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Staphylococcal scalded skin syndrome. An ultrastructural study
Journal of Cutaneous Pathology
|January 1, 1975
Summary
Staphylococcal scalded skin syndrome causes blistering in the granular layer of the epidermis due to toxin-induced desmosome disruption. This condition is ultrastructurally distinct from other toxic epidermal necrolysis forms.
Area of Science:
- Dermatology
- Pathology
- Microbiology
Background:
- Staphylococcal scalded skin syndrome (SSSS) is a blistering disease.
- It is caused by exfoliative toxins from Staphylococcus aureus.
- SSSS is also known as Ritter's disease.
Purpose of the Study:
- To investigate the ultrastructural changes in the epidermis of children with SSSS.
- To differentiate SSSS from other forms of toxic epidermal necrolysis.
Main Methods:
- Ultrastructural examination of epidermal tissue from two SSSS patients.
- Electron microscopy to analyze cellular and subcellular changes.
Main Results:
- A characteristic bullous cleavage was observed specifically within the granular layer of the epidermis.
- Desmosomes between granular cells were disrupted, with tonofilaments remaining attached to attachment plaques.
- No significant damage was noted in other epidermal layers.
- Thickened tonofilaments and dilated endoplasmic reticulum were observed in the granular layer.
- Odland bodies were abundant in areas of desmosomal disruption.
Conclusions:
- SSSS involves selective cleavage at the granular layer due to desmosome disruption.
- The ultrastructural findings support SSSS as a distinct entity separate from drug-induced toxic epidermal necrolysis.