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Staphylococcal Scalded Skin Syndrome — SCE Dermatology MCQ

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HardPaediatric DermatologyStaphylococcal Scalded Skin SyndromeSCE Dermatology

A 5-year-old girl develops a widespread blistering eruption 48 hours after starting Trimethoprim for a UTI. Biopsy shows subcorneal cleavage plane (within the granular layer). Nikolsky sign is positive. She is febrile but otherwise stable. Culture from a blister roof shows no organisms. What is the most likely diagnosis?

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Correct answer: B — Staphylococcal scalded skin syndrome

The correct answer is B, Staphylococcal scalded skin syndrome. The subcorneal cleavage plane within the granular layer, positive Nikolsky sign, fever, and widespread blistering are classic for SSSS, caused by exfoliative toxins A and B from toxigenic Staphylococcus aureus that cleave desmoglein 1 in the granular layer, producing superficial, fragile blisters. The toxin acts systemically from a remote infective focus (nasopharynx, conjunctivae, umbilicus), so the blister itself is sterile, explaining the negative culture from the blister roof. SSSS predominantly affects young children under 5 due to lower anti-toxin antibody levels and reduced renal clearance of toxin. The trimethoprim exposure is a distractor suggesting a drug reaction rather than an infective toxin-mediated process. Why the other options are wrong: A. Linear IgA disease: an autoimmune subepidermal disorder with linear IgA at the basement membrane on immunofluorescence, not a subcorneal granular layer split, and not typically triggered acutely by infection in this febrile pattern. D. Bullous impetigo: shares the same toxin and histology but is a localised infection with organisms present within the blister fluid on culture, unlike the sterile, widespread process described here. E. Pemphigus vulgaris: cleavage is suprabasal due to anti-desmoglein 3 autoantibodies, with mucosal involvement, not a subcorneal granular layer split, and is exceptionally rare in a 5 year old. C. SJS/TEN: cleavage is full-thickness at the dermoepidermal junction from keratinocyte apoptosis, mucosal involvement is prominent, and it is drug-induced via a delayed T cell mechanism, not toxin-mediated subcorneal splitting. Key point: a subcorneal, granular layer split with positive Nikolsky sign and sterile blister culture indicates toxin-mediated SSSS, not a drug reaction or autoimmune blistering disease.

Reference: DermNet NZ, Staphylococcal Scalded Skin Syndrome (SSSS), 2025, https://dermnetnz.org/topics/staphylococcal-scalded-skin-syndrome