Reappraisal of the role of endotoxin in the sepsis syndrome.

Abstract

There is strong evidence to implicate endotoxin released from gram negative bacteria in the pathogenesis of the sepsis syndrome and related conditions, but equally compelling data bring the role of endotoxin into doubt. Reappraisal of endotoxin and its release from gram negative bacteria suggests that it is not directly responsible for the complications of sepsis syndrome. Rather, release of endotoxin is a marker for the transition of gram negative organisms to cell-wall-deficient forms (L-forms) that may persist undetected despite antibiotic therapy directed against the parental form. This transition has two consequences in compromised patients: L-forms cause organ failure, and they serve as a sanctuary from which cell-wall-intact revertants may arise.