Figure 1.

The pathobiologic process of E. coli O157:H7. The complex process by which E. coli O157:H7 attaches to the intestinal mucosa starts by bacterial fimbrial attachment followed by translocation of the bacterial Tir protein into the host cell membrane. Tir serves as the receptor for the bacterial outer membrane attachment protein intimin. One or more types of Shiga toxins are released which then bind to their cellular receptors, the neutral glycolipids Gb3 and Gb4. Internalization and cellular activation of these toxins blocks ribosomal peptide elongation hence disrupting protein synthesis leading to cell death. Intestinal damage permits Shiga toxins and other bacterial factors to gain entrance to the circulation. These may reach multiple host tissues including the kidneys where damage to the microvasculature results in the potentially lethal hemolytic uremic syndrome. Treatment of this disease remains largely supportive with no widely accepted antibacterial or toxin-targeted regimen. Antibacterial agents are believed to result in bacterial lysis and release of stored toxins. One potential treatment method may rely on inhibition of toxin expression prior to administration of a bactericidal agent.