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Microbiology · Bacteriology: toxic shock syndrome toxin
Sample itemA 22-year-old woman using a high-absorbency tampon develops fever of 39.5 degrees C, hypotension, diffuse macular erythroderma and, a week later, desquamation of the palms. Which mechanism explains the massive cytokine release?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. A superantigen links MHC class II to the T-cell receptor Vbeta region, activating many T cells
Toxic shock syndrome toxin-1 of Staphylococcus aureus is a superantigen that cross-links MHC class II on antigen-presenting cells with the Vbeta region of many T-cell receptors, activating up to 20% of T cells and causing a cytokine storm with IL-2, TNF and IFN-gamma. Treatment includes removing the tampon, resuscitation, an anti-staphylococcal drug and clindamycin to suppress toxin production.
Option by option
A. Cleavage of desmoglein 1 by an exfoliative toxin
Desmoglein 1 cleavage by exfoliative toxin causes staphylococcal scalded skin syndrome, with sloughing and no shock.
B. A superantigen links MHC class II to the T-cell receptor Vbeta region, activating many T cells (correct)
Correct. Polyclonal T-cell activation by the superantigen produces shock and the rash.
C. Activation of TLR4 by lipopolysaccharide
LPS acting through TLR4 explains Gram-negative endotoxic shock, not this Gram-positive toxin-mediated syndrome.
D. ADP-ribosylation of elongation factor 2 in host cells
ADP-ribosylation of elongation factor 2 is the mechanism of diphtheria toxin and Pseudomonas exotoxin A.
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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