Trichophyton mentagrophytes delays wound healing in ob/ob mice

Abstract

A wide variety of microbial species, including Trichophyton spp., have been detected in diabetic foot ulcers (DFUs). In particular, Trichophyton spp. cause tinea pedis (i.e., athlete's foot) and onychomycosis. However, investigations regarding the correlation between Trichophyton spp. and delayed wound healing are limited to case reports. Moreover, histological changes in wounds caused by Trichophyton spp. remain unclear. In this study, we sought to confirm the delayed wound healing phenotype caused by Trichophyton mentagrophytes infection in a full-thickness excisional wound ob/ob mouse model through histopathological analysis. The inoculation of skin wounds in ob/ob mice with T. mentagrophytes sporules resulted in significant delay on wound healing. Further histopathological analyses demonstrated that the delayed wound healing in ob/ob mice was accompanied by reduced collagen fibre formation and inhibited granulation tissue formation, with spores and elongated mycelia retained in the wound bed and along the wound edges. This suggests that T. mentagrophytes colonization of wounds potentially contributes to delayed wound healing in patients with diabetes. These results suggest that neglected tinea pedis is a potential risk factor for delayed wound healing and progression to refractory wounds in patients with DFU.