Endotoxin, a lipopolysaccharide that is an essential component of the outer cell wall of gram-negative bacteria (17.1A), is spontaneously released during logarithmic bacterial growth or bacteriolysis. Therefore, endotoxemia can become the sequela to any locally extensive or systemic invasion with gram-negative bacteria such as septicemia in neonates, pleuropneumonia, peritonitis, salmonella-associated colitis, or metritis. In addition to its release during gram-negative sepsis, an endogenous source of endotoxin is contained in the lumen of the intestinal tract. Normally, endotoxin released by the resident enteric flora is restricted to the intestinal lumen by a healthy mucosal barrier. However, if the intestinal wall becomes severely inflamed or ischemic, luminal endotoxin will translocate to the peritoneal cavity, portal circulation, and, eventually, the general circulation. In mature horses, acute intestinal disease is the most common cause of endotoxemia, while in neonatal foals, endotoxemia most commonly is a consequence of gram-negative bacterial septicemia.
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