How does STEC/EHEC cause disease and what is a key severe complication?

How does STEC/EHEC cause disease and what is a key severe complication?

• A. LT/ST toxins increase cAMP/cGMP leading to watery diarrhea.
• B. Shiga toxins inhibit protein synthesis and damage microvasculature; risk of hemolytic uremic syndrome (HUS), especially in children.
• C. Attaching and effacing lesions via Type III secretion.
• D. Invades colonic mucosa causing dysentery.

Answer: (B)

Shiga toxins produced by STEC/EHEC are the main driver of disease. They enter host cells and shut down protein synthesis by inactivating the 60S ribosomal subunit, which injures endothelial cells in microvasculature. This endothelial damage underlies the bloody or hemorrhagic colitis and can lead to systemic microvascular injury. A key severe complication is hemolytic uremic syndrome, especially in children, where microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury arise from widespread endothelial damage and platelet consumption. While attaching and effacing lesions help with colonization, the toxin-mediated endothelial injury is what drives the major clinical risks.

Shiga toxins produced by STEC/EHEC are the main driver of disease. They enter host cells and shut down protein synthesis by inactivating the 60S ribosomal subunit, which injures endothelial cells in microvasculature. This endothelial damage underlies the bloody or hemorrhagic colitis and can lead to systemic microvascular injury. A key severe complication is hemolytic uremic syndrome, especially in children, where microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury arise from widespread endothelial damage and platelet consumption. While attaching and effacing lesions help with colonization, the toxin-mediated endothelial injury is what drives the major clinical risks.