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17 Cards in this Set
- Front
- Back
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Describe the classical pathway of compliment |
Antibody binds C5 binds C3 catalyses formation of C5-C6-C7 complex C8 and C9 are also required to damage the membrane and cause lysis |
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What complex does compliments classical pathway form and how does it work? |
The membrane attack complex (MAC) which forms a pore in the surface of bacteria |
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Name 2 alternative pathways to activating MAC |
Mannan binding lectin - serum protein, recognises polysaccharides Uses some of the classic pathways with other proteins |
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Name 5 methods that avoid the immune response |
Non specific - LPS avoids compliment Organism specificity Avoid the immune effector mechanism - phase variation, physical shield Diversion using vesicles Control immune receptors, down regulate complement |
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What kind of LPS can sterically hinder the MAC |
Smooth LPS is much thicker than rough LPS so the MAC proteins will get stuck on the layer |
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Describe the streptococcus pyrogenes infections |
Strep throat, impetigo, necrotising fasciitis, toxic shock |
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Describe the M protein |
Fibrillar protein - repeating 7 amino acid sequence, conserved C - terminal, variable N - terminal, occurs as a coiled dimer Covalently attached to peptidoglycan Proinflammatory - may cause toxic shock |
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How does the M protein evade the host immune response |
Binds to down regulate complement - no deposition on the surface Binds to fibrinogen and albumin - decrease in complement deposition, steric hindrance of antibodies Inhibits phagocytosis - interferes with complement opsonisation |
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Describe the characteristics of phase variation |
NOT GENETIC REGULATION The reversible ON-OFF switching in genes will show mixed populations The environment will determine which type dominates Switching will also be affected by the environment This switch can change expression of fimbrae Change the variable antigenic region - Nessesaria gonorrhoeae |
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Describe the Nessesaria gonorrohoeae bacteria |
Gram negative, diplococcus |
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Explain phase variation in Nessesaria gonorrhoreae |
PilE gene is the major pilin subunit Up to 20 silent PilS genes pilE and pilS are highly similar and can undergo RecA mediated recombination where they are swapped Neisseria are naturally transformable which adds more variation Mixed populations of other Pillus will cause the immune system to struggle |
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Explain surface sialic acids |
N.gonorrhoeae LPS is mostly absent Acquire Salic acids from the host glycoproteins and glycolipids added to LPS by sialyl transferase Forms a capsule like structure which is highly resistant Mimics host cell surface structures
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What is phase variation in E. coli |
Type 1 fimbriae in urinary pathogenic E. coli - this adheres to the bladder and allows infection as UPEC is invasive in superficial bladder epithelium |
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ON/OFF phase variation of e.coli |
314bp DNA element with 9bp inverted repeats These repeats may flip and cause FimS not to express and Type 1 fimbriae not being expressed will cause destruction of the bacteria by detection and so those expressing will dominate |
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How can bacteria 'trick' the immune response |
Destroy antigen - capsule/slime, OM vesicles (wrong target) |
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Describe and give an example of a polysaccharide capsule |
Polysaccharide outer layer Anthrax capsule is composed of poly-D-glutamic acid |
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Name 3 organisms and how they use their capsules |
Streptococcus pyrogenes - nonimmunogenic hyaluronan capsule Neisseria gonorrhoeae - sialic acids added to LPS Streptococcus pneumonia - uncapsulated strains are rapidly cleared |
