Enteropathogenic vs. enterohemorrhagic Escherichia coli (EPEC vs. EHEC): what is a major difference between these two pathotypes with respect to toxins and virulence?

Introduction:
E. coli pathotypes are distinguished by their virulence factors and clinical syndromes. This question focuses on a hallmark distinction: toxin production. Understanding these differences informs diagnosis, management, and public health responses.

Given Data / Assumptions:

• EPEC and EHEC both can form attaching-and-effacing lesions.
• Type III secretion systems are shared features for delivering effectors.
• EHEC produces Shiga toxins (Stx1/Stx2), associated with hemorrhagic colitis and HUS.
• EPEC disease is typically watery diarrhea in infants without Stx production.

Concept / Approach:
EHEC (e.g., O157:H7) carries phage-encoded Shiga-like toxins that damage intestinal microvasculature and can cause systemic complications. EPEC lacks these toxins but uses a type III secretion system to inject effectors, inducing actin rearrangements and pedestal formation. Therefore, the defining difference is Shiga-like toxin production by EHEC only.

Step-by-Step Solution:
List shared traits: A/E lesions and type III secretion are common to both. Identify unique trait: Stx production in EHEC leads to bloody diarrhea and HUS. Check each option against known virulence factors. Select the option emphasizing Shiga-like toxin as the key difference.

Verification / Alternative check:
Clinical labs may detect Stx by immunoassay or molecular methods; EPEC is identified by eae gene without stx genes.

Why Other Options Are Wrong:

• Type III secretion absence in EPEC: Incorrect; EPEC has it.
• Actin rearrangements absent in EHEC: Incorrect; both cause A/E lesions.
• Placental infection: Not a defining feature of EPEC vs. EHEC.

Common Pitfalls:
Assuming bloody diarrhea automatically means invasive disease; in EHEC it is toxin-mediated rather than invasive.

Final Answer:
EHEC secretes a Shiga-like toxin and EPEC does not.