t Heinz Red! and Gunther Sch!ag Ludwig Boltzmann Institute for
Experimental and Clinical Traumatology, Vienna, Austria The word
"sepsis" derives from the Greek meaning decay or rottenness. Tradition-
ally this term has been used to describe the process of infection
accompanied by the host's systemic inflammatory response. Based on that
understanding, previous clin- ical studies have been designed to include
only patients with positive blood cultures [1, 2]. However, the
frequent occurrence of a septic response without the demon- stration of
microorganisms in the circulation has led to a new definition and under-
standing of sepsis, mainly as the systemic response of the host to an
often unde- tectable microbiological or non-microbiological process
[3]. The general consensus is that cytokines are central to the
inflammatory response, particularly in sepsis. It is now known that not
only Gram-negative but also Gram- positive, viral, and fungal infections
initiate the complex cascades of cytokine release. Probably the most
important aspect of bacterial action is the release of toxic bacterial
products. In particular endotoxin from Gram-negative bacteria (see chap-
ter by Schade) and super antigens (see chapter by Neumann and Holzmann),
as well as pore-forming toxins [4] from Gram-positive bacteria, induce
cytokine formation. The importance of this cytokine release is evident
from both diagnostic and thera- peutic (mostly experimental) studies,
and the action of cytokines may be the key to our understanding of the
pathophysiology of the sepsis syndrome.
