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 are the main drivers of disease in STEC/EHEC. They enter host cells and inactivate the 60S ribosomal subunit by removing a specific adenine from 28S rRNA, which halts protein synthesis. This makes the toxins highly cytotoxic, with a particular impact on microvascular endothelial cells. When the small vessels are damaged, a microangiopathic process ensues, leading to platelet consumption and red blood cell destruction. The most feared outcome is hemolytic uremic syndrome, especially in children, which involves hemolytic anemia, thrombocytopenia, and acute kidney injury. So the disease result isn’t just diarrhea; it’s the toxin-mediated vascular injury that can progress to HUS. The other mechanisms described—such as toxins that raise cAMP/cGMP to cause watery diarrhea or invasiveness that causes dysentery—are characteristic of other pathogens and represent different disease pathways.