Sepsis: mechanisms of bacterial injury to the patient

Abstract In bacteremia the majority of bacterial species are killed by oxidation on the surface of erythrocytes and digested by local phagocytes in the liver and the spleen. Sepsis-causing bacteria overcome this mechanism of human innate immunity by versatile respiration, production of antioxidant e...

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Main Author: Hayk Minasyan
Format: Article
Language:English
Published: BMC 2019-02-01
Series:Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
Subjects:
Online Access:http://link.springer.com/article/10.1186/s13049-019-0596-4
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author Hayk Minasyan
author_facet Hayk Minasyan
author_sort Hayk Minasyan
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description Abstract In bacteremia the majority of bacterial species are killed by oxidation on the surface of erythrocytes and digested by local phagocytes in the liver and the spleen. Sepsis-causing bacteria overcome this mechanism of human innate immunity by versatile respiration, production of antioxidant enzymes, hemolysins, exo- and endotoxins, exopolymers and other factors that suppress host defense and provide bacterial survival. Entering the bloodstream in different forms (planktonic, encapsulated, L-form, biofilm fragments), they cause different types of sepsis (fulminant, acute, subacute, chronic, etc.). Sepsis treatment includes antibacterial therapy, support of host vital functions and restore of homeostasis. A bacterium killing is only one of numerous aspects of antibacterial therapy. The latter should inhibit the production of bacterial antioxidant enzymes and hemolysins, neutralize bacterial toxins, modulate bacterial respiration, increase host tolerance to bacterial products, facilitate host bactericidal mechanism and disperse bacterial capsule and biofilm.
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spelling doaj.art-0ed5856c4fe4451d80229dfb43cac32b2022-12-21T23:07:09ZengBMCScandinavian Journal of Trauma, Resuscitation and Emergency Medicine1757-72412019-02-0127112210.1186/s13049-019-0596-4Sepsis: mechanisms of bacterial injury to the patientHayk MinasyanAbstract In bacteremia the majority of bacterial species are killed by oxidation on the surface of erythrocytes and digested by local phagocytes in the liver and the spleen. Sepsis-causing bacteria overcome this mechanism of human innate immunity by versatile respiration, production of antioxidant enzymes, hemolysins, exo- and endotoxins, exopolymers and other factors that suppress host defense and provide bacterial survival. Entering the bloodstream in different forms (planktonic, encapsulated, L-form, biofilm fragments), they cause different types of sepsis (fulminant, acute, subacute, chronic, etc.). Sepsis treatment includes antibacterial therapy, support of host vital functions and restore of homeostasis. A bacterium killing is only one of numerous aspects of antibacterial therapy. The latter should inhibit the production of bacterial antioxidant enzymes and hemolysins, neutralize bacterial toxins, modulate bacterial respiration, increase host tolerance to bacterial products, facilitate host bactericidal mechanism and disperse bacterial capsule and biofilm.http://link.springer.com/article/10.1186/s13049-019-0596-4SepsisTreatmentAntibacterial therapyAntibioticsBactericidalsBacteriostatics
spellingShingle Hayk Minasyan
Sepsis: mechanisms of bacterial injury to the patient
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
Sepsis
Treatment
Antibacterial therapy
Antibiotics
Bactericidals
Bacteriostatics
title Sepsis: mechanisms of bacterial injury to the patient
title_full Sepsis: mechanisms of bacterial injury to the patient
title_fullStr Sepsis: mechanisms of bacterial injury to the patient
title_full_unstemmed Sepsis: mechanisms of bacterial injury to the patient
title_short Sepsis: mechanisms of bacterial injury to the patient
title_sort sepsis mechanisms of bacterial injury to the patient
topic Sepsis
Treatment
Antibacterial therapy
Antibiotics
Bactericidals
Bacteriostatics
url http://link.springer.com/article/10.1186/s13049-019-0596-4
work_keys_str_mv AT haykminasyan sepsismechanismsofbacterialinjurytothepatient