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Cytokine-Mediated Enhancement of Host Defense

  • A. J. Lechner
  • G. M. Matuschak
Conference paper
  • 90 Downloads
Part of the Yearbook of Intensive Care and Emergency Medicine book series (YEARBOOK, volume 1997)

Abstract

Despite prompt antibiotic treatment of microbial infections and aggressive intensive care of the critically ill, progression to the septic shock syndrome remains common and mortality still exceeds 50% [1, 2]. This situation has promoted the distinction between infections as microbiological phenomena, and septic shock as a complex series of deleterious host responses to such microbial invasion [1, 3]. Two factors have been important in shaping the current widely-held conception that these host-derived inflammatory responses are stereotypically activated in infected subjects regardless of the type of pathogen. The first may be termed an argument based on the clinical equivalency of pathogen-specific sepsis. Physiologic and metabolic derangements during severe infection by taxonomically diverse organisms (e.g. Gram-negative bacteria, Gram-positive bacteria, pathogenic fungi, rickettsiae, and viruses) often are clinically indistinguishable [3–5]. Thus, the inflammatory events responsible for these clinical derangements are thought to be similar. Initially manifested by the systemic inflammatory response syndrome (SIRS), these events lead to circulatory instability with respiratory distress according to the extent of infection and/or the intensity of the host response, culminating in multiple organ failure (MOF) [1,2].

Keywords

Septic Shock Biological Response Modifier Dimorphic Fungus Fungal Sepsis Candida Sepsis 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • A. J. Lechner
  • G. M. Matuschak

There are no affiliations available

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