What toxins define enterotoxigenic E. coli (ETEC) and how do they contribute to disease?

What toxins define enterotoxigenic E. coli (ETEC) and how do they contribute to disease?

• A. Heat-labile toxin (LT) and heat-stable toxin (ST); LT increases cAMP, ST increases cGMP; both cause watery diarrhea; colonization factors aid attachment.
• B. Shiga toxin and cholera toxin cause watery diarrhea.
• C. Tetanus toxin raises intracellular calcium and blocks GABA.
• D. Cholera toxin is the only toxin producing watery diarrhea.

Answer: (A)

ETEC is defined by its two enterotoxins that drive secretory diarrhea. The heat-labile toxin (LT) and heat-stable toxin (ST) are the key players. LT acts like the cholera toxin: it ADP-ribosylates the Gs alpha subunit, continually activating adenylyl cyclase and raising intracellular cAMP. The rise in cAMP stimulates the CFTR chloride channel, causing chloride and bicarbonate to flood into the intestinal lumen, with water following, which produces watery, non-inflammatory diarrhea. ST works differently but with the same end result: it activates intestinal guanylyl cyclase C, increasing cGMP inside enterocytes, which disrupts ion transport and promotes water secretion. Together, these toxins create the classic secretory diarrhea seen in traveler's diarrhea caused by ETEC. Colonization factors on ETEC help the bacteria attach to the small intestinal mucosa, concentrating toxin effect at the site of infection and enhancing disease. This attachment is why the toxins can effectively cause symptoms even though the bacteria may not invade tissue. Other toxins mentioned in the distractors are from different pathogens and have different consequences. Shiga toxin is associated with invasive disease and potential bloody diarrhea, not the toxin profile that defines ETEC. Tetanus toxin is a neurotoxin, not involved in enteric secretory diarrhea. Cholera toxin is indeed a potent secretagogue, but it is produced by Vibrio cholerae, not ETEC, so it does not define enterotoxigenic E. coli.

ETEC is defined by its two enterotoxins that drive secretory diarrhea. The heat-labile toxin (LT) and heat-stable toxin (ST) are the key players. LT acts like the cholera toxin: it ADP-ribosylates the Gs alpha subunit, continually activating adenylyl cyclase and raising intracellular cAMP. The rise in cAMP stimulates the CFTR chloride channel, causing chloride and bicarbonate to flood into the intestinal lumen, with water following, which produces watery, non-inflammatory diarrhea. ST works differently but with the same end result: it activates intestinal guanylyl cyclase C, increasing cGMP inside enterocytes, which disrupts ion transport and promotes water secretion. Together, these toxins create the classic secretory diarrhea seen in traveler's diarrhea caused by ETEC.

Colonization factors on ETEC help the bacteria attach to the small intestinal mucosa, concentrating toxin effect at the site of infection and enhancing disease. This attachment is why the toxins can effectively cause symptoms even though the bacteria may not invade tissue.

Other toxins mentioned in the distractors are from different pathogens and have different consequences. Shiga toxin is associated with invasive disease and potential bloody diarrhea, not the toxin profile that defines ETEC. Tetanus toxin is a neurotoxin, not involved in enteric secretory diarrhea. Cholera toxin is indeed a potent secretagogue, but it is produced by Vibrio cholerae, not ETEC, so it does not define enterotoxigenic E. coli.