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We identified a novel pathogenicity island inInterestingly, these strains are mainly isolated from other sources of infections and not from patients with bullous impetigo or staphylococcal scalded-skin syndrome. This strongly suggests that ETD might play a pathogenic role in a broader spectrum of bacterial infections than previously considered.

This study evaluated changes in transepidermal water loss (TEWL), skin hydration and intercorneal lipid content in dogs with atopic dermatitis (AD). TEWL and skin hydration were measured in the inguinal skin of 10 dogs with AD and 30 normal dogs. TEWL was significantly higher in both lesional skin (94.3 +/- 38.8 g/m(2)/h) and non-lesional skin (28.8 +/- 9.5) of dogs with AD than healthy controls (12.3 +/- 2.3) (P < 0.05). Water content in the lesional skin of dogs with AD (15.8 +/- 7.0 AU) was significantly lower than that of controls (24.2 +/- 8.8) (P < 0.05), whereas no significant differences were recognized in water content between non-lesional skin of dogs with AD and controls. To compare the lipid content between lesional and non-lesional skin of dogs with AD and controls, intercorneal lipids, extracted from the stratum corneum, were quantified by thin-layer chromatography. The relative amounts of ceramides in the lesional skin (24.4 +/- 5.6%) and non-lesional skin (25.6 +/- 3.8%) of dogs with AD were significantly lower than those in controls (31.4 +/- 6.9%) (P < 0.05). Conversely, no significant differences were recognized in the relative amounts of cholesterols and free fatty acids (FFA) between dogs with AD and controls. Moreover, there are statistical correlations between TEWL and the relative amounts of ceramides, but not those of cholesterols and FFA, in both lesional and non-lesional skin of dogs with AD. These results strongly suggest that decreased ceramide content accelerates TEWL in dogs with AD, similar to the situation seen in the corresponding human disease.

Staphylococcal scalded skin syndrome and its localized form, bullous impetigo, show superficial epidermal blister formation caused by exfoliative toxin A or B produced by Staphylococcus aureus. Recently we have demonstrated that exfoliative toxin A specifically cleaves desmoglein 1, a desmosomal adhesion molecule, that when inactivated results in blisters. In this study we determine the target molecule for exfoliative toxin B. Exfoliative toxin B injected in neonatal mice caused superficial epidermal blisters, abolished cell surface staining of desmoglein 1, and degraded desmoglein 1 without affecting desmoglein 3 or E-cadherin. When adenovirus-transduced cultured keratinocytes expressing exogenous mouse desmoglein 1 or desmoglein 3 were incubated with exfoliative toxin B, desmoglein 1, but not desmoglein 3, was cleaved. Furthermore, cell surface staining of desmoglein 1, but not that of desmoglein 3, was abolished when cryosections of normal human skin were incubated with exfoliative toxin B, suggesting that living cells were not necessary for exfoliative toxin B cleavage of desmoglein 1. Finally, in vitro incubation of the recombinant extracellular domains of desmoglein 1 and desmoglein 3 with exfoliative toxin B demonstrated that both mouse and human desmoglein 1, but not desmoglein 3, were directly cleaved by exfoliative toxin B in a dose-dependent fashion. These findings demonstrate that exfoliative toxin A and exfoliative toxin B cause blister formation in staphylococcal scalded skin syndrome and bullous impetigo by identical molecular pathophysiologic mechanisms.

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