Describe the mechanism by which Shiga toxin-producing E. coli (STEC) can cause edema disease in pigs.

• A. Systemic bloodstream spread
• B. Attachment via fimbriae > effacement of microvilli > Shiga toxin into enterocytes, blood vessels > necrosis of smooth muscle and endothelial cells > fluid loss
• C. Toxin inhibits potassium channels
• D. Direct coccidial replication

Answer: (B)

The mechanism being tested is that edema disease results from a Shiga toxin–producing E. coli that first attaches to and colonizes the gut, then releases Shiga toxin that damages the vascular endothelium systemically. The bacteria use fimbriae to cling to the intestinal mucosa, creating attaching-and-effacing lesions with microvilli collapse. This close association allows Shiga toxin to enter circulation from the gut and reach blood vessels, where it injures endothelial cells (and related vascular tissues), leading to endothelial necrosis and increased vascular permeability. The vascular damage manifests as edema and fluid loss, particularly in affected tissues such as the brain and head region. So, the sequence—fimbrial attachment and microvilli effacement, toxin release and vascular targeting, endothelial necrosis, and fluid leakage—best explains how STEC causes edema disease. The other ideas—simple systemic bacterial spread, toxin actions on potassium channels, or direct replication of a protozoan—don’t fit the established mechanism of toxin-mediated vascular injury following gut colonization.