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microbiology > micro 3 (CF) > Flashcards

micro 3 (CF) Flashcards

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1
Q

CFTR?

A

cistic fibrosis transmembrane regulator protein

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2
Q

How many mutations are there in the CFTR protein?

A

> 1,800

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3
Q

What is the most common mutation on the CFTR protein in CF?

A

Phe 508 del

> 80%

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4
Q

What does CFTR protein do?

A

allows Cl- ions to be secreted into the airway surface liquid

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5
Q

What happens in Phe508del CF?

A 
CFTR protein is absent
Cl- ions can't be pumped out 
airway surface liquid dehydrates
mucus attracted to cell surface
cilia can't beat properly
mucus becomes stuck
inability to clear bacteria - infections
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6
Q

4 conventional CF pathogens

A

P aeruginosa
S aureus
H influenzae
B cepacia complex

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7
Q

emerging CF pathogens

A 
Stenotrophomonas maltophilia
MRSA
M. abscessus
Achromobacter spp
Streptococcus milleri/anginosus group
Aspergillus fumigatus (Fungus)
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8
Q

What are the initial pathogens that cause CF infections?

A

H influenza

S aureus

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9
Q

What pathogens do CF infections progress to?

A

P aeruginosa

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10
Q

How to reduce cross infection in CF?

A

cohort segregation (same bacteria)
individual segregation
personal hygiene and PPE

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11
Q

What is the 1st bacteria to colonise the CF lung?

A

staphylococcus aureus

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12
Q

2 subtypes of S aureus in CF infections?

A

MRSA

small colony variants (SCV)

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13
Q

describe small colony variants?

A 
small colonies when grown on agar
< 1mm
non-pigmented
non-haemolytic
biochemical tests for ID might not work
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14
Q

What kind of metabolism do small colony variants have?

A

altered metabolism or auxotrophic

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15
Q

When do wild type change to small colony variants?

A

when stressed - antibiotics

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16
Q

What small colony variants have the strongest association with lung function?

A

SCVs that are thymidine dependent

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17
Q

What happens in children with S. aureus SCVs?

A

they have lower mean % of predicted FEV1

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18
Q

What is Pseudomonas aeruginosa?

A

G- facultatively anaerobic bacillus

usually an opportunistic pathogen

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19
Q

Where is Pseudomonas aeruginosa found?

A

UTIs
sepsis
non-CF lung infections
GI

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20
Q

What does Pseudomonas aeruginosa have multiple of?

A

efflux systems

secreted and cell based virulence factors

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21
Q

How many CF patients have Pseudomonas aeruginosa by age of 20?

A

> 50%

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22
Q

Specialised strains of Pseudomonas aeruginosa associated with CF infection

A 
Liverpool epidemic strain (LES)
Midlands1
Manchester epidemic strains
DK2 in Denmark
Aust-02 in Australia
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23
Q

How to eradicate PA infections?

A

combination of oral/IV and inhaled antibiotics

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24
Q

What is chronic colonisation with PA associated with?

A

worse lung fxn outcome

higher inflammation

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25
Q

What does PA have to overcome in the CF lung?

A

protection from the immune system

less oxygen in the mucus layer

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26
Q

What are changes in PA to adapt to CF lung regulated by?

A

quorum sensing

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27
Q

What is quorum sensing?

A

Ability to detect and respond to cell population density by gene regulation
Expression or repression of specific genes which produce phenotypes which will be beneficial

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28
Q

What 3 characteristics do bacteria need to use Quorum sensing?

A
  • Ability to produce a signaling molecule (an autoinducer)
  • Be able to detect the change in signaling molecules
  • Regulate gene expression as a result
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29
Q

How can PA use quorum sensing?

A

Biofilm formation

EPS production

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30
Q

What is T3SS?

A

needle like machinery that lets bacterial effectors

translocate directly into the cell

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31
Q

What does T3SS cause?

A

Causes tissue injury and cytotoxicity

32
Q

How many T3SS dependent effectors does PA have?

A

4

33
Q

PA 4 T3SS dependent effectors?

A

ExoS
ExoT
ExoY
ExoU

34
Q

Which T3SS effectors disrupt host cell cytoskeleton?

A

ExoS, T and U

35
Q

What can ExoU do?

A

cleave phospholipases (leads to cell death)

36
Q

How does T3SS activate immune response?

A

via IL-1 beta

37
Q

What do chronic PA infections do with T3SS?

A

they select against T3SS expressing PA

patients have antibodies against T3SS effector proteins

38
Q

What is LPS a major component of?

A

G- outer membrane

39
Q

What antigen of the outer membrane is lost in early CF infections?

A

O antigen

40
Q

What is modified/changed in the OM in CF?

A

lipid A structure

41
Q

What residues are acquired in early CF when lipid A is modified?

A

pamitate and aminoarabinose residues

42
Q

What is aminoarabinose associated with?

A

increased resistance to antimicrobial peptides and some antibiotics

43
Q

What do LPS modifications cause?

A

they make PA less visible to the immune system

44
Q

In what bacterial infections is bacteria free floating?

A

acute infections

45
Q

What is free floating bacteria called?

A

planktonic

46
Q

How are bacteria attached in chronic CF infections?

A

attached to surface and become embedded in acellular matrix

47
Q

What happens when bacteria is embedded in acellular matrix?

A

surface of epithelial airway is damaged

48
Q

What is in the matrix of PA infections?

A

alginate
PEL
PSL
extracellular DNA

49
Q

What type of communities are biofilms?

A

polymicrobial

have different micro-environments

50
Q

1st identified bacteria in biofilms

A

PA

51
Q

What other bacteria can cause biofilms?

A

B cepacia complex

52
Q

What do biofilms result in?

A

x1000 increase in resistance to antibiotics

53
Q

5 stages of biofilm formation in chronic CF

A
  1. initial attachment
  2. irreversible attachment
  3. microcolony formation
  4. maturation
  5. dispersion
54
Q

What is needed for irreversible attachment of biofilm?

A

flagella

type IV pili

55
Q

What is produced in microcolony formation stage of biofilm formation?

A

production of EPS

56
Q

What is formed in maturation stage of biofilm formation?

A

formation of 3D complexes

creates oxygen gradient (anaerobic in centre)

57
Q

What can PA switch from and to in chronic infections?

A

switches from non-mucoid to mucoid phenotype

58
Q

What causes PA to switch to mucoid?

A

large amounts of alginate produced

59
Q

What do rugose SCV use as structural components in biofilms?

A

use Pel and Psl as structural components

60
Q

What can Pel do?

A

crosslink extracellular DNA in PA biofilm matrix

61
Q

What is alginate?

A

linear polysaccharide

negatively charged

62
Q

How is alginate initially produced?

A

homopolymer of D-mannuronic acid residues

63
Q

What is alginate modified by?

A

enzymes - AlgI, AlgJ, AlgF

64
Q

What is alginate epimerized by?

A

AlgG

65
Q

What does AlgG convert D-mannuronic acid to?

A

L-guluronic acid

66
Q

What is Psl?

A

neutral pentasaccharide repeat

contains glucose, mannose, and rhamnose

67
Q

What is Pel?

A

cationic amino sugars
1→4 linked partially acetylated galactosamine and glucosamine
sugars

68
Q

How does PA invade complement?

A

produces enzymes

69
Q

What enzymes does PA produce and what do they do?

A

alkaline protease and elastase

degrade C3b

70
Q

What is downregulated by PA?

A

flagellin and T3SS

71
Q

2 other CF pathogens

A
  1. Burkholderi cepacia complex (BCC)

2. non tuberculosis mycobacteria

72
Q

How many species of BCC?

A

18

73
Q

3 types of BCC species?

A

B cenocepacia
B multivorans
B dolosa

74
Q

What 2 complexes are NTM isolates in CF from?

A

mycobacterium avium

mycobacterium abscessus complex

75
Q

What species does mycobacterium avium include?

A

4 M avium species and M intracellulare

microbiology (4 decks)

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