A neonate develops scalded skin syndrome (Ritter disease) within 48 hours of birth. The causative agent produces an exfoliative toxin (ET). Which specific property of ET explains the blister formation restricted to the superficial epidermis (stratum granulosum) WITHOUT causing dermal involvement?

• A ET is a superantigen activating Vβ-specific T cells causing localized epidermal apoptosis
• B ET directly lyses keratinocytes via pore-forming activity in the stratum granulosum
• C ET acts as a serine protease that cleaves desmoglein-1 in the superficial epidermis ✓
• D ET activates complement at the dermo-epidermal junction causing neutrophil-mediated split

Explanation

Staphylococcal exfoliative toxins (ETA and ETB) are serine proteases that specifically cleave desmoglein-1 (Dsg-1), a desmosomal cadherin expressed predominantly in the superficial layers of the epidermis (stratum granulosum). Dsg-1 cleavage disrupts cell-cell adhesion in this specific layer, producing superficial blistering at the stratum granulosum level. This is analogous to the pemphigus foliaceus mechanism (autoantibodies against Dsg-1). The dermis and deep epidermis express Dsg-3 predominantly, which is not cleaved by ET — explaining why the blister is always intraepidermal without necrosis.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.