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8 Cards in this Set
- Front
- Back
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**What cytokines are major mediators of septic shock?
What symptoms associated with Septic shock |
TNF-a IL-1
Septic Shock= fever, hypotension, DIC (disseminated intravascular coagulation), organ dysfunction |
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What are MSCRAMM's? |
Microbial Surface Components Recognizing Adhesive Matrix Molecules
A subfamily of surface adhesions that target host extracellular matrix proteins for adhesion
(Allow bacteria to bind to extracellular matrix and cause infection) |
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Endotoxins vs Exotoxins
Found in gm - or gm +?
LPS/Proteins?
Chromosomal / Phage or plasmid? |
Endotoxins= LPS, Lipid A, Gram - only, Chromosomal
Exotoxins= Proteins, both Gram - and Gram +, extracellular, phage or plasmid, converted to toxoids |
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What are the endogenous pyrogens? |
TNF-a IL-1 |
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How do Exotoxins work?
**What are the 2 types and how do they work? |
Exotoxins (AB) bind to surface and taken into cell.
b= binding unit a= active unit, causes host cell damage
2 Types: Pore-forming toxins= Form ligamers on surface and form hole (pore) in membrane, allowing passage of water and ions, causing lysis! This is how Lipid A causes septic shock.
Super antigens= combine MHC class 2 w/ T cell receptor in a polyclonal manner and avoiding antigen binding groove which causes exaggerated non productive response leading to septic shock |
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**What 3 structures confer Virulence? |
LPS, Capsule, Pili |
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**Identify the superantigen and pathology
Staph. Aureus?
Staph. Enterotoxins? |
Staph. Aureus= Toxic Shock Syndrome, (TSST-1)
Staph. Enterotoxins= vomiting, diarrhea, (SEA, SEB, SEF) (has superantigen capability in blood) |
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**What are these?
Polyclonal T-cell mitogens
Don't bind to any specific antigens, thus cause exaggerated response, and AVOID memory response (Bind to MHC class 2 and T-cell receptor outside antigen binding sites)
Stimulate non-specific T-cell responses |
Superantigens |
