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Module 2 > Biology of Neisseria Meningitides > Flashcards

Biology of Neisseria Meningitides Flashcards

1
Q

What type of bacteria is N.meningitides?

A

gram negative diplococcus

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2
Q

Where does N.meningitides reside?

A

obligate human parasite- extracellular

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3
Q

How is N.meningitides classified?

A

into serogroups based on capsular polysaccharide- A,B,C, W135, Y and X

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4
Q

Where in the body does meningococcus colonise?

A

nasopharynx

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5
Q

How is meningococcus transmitted?

A

coughing; sneezing; kissing etc

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6
Q

What are the features of meningococcus that makes it so pathogenic?

A

able to adhere to and cross host barriers; evasion; induces strong inflammatory repsonse

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7
Q

Which cellular barriers is meningococcus able to adhere to and cross?

A

epitheium of respiratory tract; endothelium and BBB

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8
Q

What is the name for the leakage that replication and damage by meningococcus in blood vessels causes?

A

meningococcal leakage

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9
Q

Where are the virulence attributes of microbes found?

A

on the cell surface

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10
Q

What is the most important factor in allowing meningococcus to adhere to and cross barriers?

A

type IV pili

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11
Q

things does Tfp allow meningococcus to do?

A

adhesion to host cells; aggregation; twitching motility; natural transformation

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12
Q

What is natural transformation?

A

gaining of genes from the environment

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13
Q

What does aggregation mediated by Tfp allow meningococcus to do?

A

form biofilms in blood vessels

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14
Q

Describe twitching motility?

A

extends and contracts- attaches then pulls itself towards

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15
Q

What protein is Tfp a polymer of?

A

pillins

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16
Q

Describe Tfp?

A

thin; long and flexible filaments- which look like a lollipop-globular head with hydrophobic residues forming the stick

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17
Q

What imaging can be used to look at the filaments?

A

cryoelectronic microscopy

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18
Q

What suggests that pilli is conserved?

A

all bacteria with pilli have the same proteins used to attach it to membrane

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19
Q

Name other type IV filamentous nanomachines?

A

secreton; competence psudeopilus; archaellum

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20
Q

Which cells have type IV filamentous nano-machines?

A

ubiquitous in prokaryotes

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21
Q

How are type IV pillins made?

A

pillins are synthesised as propeptide and stay in inner membrane; then leader sequence is cleaved and ATP is used to push pillins out of IM where pillin polymerises; uses a pore (secreton) to move through OM

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22
Q

What are the 2 types of opacity proteins?

A

Opa proteins and Opc

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23
Q

What is the function of opacity proteins?

A

role in adhesion- but nowhere near as important as type IV pilli

24
Q

Why are the opacity proteins named so?

A

presence confers opacity on bacteria in stereomicroscopy

25
Q

What is hte strucutre of opacity proteins?

A

have beta-barrel with exposed surface loops which are responsible for adhesion

26
Q

What is result of binding to OpaHS?

A

internalisation

27
Q

What is hte result of binding to OpaCEA?

A

uptake and transcytosis

28
Q

When is opa-mediated adhesion particularly important?

A

in the absene of the capsule (usually covered)

29
Q

What is the capsule?

A

water soluble high molecular weight polysaccharide made of regularly mediated subunits of sugars

30
Q

What is different about hte different serogroup polysaccharide?

A

different sugars or same sugar with different branching pattern

31
Q

What is the capsule especially important in protection against?

A

complement-mediated lysis: as complement isn’t able to access OM

32
Q

Which strains of meningococcus have a capsule?

A

all invasive strains (needed for invasion) but only 50% of carriage isolates

33
Q

What are the functions of the 3 regions of the capsule locus?

A

A-synthesis and polymerisation (different across the serogroups); B-anchoring in membrane through addition of a lipid; C-translocation across OM and IM

34
Q

What is FHbp?

A

factor H binding protein: surface lipoprotein

35
Q

What is the structure of FHbp?

A

folded into 2 beta-barrels

36
Q

What are the 2 forms of neisseria which are pathogenic?

A

gonoccocus and meningitides

37
Q

How did neisseria acquire a capsule?

A

through horizontal gene transfer

38
Q

Why is gonoccocus not invasive?

A

does not have capulse locus

39
Q

What is factor H?

A

a large, soluble glycoprotein which regulates complement by protecting host cells and tissues from famage by complement activation

40
Q

What does factor H bind?

A

host sugars and C3b- accelerating its decay

41
Q

What is FHbp an example of?

A

bacterial mimicry: binds factor H using same stereochemistry as host sugars

42
Q

What is antigenic variation?

A

non-reversible important changes in DNA sequence which alter protein sequence

43
Q

What is phase variation?

A

reversible small changes in DNA sequence which alter gene expression

44
Q

Through what mechanism does phase variation occur?

A

slipped-strand mispairing

45
Q

What induces slipped-strand mispairing?

A

repetitive sequences within genes or their promoters

46
Q

What are the 2 methods of modification of surface structures?

A

antigenic and phase variation

47
Q

Why is modification of surface structures important?

A

key in allowing bacterium to disguise itself

48
Q

How does pilin antigenic variation arise?

A

gene conversion: a silent gene can replace part of hte pilus gene (the part which ends up exposed on surface of Tfp) through homologous recombination

49
Q

Which genes in meningococcus undergo phase variation?

A

those associated with virulence

50
Q

What are porins?

A

integral OM proteins with multiple surface loops which are highly immunogenic (elicit antibodies)

51
Q

How does slip-strand mismatching work?

A

when DNA polymerase comes across certin sequences of repeated basses, stutters and makes a mistake changing the expression of the gene

52
Q

What is HGT?

A

transfer of genes between isolates in a manner other than traditional reproduction

53
Q

What is the main method of HGT?

A

natural tranformation (acquisition of free DNA)

54
Q

What mediates DNA uptake by meningococcus?

A

Tfp- binds and on retraction beings DNA across OM then another protein facilitates movement across IM

55
Q

What is LPS composed of?

A

lipid A and sugar chain which some immunotypes modified with a sialic acid addition

56
Q

How do meningococci release massive amounts of LPS into the bloodstream?

A

by releasing blebls of the outer membrane (not all gram negs do this which is why not all cause cytokine storm)

57
Q

What can the level of LPS in the patients bloodstream be correlated with?

A

infection outcome

Module 2 (38 decks)

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