Abstract

We believe that axillary granular parakeratosis, tinea pedis, and Seborrheic dermatitis are likely to be variants of eczema. All had culturable staphylococci capable of producing biofilms, as in eczema. This was confirmed on XTT assays, Congo red cultures, and PCR for gene analysis of the biofilm-forming icaD and aap genes. The pathology showed eccrine ductal occlusion that was noted on H+E and PAS stains (PAS stains positively the extracellular polysaccharide substance that makes up the bulk of the biofilm.) Toll-like receptor 2 (TLR 2) activities was found in the stratum corneum adjacent to the sweat ducts and not in its control location in the basal zone. The stratum corneum seemingly becomes altered by the fungi, yeasts, or tiny granules instead of by the filaggrin gene (1st in the double hit phenomenon); and, the sweat ducts become occluded causing activation of TLR 2. This leads to activation of the innate immune system (2nd hit), just as in eczema. Further, treatment with the mild topical corticoids and/or moisturizers helps restore the integrity of the skin.

Highlights

  • Atopic dermatitis (AD), or eczema, is thought to originate as a double-hit phenomenon to which both genetics and environment contribute [1]

  • Our results suggest a common environmental “second hit” in Seborrheic dermatitis as well as two diseases previously not considered eczematous in nature-granular parakeratosis and tinea pedis

  • Congo red staining uniformly demonstrated the presence of amyloid [17] in eccrine sweat ducts

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Summary

Introduction

Atopic dermatitis (AD), or eczema, is thought to originate as a double-hit phenomenon to which both genetics and environment contribute [1]. The “double hit” hypothesis, in which biofilm-occluded sweat ducts promote eczematous lesions, does not appear to be unique to AD, but is observed across multiple disease entities. In this paper we discuss this unanticipated, common finding in lesional skin samples from patients with Seborrheic dermatitis, granular parakeratosis and tinea pedis.

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