PATHOPHYSIOLOGY OF ACUTE INFECTIOUS DIARRHEAL DISEASESEnteropathogens gain access to the intestinal tract via oral contamination and cause diarrhea by disrupting intestinal and colonic mucosa through a variety of mechanisms. Bacteria such as Staphylococcus aureus, Bacillus cereus, and Clostridium botulinum release enterotoxins, which invoke intestinal secretion. Other pathogens, such as Shigella and enteroinvasive Escherichia coli, express invasins, which allow tissue invasion and disruption of mucosa. Many other bacteria elicit cytotoxic mediators that directly damage enteric and colonic mucosa. Enteropathogenic mechanisms of disease, therefore, are the basis for the two common clinical syndromes: inflammatory and non-inflammatory diarrhea.Inflammatory diarrheal syndromes often manifest clinically as dysentery, characterized by fever, tenesmus, abdominal pain, and frequent, small-volume stools that are often bloody. Organisms such as Shigella, Campylobacter jejuni, and enteroinvasive E. coli produce an inflammatory reaction that yields fecal leukocytes and blood on laboratory examination of stool. Patients with an inflammatory acute diarrheal illness can be quite toxic appearing and often require antibiotic treatment.Conversely, non-inflammatory diarrheal syndromes are usually self-limited and more often do not require antimicrobial therapy. Enteropathogens such as Vibrio parahaemolyticus, Cryptosporidium parvum, and Giardia lamblia as well as viral agents and toxin-producing bacteria, such as Staphylococcus aureus, Clostridium difficile, and enterotoxigenic E. coli, typically induce watery, non-bloody diarrhea without fever or significant abdominal pain. Stool examination is notable for the absence of leukocytes and blood. Typically, more than 1 L of watery stool is passed each day, and volume depletion may be profound.*66/348/5*
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