Background
Tinea pedis (athlete's foot) is the term used for a dermatophyte infection of the soles of the feet and the interdigital spaces. [1] It is a common infection, affecting an estimated 3% of the world's population. [1]
Tinea pedis is most commonly caused by Trichophyton rubrum, a dermatophyte that initially was endemic only in a small region of Southeast Asia and in parts of Africa and Australia. It is noteworthy that tinea pedis was not noted in these areas at that time, 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. War 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 forms of tinea include tinea barbae, tinea capitis, tinea corporis, tinea cruris, tinea faciei, tinea nigra, and tinea versicolor.
Pathophysiology
Dermatophytes, primarily from the genera Trichophyton and Epidermophyton, are the most common causes of tinea pedis. 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.
Etiology
T rubrum, Trichophyton interdigitale, 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 Neoscytalidium dimidiatum,Scytalidium hyalinum, and, rarely, Candida species.
The interdigital type of tinea pedis is usually caused by T rubrum. It is more pruritic in hot, humid environments. Other possible causative organisms include T 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. It was suggested that dermatophytes invade the stratum corneum, paving the way for secondary bacterial infection.
The chronic hyperkeratotic type of tinea pedis is usually caused by T rubrum. Other possible causative organisms include T interdigitale,E floccosum, and the nondermatophyte molds S hyalinum and N 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.
Trichophyton indotineae (formerly classified as type VIII T mentagrophytes) has been associated with tinea pedis and onychomycosis, but not frequently; it primarily affects the trunk and groin. [3]
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.
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.
A study from Japan found that independent risk factors for the development of tinea pedis included advanced age, male, sex, diabetes, and lower-limb ischemia. [4]
Epidemiology
Tinea pedis is thought to be the world's most common dermatophytosis. It has been estimated that as much as 3% of the world's population may have tinea pedis at a given time. [1]
The prevalence of tinea pedis increases with age. Most cases occur after puberty; childhood tinea pedis is rare. Tinea pedis affects males more commonly than females. It has no known predilection for any racial or ethnic group.
Prognosis
The prognosis for patients with tinea pedis is affected by the type of infection and any underlying conditions (eg, immunosuppression or diabetes) that may be present. In general, however, the prognosis is good when appropriate treatment is provided. Tinea pedis is not associated with significant mortality or morbidity.
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 patient education resources, see the patient education articles Athlete's Foot and Ringworm on Body.
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Tinea pedis lesion. Image courtesy of Drgnu23 (original uploader) [GFDL (https://www.gnu.org/copyleft/fdl.html) or CC-BY-SA-3.0 (https://creativecommons.org/licenses/by-sa/3.0/)], via Wikimedia Commons.
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