The biology of endotoxin.

Abstract

Approximately 100 yr ago Richard Pfeiffer, a co-worker of Robert Koch in Berlin, discovered that cholera bacteria produced, in addition to heat-labile exotoxin, another toxin (). In contrast to the secreted exotoxins this new, heat-stable toxin was found to be a constituent of the bacterial cell, and therefore Pfeiffer termed it endotoxin. Today we know that endotoxin (lipopolysaccha-ride, LPS) is the main outer membrane component of Gram-negative bacteria and plays a key role during severe Gram-negative infection, trauma, and shock (,). Despite its destructive effects, the presence of low amounts of LPS, which gain access to body fluids and organs by infection and translocation from the gut, are rather beneficial for the host, causing immunostimulation leading to enhanced resistance to infections and malignancy (). This picture changes completely when larger amounts of LPS are present in the bloodstream, as observed during severe Gram-negative bacterial infections (notably after application of antibiotics) or possibly caused by translocation of entero-bacteria from the gut. Released LPS causes various pathophysiological reactions including fever, leukopenia, tachycardia, tachypnea, hypotension, disseminated intravascular coagulation, and multiorgan failure. This may culminate in septic shock which is associated with a mortality rate of 20–50% and causes approx 100,000 deaths annually only in the United States ().