Abstract

by cutaneous bacteria, cocci may be present in lesions of bullous impetigo and the clinical presentation is more localized than with SSSS. Similar to SSSS, pemphigus foliaceous (PF) and subcorneal immunoglobulin A (IgA) pemphigus have superficial blisters caused by a split in the granular layer. In PF, Dsg1 is the target of IgG autoantibodies, thus playing a role in the similar clinical manifestations to SSSS. Both PF and subcorneal IgA pemphigus differ histologically from SSSS by having a dermal inflammatory infiltrate and by direct immunofluorescence findings that are positive for Ig deposition in the granular layer. Most reported cases of SSSS have been caused by strains of S aureus that are sensitive to semisynthetic penicillins; however, several cases of SSSS caused by methicillin-resistant S aureus (MRSA) have been reported. Patients with SSSS are best treated with a parenteral antistaphylococcal antibiotic. Because SSSS is caused by an exotoxin, the exfoliation usually persists for another 24 to 48 hours after initiating treatment, following which the appearance of new lesions should discontinue. If no improvement is seen with empiric antibiotics, MRSA should be considered and treated appropriately. Furthermore, eroded areas of skin should be covered with petrolatum gauze dressing, and any remaining blisters should be left untouched. Corticosteroids are contraindicated because they are associated with a worsening of SSSS. Additionally, attention must be given to pain management, temperature regulation, and fluid management. When treated with the appropriate antibiotics, the lesions of SSSS dry quickly and desquamate within 7 to 10 days. Because exfoliation is superficial, scarring is rare. For this series, the recommended choices are as follows: 6, b; 7, d; 8, a; 9, d; 10, c; 11, d.

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