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24 Cards in this Set

  • Front
  • Back
the three components to LPS
1. Lipid A (buried in OM)
2. Core polysaccharide
3. O specific Ant
part of LPS that varies with strain
O antigen
part of LPS which is conserved w/in species
core polysaccharide
cell wall is made out of
cell wall of gram positives has what acid has what
teichoic acids
what part of LPS is recognized on PCR
lipid A (it is a PAMP)
what cytokine is the most important in inducing endotoxin shock
steps in DIC
lipid A - Factor XII - Thrombin - Fibrin - Clotting - Depletion of Platelets - Clot dissolves - local bleeding (purpura)
why is laboratory detection of bacteria and septecemmia different
in bacteria - bacteria is transient
in septecemia - blood acts as a site of replication and transfer
Horse shoe Cra agglutinate test is very sensitive and detects what part of LPS
Lipid A
how does LPS cause endotoxic shock
LBP binds LPS
LBP-LPS binds SCD14 (delivers LPS to CD14)
LPSmCD14 bind TLR4/MD-2 Rece
release of TNF, IL1,6,9
innate response, inflammation, activates acquired immunmity, mediator synthesis
what inhibirs mediator synthesis in endotoxic shock
Prostaglandin E2
three main symptoms of endotoxic shock
1. Fever, Hypotension, Fibrinolysis
two things that lead to hypotension in endotoxic shock
endotoxin vs. exotoxin
denatured by boiling?
Forms Toxoid
endotoxin is not denatured by boiling, exotoxin is

both are antigenic

only exotoxin can form toxoid
High or low potency

endotoxin vs. exotoxin
exotoxin has high Potency AND Speficity

endotoxin has low potency and spcificity
endotoxin vs. exotoxin

enzymatic activity?
exotoxin yes

endotoxin no
fever inducing

endtotoxin vs exotoxin
yes endotoxin, sometimes exotoxin does
two purposes of the O antigen
1. variable surface (protection)
2. permeability barrier
can Gram cause endotoxin response
no exactly but CM can cause similar response when lysed
is endotoxin secreted
no - released when cell lysed
what accounts fore the variability in outcome due to endotoxic shock
the polysaccharide O antigen influences the activity of lipid A
The TWO strongest mediators fo toxic shock
TNF and IL-1
the two consequences of DIC
localized necrosis
generalized bleeding