![]() ![]() Gentle rubbing of the skin causes exfoliation ( Nikolsky sign is positive).Exposure of the underlying, moist, reddish tissue leaves the skin with a burned-like appearance.Blisters easily rupture leading to the top layer of the skin (epidermis) peeling off easily, often in large sheets.Fluid contents range from a sterile cloudy fluid to frank yellow pus.Frequently occur in areas of friction (such as axillae, groin, and buttocks), the centre of the face and body orifices (such as the nose and ears).Following the rash, the formation of large fluid-filled blisters.In newborns, lesions can be found around the umbilical cord.Typically starts on the face and flexural regions (groin, axillae, and neck), then spreads rapidly to other parts of the body including the arms, legs, and trunk.A red rash with wrinkled tissue or paper-like consistency.These can rupture easily leaving tender patches of skin that look like a burn. Within 24–48 hours, a painful widespread red rash develops on the skin followed by the formation of large, fragile, fluid-filled blisters ( bullae). SSSS tends to start with nonspecific symptoms in children this may include irritability, lethargy, and fever. What are the clinical features of staphylococcal scalded skin syndrome? These toxins then spread to the skin via the circulating blood and target the desmoglein-1 protein in the epidermis leading to the blistering and sloughing typified by the condition. The initial localised infection often starts from sites such as the ears, eyes ( conjunctiva) or throat, especially in children, or infected wounds. Desmoglein-1 is absent from mucosal epithelium, which explains why mucosae are unaffected in SSSS. Loss of the epidermal layer and associated blistering occurs.ĭepending on disease severity, the resultant effect can range from a localised area of skin loss to total body blistering and sloughing.The desmoglein-1 protein is broken down leading to the skin cells becoming loose and “unstuck”.Desmoglein-1 is responsible for maintaining cell-to-cell adherence within the epidermis and preserving skin integrity.These toxins bind to a specific desmosome present in the epidermis known as desmoglein-1.aureus releases two exotoxins ( exfoliative toxins A and B) SSSS starts from a localised infection caused by toxigenic Staphylococcus aureus (approximately 5% of strains). What causes staphylococcal scalded skin syndrome? The estimated prevalence of SSSS based on studies undertaken in Europe has been reported to range from 0.09 to 0.56 cases per million people, with an equal male to female ratio seen in children. Renal clearance system: reduced toxin clearance.Īlthough rare, cases have been reported in older children and adults, and would characteristically involve those who are immunosuppressed or have severe renal impairment/ chronic renal disease.Immune system: lack of protective antibodies to exotoxins.The higher incidence in this age group is thought to be a consequence of an immature: SSSS is predominantly seen in children younger than 5 years with a peak age being reported between 2 to 3 years of age. Click here for more images Who gets staphylococcal scalded skin syndrome? ![]()
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