ABSTRACT
Staphylococcal scalded skin syndrome (SSSS) is a blistering disease of the skin caused by an infection with certain strains of Staphylococcus aureus. In vitro studies have suggested that exfoliative toxins secreted by these bacteria cleave the desmosomal adhesion molecule desmoglein 1 leading to loss of cell-cell contact in the superficial epidermis. In this study we investigated the fate of desmoglein 1 in biopsies of patients with SSSS to see whether the ectodomain of desmoglein 1 is cleaved. Our data largely confirm previous in vitro data. The different biopsies demonstrated the loss of the ectodomain of desmoglein 1 to different degrees. The endodomain of desmoglein 1 meanwhile remained present. Most remarkably, in one of our patients, the immunofluorescent analysis demonstrated that not desmoglein1 but desmocollin 1, another desmosomal cadherin, became affected. This raises the question if other toxins and/or other bacteria than Staphylococcus aureus might also induce SSSS.
