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. 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. 
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.
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.
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.
Tinea pedis has no predilection for any racial or ethnic group.
Tinea pedis more commonly affects males compared with females.
The prevalence of tinea pedis increases with age. Most cases occur after puberty. Childhood tinea pedis is rare.
The type of tinea pedis infection and underlying conditions (eg, immunosuppression, diabetes) affect the prognosis; however, with appropriate treatment, the prognosis is generally good. Tinea pedis is not associated with significant mortality or morbidity.
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.
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