Etiology and Pathophysiology of Tinea Pedis
Tinea pedis is a superficial dermatophyte infection of the feet caused predominantly by Trichophyton rubrum, followed by T. mentagrophytes (also known as T. interdigitale) and less commonly Epidermophyton floccosum. 1, 2, 3
Causative Organisms
T. rubrum is the most prevalent etiologic agent globally, accounting for the majority of tinea pedis cases, with T. mentagrophytes var. interdigitale as the second most common pathogen. 1, 2, 3
These anthropophilic dermatophytes have undergone clonal global spread during the second half of the twentieth century, correlating with increased urbanization, use of sports facilities, and demographic shifts. 3
Non-dermatophyte molds (Fusarium, Aspergillus, Scopulariopsis) and yeasts can occasionally cause tinea pedis, though dermatophytes remain the primary pathogens in 84.8% of cases. 4, 5
Pathophysiologic Mechanisms
Fungal Virulence Factors
Dermatophytes possess expanded gene families encoding LysM domain-containing proteins that bind chitin and related carbohydrates, facilitating adherence to keratinized tissues and potentially modulating host immune recognition. 6
These organisms are enriched for multiple classes of proteases (keratinases) that degrade keratin, enabling fungal growth and nutrient acquisition from the stratum corneum, hair, and nails. 6
Dermatophyte genomes encode novel fungus-specific kinases and pseudokinases that may regulate signaling pathways involved in chronic infection establishment and immune evasion. 6
Secondary metabolite synthesis pathways are abundant in dermatophyte genomes, potentially producing compounds that facilitate tissue invasion or suppress local immune responses. 6
Transmission and Infection Establishment
Household transmission among family members is the most common route of infection, with indirect contact through contaminated footwear, floors, and bathing facilities serving as major vectors. 2, 4
Fungal elements can spread from the foot to other body sites via direct contact or contaminated hands, with concomitant dermatophytosis at other locations confirmed in 25% of cases. 7, 8
Footwear can harbor large numbers of viable dermatophyte spores, acting as a persistent reservoir for reinfection even after successful treatment. 7
Predisposing Risk Factors
Environmental and Occupational
Athletes demonstrate infection rates up to 22-23% compared to 8% in the general population, with a 15-fold higher prevalence of onychomycosis that can spread to cause tinea pedis. 1, 9
Warm, humid environments activate dormant fungal elements, with periods of increased warmth and humidity or impaired immunity triggering clinical disease. 1
Occlusive footwear, synthetic materials that retain sweat, water sports, and communal bathing facilities significantly increase exposure to infectious dermatophytes. 1
Host Factors
Male gender, adolescent and adult age (peak incidence 16-45 years), and obesity are established demographic risk factors. 1, 7, 2
Diabetic patients are almost three times more likely to develop tinea pedis and onychomycosis, with poor peripheral circulation, neuropathy, and impaired wound healing contributing to infection susceptibility and complications. 1
Genetic susceptibility exists, with familial patterns of T. rubrum infection showing autosomal dominant inheritance patterns, suggesting host immune factors influence infection establishment. 1
Repeated nail trauma, hyperhidrosis, and immunosuppression (HIV infection, immunosuppressive medications) compromise skin barrier function and local immune defenses. 1, 5
Clinical Progression
Fungal invasion of the nail can spread to the foot when activated by environmental triggers, and conversely, tinea pedis serves as a reservoir for onychomycosis development. 1
Concomitant onychomycosis is present in up to one-third of tinea pedis cases, requiring extended treatment and serving as a persistent source of reinfection. 1, 7
In diabetic patients, diseased nails with sharp edges can cause pressure erosion and skin injury that goes unnoticed due to sensory neuropathy, creating entry points for secondary bacterial infection and potentially limb-threatening complications. 1