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20 Cards in this Set
- Front
- Back
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3 mech of host cell lysis + ex's
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1 Toxins - RBC lysis from Clostridia toxin in Gas Gangrene
-lecithinase (lipase) 2 - intracellular growth --> lysis. Rickettsae growth kills host cells in RMSF (endothelial cells) 3 - Cell Mediated immunity erradication of infected cells - TB |
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7 questions for a toxin?
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does it, isolated, cause damage? does it contribute to virulence?
can a specific AB prev/alleviate if AB'd, is disease process effected? --> What is the mech? Why does it target spec. cells? Is it only toxin, or interact w others? |
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What is the reason/theory behind most toxins being held on plasmids?
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Toxins are not required for bacterial growth, are dispensible. However they may be essential for colonization, obtaining nutrients, etc
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Exotoxins -
Type 1 secretion? Type 2 |
1 - autotransport built into toxin
2 - mech built into bacterial CM |
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Where is the B domain in exotoxins? Cytotoxin IIIs?
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B domain is built into toxin in exotoxins, is part of parent cell in cytotoxin t3s
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What Bact use ADP Ribosylation?
How are their effects different? |
Diptheriae - shuts down EF-2, inhib
growth exotoxin A of P.Aeruginosa - Cholera - excess cAMP (lock GTP) massive fluid release B.Pertussis - Also G-protein, diff site |
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***TABLE9.1**** ON IPAD
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^____^;
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How are exotoxins activated?
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commonly by breaking of a disulfide bond
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To what genus do botulism and tetanus belong to?
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The anaerobic spore-forming Clostridium
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What constitutes true intoxication?
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Damage in the absence of the microbe (Botulism)
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General mechanism of TypeIII Cytotoxins?
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Degradation of the host cell cytoskeleton. Phagocytosis requires an operational actin skeleton
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What arm do endotoxins initiate?
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The innate immune system
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**Pattern Recognition Receptors**
Activate? Catalyst to? G- G+ Fungal Mycobacterial |
Activates Innate, catalyses activation of Adaptive
LPS lipoteichoic acid mannans (yeast) lipoglycans |
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Reactions to Endotoxin + Effect
1 - Macrophages 2 - Neutrophils 3 - B Lymphocytes 4 - Complement |
1 - ^IL-1, TNF --> FeverAcutePhaseR
2 - Kinnin System --> Vasodilation 3 - activation / AB synthesis (via IL-1) 4 - Alt Pathway, Inflammation -MAC,Anaphylaxis, Neut Activati |
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How does the release of endotoxin lead to DIC?
Where is this most severe? What disease of this type is caused by Meningococci |
endotoxin causes serious coag by activiating Hageman Factor (XII), Granule release from platelets, and release of neutrophil clot stabilizers
This is most severe in the kidney Waterhouse-Friedrichson, an acute infarction of the adrenal glands |
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Mechanism of bacterial sepsis?
Common bacteria? |
massive endotoxin release triggers mass infection by gram negative bacterias and leads to Shock
E.Coli, P.aeruginosa, Meningococcci |
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prototypical homogenous pore former? similar to? advantages?
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Alpha hemolytics from staph, very similar to MAC complex, cannot be broken down by many common proteases
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Heterogenous pore forming toxin?
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Stretolysin-O which binds to the cholesterol of RBCs
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function of exoenzymes?
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commonly to break down host tissues
-hyalurinidase, deoxyribonuclease, streptokinase |
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Immunization against toxins?
New Techniques? |
use of antitoxins or toxoids(inactivated versions)
interest in focusing solely on B domain |
