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Staphylococcal Scalded Skin Syndrome. An Ultrastructural Study
Author(s) -
Dobbeleer G.,
Achten G.
Publication year - 1975
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/j.1600-0560.1975.tb00212.x
Subject(s) - staphylococcal scalded skin syndrome , ultrastructure , toxic epidermal necrolysis , granular layer , endoplasmic reticulum , desmosome , pathology , staphylococcus aureus , epidermis (zoology) , cleavage (geology) , desquamation , ichthyosis , chemistry , dermatology , medicine , biology , anatomy , microbiology and biotechnology , bacteria , cell , paleontology , biochemistry , fracture (geology) , cerebellum , genetics
The authors investigated the ultrastructure of the epidermis of two children who suffered from the staphylococcal scalded skin syndrome (or the Ritter's type of toxic epidermal necrolysis). This syndrome is attributed to the action of an exfoliative toxin produced by Staphylococcus aureus phage group II. A characteristic bullous cleavage was selectively observed at the level of the granular layer, without any damage in other epidermal layers. This cleavage was the result of disruption of desmosomes between granular cells in two halves, each half desmosome conserving the tonofilaments which were attached to its attachment plaque. No remarkable cytoplasmic alteration occurred in the granular layer, with the exception of the development of thickened tonofilaments among dilated endoplasmic reticulum. Odland bodies were particularly numerous in the areas of desmosomal disruption. This syndrome must be considered as an entity clinically, histologically and ultrastructurally separate from the drug form of toxic epidermal necrolysis.