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ZZPathology undergraduate year 3, first term. > Bacteriology - biofilms, extracellular survival > Flashcards

Bacteriology - biofilms, extracellular survival Flashcards

1
Q

Dynamic biofilm environments

A 
Physico-chemical gradients
Enzymes
Water channels 
Gene transfer
Cell to cell communication
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2
Q

EPS constituents

A

Polysaccharides, DNA, proteins, water, lipids and biosurfactants, minerals.

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3
Q

Proteus mirabilis biofilm

A

Crystalline; cells in calcium apatite base.

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4
Q

Biofilm formation steps.

A

Initial attachment –> multiplication –> a flat biofilm.
OR
Initial attachment leads to an aggregate formation, leading to a structured Biofilm 1 (motile cap) or a structured biofilm II (due to clonal growth).
EITHER
Then lead to dispersion or detachment.

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5
Q

Pseudomonas stage III biofilm

A

LasI and RhlI are active, type IV pili are being made, extracellular DNA is found. GacA and rhlA are expressed.

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6
Q

Pseudomonas stage IV biofilm

A

PQS active. Matrix contains PSL, PEL and DNA.

Denitrification genes active, rhlA expressed. Alginate made.

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7
Q

Pseudomonas stage V biofilm

A

rhamnolipid (rhlA and rhlB). SadA expressed. Flagella made.

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8
Q

Alginate

A

Scavenges free radicals, prevents phagocytosis, protects from defensins.

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9
Q

Conversion to mucoidy in P. aeruginosa.

A

Stress reveals WVF on MucE.
WVF binds PDZ domain of AlgW, activating AlgW.
AlgW cleaves anti-sigma factor MucA, which releases AlgU which it has been sequestering.
AlgU activates alginate biosynthesis genes.

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10
Q

Alginate synthesis regulation

A

By stress (leads to MucE/AlgW/MucA/AlgU) and high c-di-GMP.

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11
Q

c-di-GMP and alginate synthesis

A

c-di-GMP binds Alg44 PilZ domain which helps co-ordinate alginate polymerisation and export.

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12
Q

Importance of adhesion in UPEC.

A

Contributes to colonisation, biofilm formation, apoptosis and exfoliation.

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13
Q

Biofilms in E. Coli.

A

Colanic acid rather than alginate.

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14
Q

What is EPS?

A

Extracellular polymeric substances.

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15
Q

Stabilisation of EPS matrix

A 
Repulsive forces (e.g. between acidic groups) prevent collapse. 
Ionic/electostatic/hydrogen bonds/van der Waals stick it together.
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16
Q

Biofilm formation pathway

A

reversible attachment, irreversible attachment, microcolony formation, mature biofilm, biofilm dispersal.

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17
Q

Biofilms - pathology

A

Phagocytosis cannot occur, but phagocytic enzymes are released. Damage tissues around the biofilm.
Motile bacteria are released from the biofilms.

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18
Q

Biofilm dispersal - swarming

A

Pseudomonas, Proteus mirabilis.

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19
Q

Biofilm dispersal - swimming

A

Pseudomonas.

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20
Q

Biofilm dispersal - clumping

A

Staph aureus, Mycobacterium tuberculosis

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21
Q

Biofilm dispersal - rolling

A

Staph aureus

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22
Q

Biofilm dispersal - sliding

A

Mycobacterium tuberculosis.

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23
Q

Types of motility in Pseudomonas biofilms

A

Flagella based in early stages and in late dispersal.

Twitching important in complex biofilm structures - mutants make flat biofilms.

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24
Q

HAP signalling pathways in biofilm formation

A

GacSA, sadARS.

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25
Q

Pseudomonas biofilms stage 1 and 2 as therapy targets.

A

Multicomponent vaccines, antibiotic therapies, quorum sensing inhibitors e.g. furanones. PREVENT FORMATION.

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26
Q

Pseudomonas biofilms stage 3 as a therapy target.

A

A few antibiotics still have effects.
Anti-inflammatories
Anti-biofilm agents.

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27
Q

Pseudomonas biofilms stage 4 as a therapy target. Alginate covered biofilm.

A

Alginate lyase, anaerobic growth inhibitors, DNase, novel antibiotics?

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28
Q

How do E. Coli colonise the host urinary tract?

A

Motility, adhesion, intracellular biofilms, extracellular biofilms, immune evasion.

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29
Q

How does E. coli damage the urinary tract?

A

Immune response, protein toxins.

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30
Q

UPEC motility

A

Flagella mediated, chemoattraction.

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31
Q

Phosphorylation pathway of chemoattraction

A

Empty receptor –> CheA –> CheY –> FliM –> tumble.

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32
Q

FliM

A

Switch motor protein in flagellar motor. Phosphorylation causes a switch to CW rotation.

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33
Q

Adhesion proteins expressed by UPEC

A

Curli pili
P-pili
Type 1 pili
S pili and Dr pili

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34
Q

Curli pili on E. coli

A

csgDEFG operon –> important in initial adhesion.

CsgA is exported by CsgG

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35
Q

Exfoliation in UPEC

A

Exposes lower level of epithelium; FimH binds CD48 as well as other receptors; internalised in actin-bound antibiotic non-susceptible non-immunogenic vesicles.

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36
Q

Intracellular invasion by UPEC

A

Zipper mechanism. FimH binds integrins –> clustering –> signalling –> internalisation.
Hijacks the Rab27b fusiform vesicular trafficking pathway.

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37
Q

Signalling for internalisation in UPEC

A

1) FAK complexes with PI3K –> PIPs –> changed actin dynamics.
2) Activation of Rac1 –> α-actinin and vinculin –> local changes to actin.

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38
Q

Intracellular UPEC

A

Quiescent, expelled or replication.

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39
Q

Intracellular UPEC - expelled

A

Probably by Rab27b fusiform vesicular pathway.

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40
Q

Intracellular UPEC - quiescent

A

Form reservoir, resistant to antibiotics

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41
Q

Intracellular UPEC - multiplication

A

Has to escape vesicle.
Requires adhesion pili to form communities, otherwise distributed.
Differentiate into filamentous and flagellated forms.

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42
Q

Filamentous UPEC from IBCs

A

Less prone to phagocytosis.

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43
Q

Immune response to UPEC

A

LPS –> TLR4 –> NFkB –> neutrophil recruitment (lots of inflammation) and production of IL-6 and IL-8. Thought to make epithelial cells more resistant to invasion.

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44
Q

Immune evasion by UPEC

A

LPS; use different forms to decrease immunogenicity. Phase variation of FimH.
Filamentous form less prone to phagocytosis
Stabilise IkB to decrease NFkB activation. Alter immune response using HlyA.

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45
Q

UPEC; protein toxins

A

HlyA, CNF1, Sat and Vat.

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46
Q

HlyA

A

RTX protein toxin, associated with increased severity in UTIs.

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47
Q

HlyA - synthesis and export.

A

Two genes for synthesis, ditto for export.
Fatty acid chains attached by HlyC.
Exported by HlyB pump associated with TolC.

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48
Q

HlyA - effects (5)

A

Release of iron and other nutrients by cytolysis.
Promotes exfoliation.
Promotes expression mesotrypsin –l NFkB.
Fine tunes immune response by causing Ca++ fluxes in renal cells.
Immune cell dysfunction

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49
Q

CNF; binding, entry into cytosol, effects.

A

Binds laminin, uptake by endocytosis, transfer into cytoplasm with acidification, effects are aberrant Rho activation and subsequent Rho degradation.

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50
Q

Vat and Sat toxin delivery

A

Blebbing forms outer membrane vesicles which allow for concentrated burst of toxin delivery to the host cell.

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51
Q

Type 1 pilus structure

A

FimH (adhesin), FimG, FimF, then right hand helix of FimA attached to OM secretion system at base (FimD)

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52
Q

Pap pilus structure

A

PapG, PapF, PapE (5-10), PapK and PapA attached to PapC secretion system at base.

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53
Q

Adhesins; FimH/PapG

A

Pilin domain + lectin domain for binding to host surfaces. Phase variation leads to expression of adhesin switched on in the host.

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54
Q

EPEC initial adhesion

A

Due to bundle forming pili

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55
Q

bundle forming pili (EPEC)

A

long range plasmid associated Type IV pilus. Encoded by bfp operon.

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56
Q

Possible importance of A/E lesions

A

1) Efficient delivery of other proteins
2) Resistance to bulk flow
3) Antiphagocytic

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57
Q

Importance of biofilms

A
  • Avoid predation by single cells (either immune or such as amoeba)
  • Increased tolerance to antibiotics
  • Some evidence that there is a subdivision of labour.
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58
Q

Bacterial motility in biofilm formation

A

Non-motile bacteria form microcolonies
• Cells migrate to form flat colonies.
• Formation of mushroom shaped colonies depends on migration of motile bacteria to colonise already established microcolonies.

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59
Q

Role of extracellular matrix

A

Scaffold, cell attachment, cell-to-cell interactions, antimicrobial tolerance.

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60
Q

Pel

A

Glucose rich and reported to be involved in formation of liquid-air pellicles.

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61
Q

Psl

A

important in cell-to-surface and cell-to-cell binding.

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62
Q

Type IV pili in biofilms

A

Adhesion. Also bind DNA and act as cross-linkers

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63
Q

Psl crosslinks with…

A

CdrA

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64
Q

Rhamnolipid

A

a biosurfactant produced in iron-limiting conditions which stimulates surface motility. Affects biofilm structure and formation.

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65
Q

LasI signal

A

3-O-C12-HSL

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66
Q

RhlI signal

A

C4-HSL

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67
Q

Subpopulations in biofilms

A

 Secreted products may be of use to all bacteria: e.g. rhamnolipid, pyoverdine.
 Some evidence that sub-populations have different roles e.g. in formation of mushroom-shaped colonies.

68
Q

Mechanisms of biofilm dispersal

A

 Controlled by low c-di-GMP. Biofilm dispersal locus makes BdlA which is a chemotaxis regulator affecting c-di-GMP levels.
 RbdA decreases Pel and Psl synthesis, and increases rhamnolipid synthesis.

69
Q

Antimicrobial tolerance in biofilms is due to …

A

Restricted penetration.
Different physiological activity.
Presence of persisters.
Inducible anti-microbial resistance factors.

70
Q

High c-di-GMP results in…

A 
o	Pel production
o	Psl production
o	Alg44 production
o	Type IV pili
o	Cup fimbriae in P. aeruginosa.
71
Q

Controlling biofilms

A

Use quorum sensing
Use c-di-GMP
Use antibiotic combination therapies
Use implants which target antimicrobial surfaces.

72
Q

Restricted penetration in biofilms

A

DNA is positive, shields from AMPs and cationic antimicrobials. Mucoidy.

73
Q

Different physiological activity in biofilms.

A

Inner part of biofilm has low metabolic activity.

74
Q

Inducible antimicrobial resistance factors in biofilms - P. aeruginosa

A

MexAB-OprM efflux pump. Pmr operon mediated LPS modification.

75
Q

Identifying quorum inhibitors.

A

 Chemical biology approaches
 Structural based virtual screening
 Isolated from food sources

76
Q

c-di-GMP inhibitors

A

o Genetic manipulation suggests that this would work.

o Novel benzimidazole agent.

77
Q

Theory behind antibiotic combination therapies

A

o Targetting different subpopulations with different metabolic activity.

78
Q

Extracellular survival general plan

A
  • Avoid complement
  • Avoid recognition
  • Avoid effector arm
79
Q

Complement initiation

A

Classical, MB-lectin and alternative

80
Q

Complement initiation - classical

A
  • Antigen:antibody

* C1q, C1r, C1s, C4 and C2

81
Q

Complement initiation - MB-lectin.

A
  • Mannose binding lectin binds mannose on surfaces

* MBL, MASP-1, MASP-2, C4, C2.

82
Q

Complement initiation - alternative pathway.

A
  • Pathogen surfaces

* C3, Factor B, Factor D.

83
Q

C3 convertase

84
Q

C3 convertase effects

A

Cleaves C3 to give C3b, a C5 convertase important in MAC.
Binds complement receptors on macrophages
• Opsonise pathogens,
• Remove immune complexes.

85
Q

Blocking C3 convertase activity

A

 Blocked by Factor H and factor I.
Pathogens acquire regulators for resistance
• Factor H, FHL1, C4BP, CFHR.

86
Q

IgA proportion of Ig in serum

A

15-20% total serum

87
Q

IgA found in

A

mucus, saliva, milk

88
Q

IgA structure

A

2 identical Fab regions bound by hinge to Fc, binds host cells
In secretions is dimerised by J chain and secretory component S-IgA1

89
Q

IgA targetted by bacteria

A

Proteases. Zinc metalloproteases or serine proteases.

90
Q

Staph aureus avoiding complement

A

Avoid initiation
Bind C3 to avoid conversion to C3b
Acquire complement regulators.

91
Q

Staph aureus - binding C3

92
Q

Staph aureus avoiding initiation of complement

A

Aureolysin, or acquiring plasminogen from the host.

93
Q

S. pyogenes anti-complement

A

GAPDH to bind C5a.

SIC.

94
Q

Strep IgA protease.

A

Specific for IgA1
Cleaved fragments compete with uncleaved.
Zinc metalloprotease

95
Q

Proteases with specificity for IgA1

A

Cleaving at specific sites between Pro-Ser or Pro-Thr present in longer more flexible hinge region.
Fragments compete with IgA for binding to pathogens.

96
Q

Zinc metalloproteases - structure

A

signal sequence, anchoring domain, autoproteolytic cleavage sites, and protease domain

97
Q

Zinc metalloproteases - synthesis.

A

 Synthesised, inserted into membrane, autoproteolytically cleaved, but protease domain remains associated with bacterial surface as non-covalently binds N-terminal domain.

98
Q

B burgdorferi anti-complement

A

o CD59-like protein

o CRASP-1

99
Q

Neisseria - avoiding innate.

A

Capsule to avoid phagocytosis
Mimic or recruit host proteins to avoid complement.
Divert complement using blebs.

100
Q

Neisseria importance of capsule

A

Major virulence determinant. meningococci rely on this partially for serum resistance and virulence. Unencapsulated are sensitive to killing by serum, but do not cause disease in complement deficient (encapsulated do); probably due to anti-phagocytic properties.

101
Q

Importance of complement in Neisseia killing

A

o Deficiency (acquired or inherited) in complement leads to susceptibility to disease. (seminal study by Goldschneider showed importance of complement)

102
Q

Neisseria avoiding complement - mimicing host proteins.

A

Avoid recognition - Group B capsule repeating unit is identical to NCAM, a host adhesion protein.
Carbs on LOS mimic host carbs.
C4BP inactivates C3 convertase.

103
Q

Neisseria acquiring host proteins

A

Factor H

Vitronectin

104
Q

Neisseria acquiring factor H - proteins.

A

Gonococci: porin
meningococci: Factor H binding protein, Neisseria surface protein A ad sialylated lipo-oligosaccharide. Not PorB3 despite homology to porin.

105
Q

Neisseria acquiring factor H; tropism.

A

Species specific complement evasion. Human pathogens’ factor H binding proteins –> only binds chimpanzee factor H poorly, and rhesus macaque factor H barely detectably.

106
Q

Neisseria acquiring factor H; convergent evolution.

A

• Factor H binding proteins in different Neisseria bind the same domains 6&7 as each other, which is the same as that used by host cell surface molecules – convergent evolution.

107
Q

Role of factor H

A

H is the co-factor for factor I medicated cleavage of C3b to iC3b. Factor H also causes decay acceleration.

108
Q

Gonococci factor H binding.

A

Uses porin.
Also uses sialylated LOS. Does not have serum resistance if LOS not sialylated for some strains. Decreases binding of antibodies and increases binding of fH.

109
Q

Neisseria acquiring host proteins: vitronectin.

A

Inhibits the terminal complement complex at various stages; occupies metastable membrane binding site of nascent MAC. Can also block C9 polymerisation.

110
Q

Neisseria: decreasing recognition

A

Antigenic variation –> phase variation and DNA sequence variation.

111
Q

Phase variation

A

Switches on or off due to strand slippage at polyG or poly C tracts.
Genes, promoters, genes involved in biosynthesis, glycosyltransferases for LOS synthesis.

112
Q

Phase variation: polyG strand slippage.

A

Variation in PilC and IgtA.

113
Q

Phase variation: polyC strand slippage

A

Opa/Opc,

SiaD

114
Q

Neisseria: DNA sequence variation.

A

PilE silent genes being copied

Pilin on/off

115
Q

Neisseria PilE

A

Major pilin protein.
Silent genes lack a promoter, ribosome binding site and the first 35-43 codons.
Parts of these are copied into the PilE locus.
Unusual type of homologous recombination.

116
Q

Neisseria pilin DNA variation - ways to switch off pilin synthesis.

A

Truncation - Some silent genes code stop codons in coding regions. Recombination.
Non-assembly - If PilC (tip adhesin) switched off in both alleles in gonococcus, then pilus is not assembled. Phase variation.
Non-export - Some variant sequences have poor interactions with the machinery, and do not form pilins. Recombination.
Non-export - Formation of L-pilin which is not exported across OM leads to phase variation by aberrent recombination.

117
Q

Neisseria PilE

A

Silent genes lack a promoter, ribosome binding site and the first 35-43 codons.
Parts of these are copied into the PilE locus.
Recombination tracts are bordered by regions of microhomology.

118
Q

Neisseria pilin DNA variation.

A

Some silent genes code stop codons in coding regions. If PilC switched off in both alleles in gonococcus, then pilus is not assembled.
Some variant sequences have poor interactions with the machinery, and do not form pilins.

119
Q

Neisseria avoiding the effector arm of the adaptive immune response.

A

Cleave IgA

Avoid phagocytosis with a slimy capsule.

120
Q

Yersinia anti-complement activity.

A

 YadA = fibrillar surface structure attachment to mammalian cells and ECM. Stalk does Factor H binding and serum resistance.

121
Q

Yersinia adhesins

A

YadA
Inv
Ail

122
Q

YadA

A

fibrillar surface structure attachment to mammalian cells and ECM.
Important for initial attachment before T3SS inserted into host membrane.

123
Q

YadA structure

A

o Head performs neutrophil, collagen and autoagglutination.
o Stalk does Factor H binding and serum resistance.

124
Q

Inv

A

promotes uptake into host cells

125
Q

YadA and Inv

A

Both autotransporters.

126
Q

T3SS for YOPS in yersinia

A

Similar to flagella synthesis. Basal body, needle, rings in membranes, ring for insertion into host membrane.

127
Q

Yersinia T3SS needle

A

Needle made of YscF. Plugged by LcrV.

Measured using molecular ruler.

128
Q

Yersinia subverting macrophage function

A

Disrupt host cytoskeleton

Trigger macrophage apoptosis.

129
Q

Yersinia subverting macrophage function - disrupting host cytoskeleton.

A

Target Rho GTPases

Use YopH.

130
Q

Yersinia subverting macrophage function - Targetting Rho GTPases

A

o GAP mimic YopE
o GDI mimic YopO
o Cysteine protease YopT

131
Q

YopH

A

• YopH is a tyrosine phosphatase that interferes with host cell adhesion and signal transduction.
Prevents cell survival by inhibiting PI3K-akt signaling.

132
Q

Yersinia subverting macrophage function - triggering apoptosis.

A

YopJ and Yop H

133
Q

YopJ

A

• YopJ inhibits MAPK and NFkB signaling, simulating apoptosis.

134
Q

Autotransporters in OM. Crossing IM.

135
Q

Autotransporters in OM. In periplasm

A
  • Chaperones like Skp and SurA bind passenger and B domain and DegP binds passenger domain.
  • DegP = quality control mechanism.
136
Q

Autotransporters in OM. Insertion into OM

A
  • Targeted to B-barrel assembly machinery, Bam complex in OM. Inserts barrels into OM.
  • Barrel then autotransports passenger domain extracellularly.
137
Q

Capsules - protein

A

Bacillus anthracis. But usually capsules are carbohydrate.

138
Q

Purpose of capsules

A

Protect from desiccation, act as adhesin, evasion of host defences.

139
Q

LPS

A

Attached to OM of Gram -ive.

140
Q

Difference between antigenic and phase variation.

A

Antigenic variation promotes change of surface antigens at a higher rate than normal.
Phase variation switches structures or proteins on or off.

141
Q

Neisseria surface components

A

Capsule, type IV pili, Opa (gonococcus) or Opc (meningococcus), lipo-oligosaccharide.

142
Q

Neisseria-host interactions

A

Pili for initial adhesion. Opa/Opc for tight adherence and cell tropism, invasion and transcytosis. Capsule prevents phagocytosis. Sialic acid element of capsule helps evasion.

143
Q

Opa/Opc function

A

Neisseria. Tight adherence and cell tropism. Binds CD66. Meningococci have 3-4 opc genes, gonococci have 11 opa genes.

144
Q

SiaD function

A

Neisseria sialylation enzyme for the capsule.

145
Q

LgtA function

A

ligates lipo-oligosaccharide terminal sugars.

146
Q

PilS

A

Partial gene copies of PilE (Neisseria). Silent. There are 17.

147
Q

Neisseria homologous recombination in pilin genes.

A

Recombination tracts, or mini-cassettes, are bordered by regions of microhomology. Requires only short region of homology.
Naturally transformable - can use DNA from environment.

148
Q

Mini-cassettes in Neisseria

A

Sequence variability doesn’t perfectly match mini-cassettes; what is important is the functional conservation. There is a hypervariable area, mc2.

149
Q

Neisseria: variation in pilin

A

Antigenic variation by homologous recombination.

Formation of L-pilin which is not exported across OM leads to phase variation by aberrent recombination.

150
Q

Neisseria - formation of S pilin

A

Signal sequence is normally removed before pilus assembly, but after aberrent recombination, it can be removed at +40, leading to soluble secreted S-pilin, which acts as a molecular decoy.

151
Q

PilC polyG slippage

A

10 or 13 Gs = in frame

11 or 12 Gs = out of frame.

152
Q

When does polyG slippage occur for phase variation in Neisseria?

A

During DNA repair.

During replication.

153
Q

How does polyG strand slippage occur in DNA repair?

A

Single strand break –> exonuclease degradation. Mispairing during DNA synthesis –> altered number of repeat units.

154
Q

How does polyG strand slippage occur in DNA replication?

A

Parent strand loops out and repair process removes looped-out repeat. Daughter strand is shorter.
Lagging strand can slip back one repeat during synthesis. Daughter strand is longer.

155
Q

Opa/Opc variation

A

Repeat sequence CTTCT. - Opc ON/OFF
In frame = multiples of 3. Out of frame = not multiples of 3 (2, 4, 5, 7 etc).
Opc polyC tract can act as a dimmer switch.Alters distance between -35 and -10 sequences, hence sigma factor binding and expression. 10 residues is off, 14 is on, and 12 is on with high expression.

156
Q

Ways to apply phase variation (Neisseria).

A

ON/OFF.

Dimmer switch.

157
Q

Ways to apply recombination (Neisseria)

A

Variation.
ON/OFF - truncation, non-export.
Secretion of molecular decoy.

158
Q

Ways to cause variation

A 
Antigenic variation (Neisseria)
Phase variation by strand slippage (Neisseria).
Phase variation by invertible elements (E. coli and salmonella)
159
Q

Phase variation by invertible elements

A

E. coli and salmonella, in fimbriae and flagella. Recombination sites within the promoter are in opposite orientation leading to switching of gene expression.

160
Q

Ways to cause variation

A 
Antigenic variation (Neisseria) - homologous recombination. 
Antigenic variation - gene conversion (Borrelia).
Antigenic variation - segmental recombination (Borrelia).
Phase variation by strand slippage (Neisseria).
Phase variation by invertible elements (E. coli and salmonella)
Phase variation by BvgAS two component system.
161
Q

Phase variation by invertible elements

A

E. coli and salmonella, in fimbriae and flagella. Recombination sites within the promoter are in opposite orientation leading to switching of gene expression. Temperature dependence

162
Q

Phase variation by invertible elements temperature dependence

A

FimB and FimE recombinases are used. FimB switches either way, with higher activity at 37-40 degrees. FimE favours the OFF switch and is more active at lower termperatures, so fimbriae are switched on in hosts.

163
Q

Segmental recombination B. burgdorferi.

A

In vlsE. 6 variable regions continuously recombine in surface lipoprotein VlsE in mammalian infections.

164
Q

Gene conversion in Borrelia.

A

Structure = upstream homology sequence, coding region, variable gap and downstream homology sequence. Homology sequences contribute to expression switching, with order being determined by homology in UHS, and distance between coding sequence and DHS.

165
Q

YopE

A

GAP activity decreases Rho activity. So YopE decreases polymerisation of actin cytoskeleton and hence decreases uptake.

166
Q

YopO

A

Specifically targets Rac. Prevents Rac activation, although in vitro it can act on both Rac and Rho.

ZZPathology undergraduate year 3, first term. (15 decks)

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