Which statement about EAEC and ETEC pathogenesis is accurate?

Which statement about EAEC and ETEC pathogenesis is accurate?

• A. ETEC invades whereas EAEC forms biofilms.
• B. EAEC forms biofilms and aggregates on mucosa; ETEC relies on adhesins and toxins without invasion.
• C. Both invade mucosa.
• D. Neither produces toxins.

Answer: (B)

The main idea being tested is how these two diarrheagenic pathotypes cause disease without invading tissue, using different strategies: EAEC relies on adhesion patterns and biofilm formation, while ETEC uses toxins produced alongside specific adhesins to attach to the mucosa. EAEC forms biofilms and aggregates on the mucosal surface using aggregative adherence factors, creating a sticky, multilayered lining that helps it persist on the intestinal mucosa. This adherent biofilm lifestyle drives disease without invading the epithelial tissue. ETEC, on the other hand, does not invade; it attaches to the small intestine using adhesins (colonization factor antigens) and produces enterotoxins (LT and ST) that stimulate secretion and watery diarrhea. The combination of adherence plus toxins is the key mechanism, not tissue invasion. The other options misstate these mechanisms: invading mucosa isn’t characteristic of ETEC, and EAEC’s hallmark isn’t invasion but biofilm-based adherence; saying neither produces toxins ignores ETEC’s well-established toxin-mediated pathogenesis.

The main idea being tested is how these two diarrheagenic pathotypes cause disease without invading tissue, using different strategies: EAEC relies on adhesion patterns and biofilm formation, while ETEC uses toxins produced alongside specific adhesins to attach to the mucosa.

EAEC forms biofilms and aggregates on the mucosal surface using aggregative adherence factors, creating a sticky, multilayered lining that helps it persist on the intestinal mucosa. This adherent biofilm lifestyle drives disease without invading the epithelial tissue. ETEC, on the other hand, does not invade; it attaches to the small intestine using adhesins (colonization factor antigens) and produces enterotoxins (LT and ST) that stimulate secretion and watery diarrhea. The combination of adherence plus toxins is the key mechanism, not tissue invasion.

The other options misstate these mechanisms: invading mucosa isn’t characteristic of ETEC, and EAEC’s hallmark isn’t invasion but biofilm-based adherence; saying neither produces toxins ignores ETEC’s well-established toxin-mediated pathogenesis.