How does enteropathogenic E. coli (EPEC) cause disease?

How does enteropathogenic E. coli (EPEC) cause disease?

• A. Attachment via fimbriae and Shiga toxin production.
• B. Through invasive necrosis.
• C. Toxins cholera-like.
• D. Attachment via intimin > effacement > microcolony formation; T3SS secretes effector proteins into host cell; colonize lower and small intestine; attach and efface = enterocyte necrosis and villi stunting; maldigestion and malabsorption; no toxin production.

Answer: (D)

EPEC causes disease through a unique attaching and effacing mechanism rather than toxin production. The bacteria use intimin to tightly attach to enterocytes, with the Tir effector protein being injected into the host cell by a Type III secretion system. This triggers cytoskeletal rearrangements that form pedestals beneath the bacteria and erase the microvilli, creating microcolonies on the enterocyte surface. As EPEC colonizes both the lower and small intestine, the loss of microvilli and disruption of absorptive surfaces lead to maldigestion and malabsorption, manifesting as watery diarrhea. Crucially, this pathogenesis relies on adherence and effacement rather than toxin-mediated injury, so no toxin production occurs. Other options imply toxin production or invasive damage that isn’t characteristic of EPEC.

EPEC causes disease through a unique attaching and effacing mechanism rather than toxin production. The bacteria use intimin to tightly attach to enterocytes, with the Tir effector protein being injected into the host cell by a Type III secretion system. This triggers cytoskeletal rearrangements that form pedestals beneath the bacteria and erase the microvilli, creating microcolonies on the enterocyte surface. As EPEC colonizes both the lower and small intestine, the loss of microvilli and disruption of absorptive surfaces lead to maldigestion and malabsorption, manifesting as watery diarrhea. Crucially, this pathogenesis relies on adherence and effacement rather than toxin-mediated injury, so no toxin production occurs. Other options imply toxin production or invasive damage that isn’t characteristic of EPEC.