Which mechanism of pathophysiology is associated with EHEC infection?

Enterohemorrhagic Escherichia coli (EHEC), particularly the strain O157:H7, is known for producing Shiga toxin. The mechanism through which this toxin exerts its pathogenic effects involves inactivation of the 60S ribosomal subunit of host cells. By modifying the ribosomal RNA within the ribosome, Shiga toxin inhibits protein synthesis. This inhibition leads to the death of the host cell and contributes to the severe gastrointestinal symptoms and potential complications like hemolytic uremic syndrome that are associated with EHEC infections.

This mechanism is critical in understanding the severity of the disease caused by EHEC, as it not only disrupts normal cellular function but also plays a significant role in the organism's ability to cause harm. The other options, such as inhibition of RNA synthesis, disruption of bacterial cell wall synthesis, and inhibition of DNA replication, relate to different mechanisms of action that do not accurately describe how EHEC, through its toxin, affects host cells. The focus on ribosomal inactivation underscores the unique pathogenic strategy employed by EHEC, distinguishing it from other bacterial infections.