Pathophysiology

Viral pathogens cause acute gastroenteritis by tissue invasion and a directly cytopathic effect to small intestinal villous cells. As a consequence, there is villous damage and decreased intestinal absorption of nutrients, electrolytes, and water, resulting in watery diarrhea. Villous injury also results in reduced disaccharidase levels and diminished total mucosal glucose-coupled sodium transport. The end result is a decrease in intestinal water absorption. The volume of fluid delivered from the lumen of the damaged small intestine exceeds the colon's limited ability for fluid absorption, and the net result is watery diarrhea.

Bacteria cause diarrhea by a variety of mechanisms, including production of enterotoxins and cytotoxins and invasion of the mucosal absorptive surface. Enteric infections with E. coli are prototypic for understanding several of these pathogenic processes. ETEC and EPEC adhere to the mucosa and produce enterotoxins or damage the microvilli, respectively. Certain strains of EHEC invade the colonic mucosa, resulting in inflammation and an illness similar to shigellosis. EHEC serotype O157:H7 typically produces a hemorrhagic colitis with little inflammation and may produce verotoxins that have been implicated in causing hemolytic-uremic syndrome (HUS).6 Antibiotic-associated diarrhea and colitis due to cytotoxigenic Clostridium difficile may result in a similar pattern of diarrhea.

Bacterial toxins may also be ingested directly in food. The most common are heat-stable toxins produced by Staphylococcus aureus present in improperly stored or prepared meats, poultry, and dairy products. Bacillus cereus also produces a heat-stable toxin typically ingested with boiled or fried rice. Although Shigella is considered a prototype organism causing dysentery, it can also produce a toxin that causes watery diarrhea, encephalopathy, or seizures. Parasitic infestations may cause diarrhea by a variety of mechanisms similar to those discussed for viral gastroenteritis.

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