Endotoxin is lipopolysaccharide (LPS), a structural component of the outer membrane of gram-negative bacteria. It is not secreted by living bacteria but released in large quantities when gram-negative cells lyse — are destroyed — either by the immune system, by antibiotics, or by the ischemic death of gut tissue. In horses, endotoxin absorption is one of the most clinically significant events in severe gastrointestinal illness.
The healthy equine gut contains a large resident population of gram-negative bacteria. Under normal conditions the intact mucosal barrier prevents LPS from entering the bloodstream in significant amounts. When gut perfusion is compromised — as occurs in strangulating obstruction, severe large colon displacement, or prolonged ileus — the mucosal barrier fails and endotoxin translocates into the portal circulation. Once systemic, LPS binds toll-like receptor 4 (TLR4) on macrophages and monocytes, triggering a cytokine cascade that produces fever, tachycardia, injected mucous membranes, and in severe cases, distributive shock. This is equine endotoxemia.
The most dangerous downstream consequence of endotoxemia in the horse is laminitis. Endotoxin directly activates vasoactive mediators and platelet aggregation pathways in the laminar vasculature of the hoof, causing the ischemic damage that underlies acute laminitis. Horses that survive endotoxemic colic frequently develop laminitis as a secondary complication within 24 to 72 hours. Monitoring the hoof for heat and digital pulse is standard post-colic protocol for this reason.
Treatment targets both endotoxin itself and the inflammatory response it triggers. Polymyxin B binds and neutralizes circulating LPS directly and is the most specific anti-endotoxin agent in equine practice. Flunixin meglumine (Banamine) at full anti-endotoxin dose (0.25 mg/kg IV four times daily) blunts the prostaglandin arm of the inflammatory response. Intravenous fluids support perfusion and dilute circulating endotoxin. Recognition of early colic warning signs and rapid veterinary intervention reduces the duration of gut compromise and therefore the endotoxin load absorbed. See also laminitis as the primary downstream complication of endotoxemia, and recognizing colic in the first 30 minutes to limit gut compromise before endotoxin absorption begins.
Further Reading: The molecular biology of lipopolysaccharide and its role in gram-negative sepsis is detailed on Wikipedia’s Lipopolysaccharide article. For the equine-specific clinical picture — how endotoxemia manifests in horses with colic and its treatment — see Utah State University Extension’s overview at USU Extension: Endotoxemia in Horses.