Staphylococcal scalded skin syndrome pathophysiology: Difference between revisions
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==Overview== | |||
The [[syndrome]] is induced by epidermolytic [[exotoxin]]s ([[exfoliatin]])<ref>{{DorlandsDict|three/000037652|exfoliatin}}</ref> A and B, which are released by ''S. aureus'' and cause detachment within the epidermal layer; by breaking down tight-junctions. One of the exotoxins is produced by the bacterial chromosome, while the other is produced by a [[plasmid]]. (Bacterial plasmids are pieces of self-replicating DNA that often code for secondary characteristics, such as antibiotic resistance, and toxin production.) These exotoxins are proteases that cleave desmoglein-1, which normally holds the [[Stratum granulosum|granulosum]] and [[Stratum spinosum|spinosum]] layers together. | |||
==References== | ==References== | ||
Revision as of 15:25, 11 December 2012
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Staphylococcal scalded skin syndrome Microchapters |
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Differentiating Staphylococcal scalded skin syndrome from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Staphylococcal scalded skin syndrome pathophysiology On the Web |
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Staphylococcal scalded skin syndrome pathophysiology in the news |
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Blogs on Staphylococcal scalded skin syndrome pathophysiology |
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Directions to Hospitals Treating Staphylococcal scalded skin syndrome |
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Risk calculators and risk factors for Staphylococcal scalded skin syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
The syndrome is induced by epidermolytic exotoxins (exfoliatin)[1] A and B, which are released by S. aureus and cause detachment within the epidermal layer; by breaking down tight-junctions. One of the exotoxins is produced by the bacterial chromosome, while the other is produced by a plasmid. (Bacterial plasmids are pieces of self-replicating DNA that often code for secondary characteristics, such as antibiotic resistance, and toxin production.) These exotoxins are proteases that cleave desmoglein-1, which normally holds the granulosum and spinosum layers together.