Abstract

Tinea pedis, “fungus of the foot,” involves marked toeweb scaling, a “moccasin” pattern of scaling on the soles, and maceration. Dermatophytes including Trichophyton rubrum, Trichophyton mentagrophytes, and Epidermophyton floccosum are responsible. T. rubrum is ubiquitous, especially in locker rooms and showers (causing “athlete’s foot”). The same phenomenon is occurring in tinea pedis as in eczema. The difference is that in tinea pedis the fungus disrupts the stratum corneum and plays the role that genetic abnormalities play in eczema. Axillary granular parakeratosis, a rare disease with an unknown cause, presents clinically with a pruritic, hyperpigmented or dull red hyperkeratotic plaque in the axilla. In our examination of multiple sections of a specimen from axillary granular parakeratosis, we found periodic acid–Schiff positive occluded sweat ducts in the upper epidermis and proximal stratum corneum. We believe the occlusions arise from staphylococcal biofilms similar to those seen in miliaria, and the granules play the role of genetic abnormalities in eczema. In seborrheic dermatitis, biofilm-producing staphylococci and occluded sweat ducts form the environmental “hit” of the double-hit phenomenon and yeasts play the role of the genetic abnormalities in eczema. Management of seborrheic dermatitis usually involves bland shampoo and infrequent use of soap. The response is similar to eczema because it truly is eczema. “Cradle cap” is similar.

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