Biology of Neisseria Meningitides Flashcards Preview

Module 2 > Biology of Neisseria Meningitides > Flashcards

Flashcards in Biology of Neisseria Meningitides Deck (57):
1

What type of bacteria is N.meningitides?

gram negative diplococcus

2

Where does N.meningitides reside?

obligate human parasite- extracellular

3

How is N.meningitides classified?

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

4

Where in the body does meningococcus colonise?

nasopharynx

5

How is meningococcus transmitted?

coughing; sneezing; kissing etc

6

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

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

7

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

epitheium of respiratory tract; endothelium and BBB

8

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

meningococcal leakage

9

Where are the virulence attributes of microbes found?

on the cell surface

10

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

type IV pili

11

things does Tfp allow meningococcus to do?

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

12

What is natural transformation?

gaining of genes from the environment

13

What does aggregation mediated by Tfp allow meningococcus to do?

form biofilms in blood vessels

14

Describe twitching motility?

extends and contracts- attaches then pulls itself towards

15

What protein is Tfp a polymer of?

pillins

16

Describe Tfp?

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

17

What imaging can be used to look at the filaments?

cryoelectronic microscopy

18

What suggests that pilli is conserved?

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

19

Name other type IV filamentous nanomachines?

secreton; competence psudeopilus; archaellum

20

Which cells have type IV filamentous nano-machines?

ubiquitous in prokaryotes

21

How are type IV pillins made?

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

22

What are the 2 types of opacity proteins?

Opa proteins and Opc

23

What is the function of opacity proteins?

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

24

Why are the opacity proteins named so?

presence confers opacity on bacteria in stereomicroscopy

25

What is hte strucutre of opacity proteins?

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

26

What is result of binding to OpaHS?

internalisation

27

What is hte result of binding to OpaCEA?

uptake and transcytosis

28

When is opa-mediated adhesion particularly important?

in the absene of the capsule (usually covered)

29

What is the capsule?

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

30

What is different about hte different serogroup polysaccharide?

different sugars or same sugar with different branching pattern

31

What is the capsule especially important in protection against?

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

32

Which strains of meningococcus have a capsule?

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

33

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

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

34

What is FHbp?

factor H binding protein: surface lipoprotein

35

What is the structure of FHbp?

folded into 2 beta-barrels

36

What are the 2 forms of neisseria which are pathogenic?

gonoccocus and meningitides

37

How did neisseria acquire a capsule?

through horizontal gene transfer

38

Why is gonoccocus not invasive?

does not have capulse locus

39

What is factor H?

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

40

What does factor H bind?

host sugars and C3b- accelerating its decay

41

What is FHbp an example of?

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

42

What is antigenic variation?

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

43

What is phase variation?

reversible small changes in DNA sequence which alter gene expression

44

Through what mechanism does phase variation occur?

slipped-strand mispairing

45

What induces slipped-strand mispairing?

repetitive sequences within genes or their promoters

46

What are the 2 methods of modification of surface structures?

antigenic and phase variation

47

Why is modification of surface structures important?

key in allowing bacterium to disguise itself

48

How does pilin antigenic variation arise?

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

Which genes in meningococcus undergo phase variation?

those associated with virulence

50

What are porins?

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

51

How does slip-strand mismatching work?

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

52

What is HGT?

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

53

What is the main method of HGT?

natural tranformation (acquisition of free DNA)

54

What mediates DNA uptake by meningococcus?

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

55

What is LPS composed of?

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

56

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

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

57

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

infection outcome