 1999:Unit 17-9; 1-11.
Elewski BE. Cutaneous mycoses in children. Br J Dermatol. Jun 1996;134 Suppl 46:7-11: discussion 37-8. [Medline].
Elewski BE. Mechanisms of action of systemic antifungal agents. J Am Acad Dermatol. May 1993;28(5 Pt 1):S28-S34. [Medline].
Elewski BE. Trichophyton rubrum: Dermatophytoses in evolution. Adv Dermatol. 1994;9:110-11.
Elewski BE, Haley HR, Robbins CM. The use of 40% urea cream in the treatment of moccasin tinea pedis. Cutis. May 2004;73(5):355-7. [Medline].
Elewski BE, Malden MA. Cutaneous Fungal Infections. 2nd ed. London: Blackwell Science; 1998:13-72, 321-46.
Freedberg IM, Eisen AZ, Wolff K, et al. Fitzpatrick's Dermatology in General Medicine. 5th ed. New York, NY: McGraw-Hill; 1999:2349-51.
Leyden JJ. Progression of interdigital infections from simplex to complex. J Am Acad Dermatol. May 1993;28(5 Pt 1):S7-S11. [Medline].
Leyden JJ, Kligman AM. Interdigital athlete's foot. The interaction of dermatophytes and resident bacteria. Arch Dermatol. Oct 1978;114(10):1466-72. [Medline].
Malcolm B. Tinea pedis. Practitioner. Mar 1998;242(1584):225. [Medline].
Medical Economics Staff. Physicians' Desk Reference. 53rd ed. Montvale, NJ: Thomson Healthcare; 1999.
Mitchell JH. Ringworm of hands and feet. J Am Med Assoc. Jun 9 1951;146(6):541-6. [Medline].
Noble SL, Forbes RC, Stamm PL. Diagnosis and management of common tinea infections. Am Fam Physician. Jul 1998;58(1):163-74, 177-8. [Medline].
Pellizzari C. Recherche sur Trichophyton tonsurans. G Ital Mal Veneree. 1888;29:8.
Resnik SS, Lewis LA, Cohen BH. The athlete's foot. Cutis. Sep 1977;20(3):351-3, 355. [Medline].
Rippon JW. Medical Mycology: The Pathogenic Fungi and the Pathogenic Actinomycetes. 3rd ed. Philadelphia, Pa: WB Saunders; 1988:169-275.
Watanabe K, Taniguchi H, Katoh T. Adhesion of dermatophytes to healthy feet and its simple treatment. Mycoses. 2000;43(1-2):45-50. [Medline].
Weidman FD. Laboratory aspects of epidermophytosis. Arch Dermatol. 1927;15:415-50.
Further Reading
Keywords
athlete's foot, ringworm of the feet, dermatophytosis, dermatophytid, Trichophyton rubrum, T rubrum, Trichophyton mentagrophytes, T mentagrophytes, Epidermophyton floccosum, E floccosum, Scytalidium hyalinum, S hyalinum, Scytalidium dimidiatum, S dimidiatum
