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Microbiology · Bacteriology: staphylococcal exfoliative toxin
Sample itemA 10-day-old neonate has fever, perioral erythema and flaccid blisters that rupture to leave moist red skin. Gentle rubbing produces skin separation, the mouth is spared, and blister fluid is sterile on culture. Which molecular event explains the lesions?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Cleavage of desmoglein-1 in the stratum granulosum by a staphylococcal serine protease
This is staphylococcal scalded skin syndrome. Phage group II Staphylococcus aureus produces exfoliative toxins A and B, serine proteases that cleave desmoglein-1 and split the granular layer. The toxin is carried through blood from a distant focus, so the blister fluid is sterile and mucosae are spared because they lack desmoglein-1 as the main adhesion molecule.
Option by option
A. Antibody attack on BP180 at the dermo-epidermal junction
BP180 antibodies cause bullous pemphigoid with subepidermal blisters, mostly in the elderly.
B. Cleavage of desmoglein-1 in the stratum granulosum by a staphylococcal serine protease (correct)
Correct. Exfoliative toxin cleaves desmoglein-1 and causes superficial epidermal splitting.
C. Autoantibodies against desmoglein-3 in the suprabasal layer
Desmoglein-3 autoantibodies cause pemphigus vulgaris in adults, with mucosal erosions.
D. Mutation of keratin 5 and 14 in the basal layer
Keratin mutations cause epidermolysis bullosa simplex, which is inherited and not febrile.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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