To What Extent Are the Terminal Stages of Sepsis, Septic Shock, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome Actually Driven by a Prion/Amyloid Form of Fibrin?

Sepsis is a diseasewith highmortality.1–7However, the original notion of sepsis as the invasion of blood and tissues by pathogenic microorganisms has long come to be replaced, in the antibiotic era, by the recognition that in many cases, the main causes of death arise not so much from the replication of the pathogen per se but from the host’s “innate immune” response to the pathogen.8–11 In particular, microbial replication is not even necessary (and most bacteria in nature are dormant12–16), as this response is driven by very potent17 inflammation-inducing agents such as the lipopolysaccharides (LPSs) of gram-negative bacteria18 and equivalent cell wall materials such as lipoteichoic acids from gram-positive bacteria.19–22 To this end, such release may even be worsened (i.e., the Jarisch–Herxheimer reaction23–26) by antibiotic