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Pathophysiology Gastroenteritis is a nonspecific term for various pathologic states of the gastrointestinal tract.

Infectious agents usually cause acute gastroenteritis. These agents cause diarrhea by adherence, mucosal invasion, enterotoxin production, and/or cytotoxin production. These mechanisms result in increased fluid secretion and/or decreased absorption. This produces an increased luminal fluid content that cannot be adequately reabsorbed, leading to dehydration and the loss of electrolytes and nutrients. The small intestine is the prime absorptive surface. The colon then absorbs additional fluid, transforming a relatively liquid fecal stream in the cecum to well-formed solid stool in the rectosigmoid. Disorders of the small intestine result in increased amounts of diarrheal fluid with a concomitantly greater loss of electrolytes and nutrients.
Microorganisms may produce toxins that facilitate infection. Enterotoxins are generated by bacteria (ie, enterotoxigenic Escherichia coli, Vibrio cholera, Rotavirus) that act directly on secretory mechanisms and produce typical, copious watery (rice water) diarrhea, but with no mucosal invasion. The toxin binds to specific enterocyte membrane receptors thus activating the adenyl.cyclase through the stimulation of an enterocyte G protein. The resulting increase in the cyclase adenosine monophosphate (cAMP) in turn activates specific signaling proteins, including opening of chloride channels. Intestinal fluid secretion is predominantly due to electrogenic chloride secretion thru the activation of cystic fibrosis transmembrane regulator chloride channel, located on the apical part of the enterocyte. Stimulation of chloride secretion is largely mediated by the upregulation of the intracellular mediator cAMP. Other enterotoxins stimulate intestinal secretion through activation of guanosine monophospate or a rise in the intracellular calcium concentration. Rotavirus produces a non-structural protein (NSP+) that stimulates calcium-mediated chloride secretion. Cytotoxin production by bacteria (ie, Shigella dysenteriae, Vibrio parahaemolyticus, Clostridium difficile,enterohemorrhagic E coli) results in mucosal cell destruction that leads to bloody stools with inflammatory cells. A resulting decreased absorptive ability occurs. For instance, shigella spp. cause gastroenteritis through invasion of superficial colonic mucosa, which they invade through the M cells located over the payers patches. After phagocytosis of the invading pathogen by the macrophages, apoptosis of macrophages, multiplication and spread of bacteria to adjacent cells, release of inflammatory mediators ( IL-1 IL-8), transmigration of neutrophils into the lumen of the colon, neutrophil necrosis and degaranulation, further breach of the epithelial barrier and finally mucosal destruction follows. Enterocyte invasion is the preferred method by which microbes such as Shigella and Campylobacter organisms and enteroinvasive E coli cause destruction and inflammatory diarrhea. Similarly, Salmonella and Yersinia species also invade cells but do

not cause cell death. Hence, dysentery does not usually occur. However, these bacteria invade the bloodstream across the lamina propria and cause enteric fever such as typhoid. In addition to the ingestion of pathogenic organisms or toxins, other intrinsic factors can lead to infection. An alteration of normal bowel flora can create a biologic void that is filled by pathogens. This occurs most commonly after antibiotic administration, but infants are also at risk prior to colonization with normal bowel flora.