Bacterial Gastroenteritis

Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.

Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid receptor globotriaosylceramide (Gb3), initiating toxin uptake via tubular membrane invaginations and retrograde transport through the Golgi and endoplasmic reticulum to the cytosol. There, the A1 subunit cleaves a specific adenine base from the 28S rRNA of the 60S ribosomal subunit, halting translation, inducing vascular endothelial cell damage, bloody diarrhea, and potentially hemolytic uremic syndrome.

Importantly, the genes encoding Shiga toxins (stx1 and stx2) are not native to the E. coli chromosome but are carried by lysogenic bacteriophages—viruses that have integrated into the bacterial genome. This phage-mediated horizontal gene transfer allows non-toxigenic E. coli strains to acquire toxin-producing capability, contributing to the emergence of new pathogenic variants.

Enteropathogenic E. coli (EPEC) and some STEC use a Type III secretion system (T3SS) to insert virulence proteins directly into intestinal epithelial cells. The T3SS apparatus—a basal body with an extracellular needle—is tightly regulated and injects effectors such as Tir into host cells, while surface factors such as intimin and bundle-forming pili (BFP) mediate bacterial attachment. These effectors induce actin re‑organization, effacing microvilli and forming pedestal structures beneath adherent bacteria. The result is impaired nutrient absorption and watery diarrhea.

Recent genomic classification frameworks highlight key virulence markers—such as the LEE pathogenicity island (T3SS encoding) and co‑occurrence of stx and eae genes—to distinguish STEC from other pathotypes. Additionally, STECs continue to generate large outbreaks globally, especially in regions with limited surveillance, underlining the ongoing threat they pose to public health.