Sepsis: Pathophysiology and Treatment
Journal Title: Journal of Intensive and Critical Care - Year 2017, Vol 3, Issue 2
Abstract
Few pathogens cause sepsis. The majority of sepsis causing bacteria is facultative anaerobes. This type of respiration is the most flexible and it facilitates pathogen survival, proliferation and dissemination in human tissues and blood. Other conditions for causing sepsis are thick slime layer and capsule, as well as production of antioxidant enzymes and substances (superoxide dismutase (SOD), catalase and glutathione) that protect bacteria against oxidative stress caused by reactive oxygen species of erythrocytes and leukocytes [1]. Pathogens need pore forming and membrane destroying enzymes and toxins for penetrating erythrocytes. Initial pathogen-host interaction occurs in the tissues where blood coagulation, resident and transmigrated leukocytes, platelets, complement proteins and NETs are the first line of innate antibacterial immunity. If bacteria survive in the tissues, they start to produce especially thick capsule and form biofilm. After overcoming the tissue barrier, pathogens enter the bloodstream and cause bacteremia. The latter transforms to sepsis when microbes survive oxidation on the surface of erythrocytes. Septic shock develops when bacteria enter erythrocytes, survive oxidation by oxygen released from oxyhemoglobin, proliferate inside erythrocytes and cause premature abundant release of oxygen from erythrocytes before their entering capillaries [2]. Premature release of oxygen has consequences: a) oxidation of blood plasma components (proteins, immune complexes, regulatory hormones, peptides, amino acids, lipids, vitamins and other substances necessary for cell nutrition, proliferation, protection, energy production, functioning, etc.); b) failure of oxygen delivery to cells and multi-organ hypoxia; c) disseminated intravascular coagulation with further massive haemorrhages because of consumption of blood coagulation factors. As a result, multiple organ dysfunctions develop.
Authors and Affiliations
Hayk Minasyan
Keywords
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- EP ID EP300716
- DOI 10.21767/2471-8505.100083
- Views 45
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