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Infection And Immunity > Biofilms and Complement Resistance > Flashcards

Biofilms and Complement Resistance Flashcards

1
Q

name 3 types of biofilms

A
  1. Mixed communities of interdependent bacteria (synotrophism)
  2. Single species biofilms
  3. Matrix of exopolysaccharide and/or DNA
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2
Q

whats the Structure of Biofilms

A
  • Three-dimensional structure (flat or larger structures)
  • Interspersed by water channels permitting circulation of nutrients and oxygen
  • But variable environments (e.g. low oxygen in centre)
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3
Q

what is Exopolysaccharide

A 
Secreted polysaccharides
Wide array of types
Some species produce only one type and
others multiple types
Often appear as mucoid colonies on plates,
frequently slow-growing
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4
Q

give 2 examples of Exopolysaccharides

A
  • staphylococci produce a slime substance PIA or PNAG

- E. coli produces colanic acid

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5
Q

how do Biofilms work in Pathogenesis

A
  • Attachment to host tissues
  • Increase metabolic efficiency of community Obtain a high density of microorganisms
  • Gene transfer
  • Protection from antimicrobial agents (antibiotics), immune effectors and phagocytosis
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6
Q

how do Biofilms provide Resistance to Antimicrobial agents

A
  • Prevent antimicrobial agents from reaching bacterial cells
  • Nutrient-starved, slow-growing bacterial cells are resistant to many antimicrobial agents
  • Distinct biofilm-associated phenotypic state resistant to agents
  • Source of re-infection after killing of planktonic cells
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7
Q

whats the prevalence of Cystic Fibrosis?

A

affects 70,000 people/annum worldwide

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8
Q

how does infection occur in cystic fibrosis

A
  • Mutation in cystic fibrosis transmembrane conductance regulator (CFTR)
  • CFTR-defect lung leads to defects in mucociliary clearance, accumulation of mucus and poor clearance of bacteria
  • Gradual decrease in lung function further impacted by exacerbations
  • Initial colonisation by H. influenzae and Staphylococcus aureus is followed by colonisation by Pseudomonas aeruginosa
  • P. aeruginosa predictor of morbidity and mortality
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9
Q

P. aeruginosa’s role in Cystic Fibrosis

A
  1. Initial colonisation is by planktonic cells
  2. Switch to mucoid phenotype and biofilm production associated with poor clearance
  3. Exopolysaccharide production and anaerobic state associated with antibiotic resistance and inhibition of immune clearance
  4. P. aeruginosa produces large number of virulence factors many regulated by quorum- sensing control mechanisms
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10
Q

describe Formation of Biofilms by P. aeruginosa

A
  • Attachment facilitated by biofilms = flat
  • Initial attachment by flagella, Down-regulation of flagella Siderophore production Type IV pili, twitching motility = structured
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11
Q

what is the structure of the P. aeruginosa Matrix?

A
  1. Alginate – acetylated polymer of nonrepetitive monomers of beta-1,4-linked L-guluronic and D- mannuronic acids
  2. Psl – mannose-rich and galactose-rich polysaccharide
  3. Pel – glucose-rich polymer DNA and Protein
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12
Q

Functions of Psl and Pel

A

Initial attachment
Differentiation
Pellicle-type biofilms

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13
Q

explain P. aeruginosa Biofilms in CF

A
  1. Initial Colonisation of CF lung by Non-mucoid strains
  2. Repression of algU by mucABCD
  3. Progression to Mucoid strains producing alginate (frequent mutation in negative regulator mucA)
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14
Q

Functions of Alginate?

A
  1. alginate-antibodies antimicrobial compounds antibiotics
  2. adsorbed by ROS bactericidal and causing Tissue damage
  3. IFNg-activated phagocyte
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15
Q

what are Dental Biofilms?

A

+ Dental biofilms (plaque) is a prerequisite to dental caries
+ Dental biofilms consistent of a heterogenous mix of bacterial species which undergoes temporal changes
+ Metabolism of bacteria in the plaque generates acid leading to removal of the enamel and tooth decay

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16
Q

what are the Temporal Changes in Dental Plaque

A
  1. Primary Colonisers
    Bind to pellicle (proteins/glycoproteins) First streptococci (S. mutans) Later actinomycetes Synthesize gluten
  2. Bridge Bacteria Fusobacterium Aggregate with primary colonisers
  3. Late Colonisers Pathogens Porphyromonas ginivalis Bacteriodes forsythus Actinobacillus actinomycetiemcomitans Treponema denticola
17
Q

whats the structure of Dental Biofilm Matrix?

A

+ Sucrose primary substrate for Extracellular PolySaccharides (EPS)
+ Synthesized by glucosyl- > fructosyly- transferases
+ S. mutans synthesize alpha(1-3)-linked insoluble glucans, alpha(1-6)-linked soluble glucans alpha(2- 6)-linked fructans
+ Form porous/bulky biofilms facilitating fermentation and acid production as well as adherence

18
Q

name 3 Biofilms and their Implant Infections

A
  1. Endotracheal tube- P. aeruginosa=Pneumonia
  2. Joint replacement- S. epidermis=Septicaemia
  3. Prosthetic valve- S.epidermis=Endocarditis
19
Q

Biofilm Summary

A
  1.  Biofilms are structured communities that form when planktonic bacteria adhere to host surfaces and secrete exopolysaccharides and/or DNA
  2.  Biofilms facilitate attachment and immune evasion by mediating resistance to phagocytosis, immune effectors and antibiotics
  3.  Biofilms, alginate production and QS-regulated virulence factors contribute to pathogenesis of P. aeruginosa during cystic fibrosis
  4.  Dental biofilms contribute to disease by recruiting pathogenic organisms and changing the biochemical characteristics of bacterial communities
20
Q

what is Complement Resistance?

A

+ Resistance to deposition of complement effectors
+ Masking of ligands for complement activators
+ Ineffective complement-activation
+ Recruitment of complement regulators to prevent activation

21
Q

what is Moraxella catarrhalis?

A

+ M. catarrhalis is a Gram negative diplococcus
+ Frequent cause of otitis media, sinusitis and lower respiratory tract infections in people with pulmonary problems
+ Common commensal of pharynx of children + Two ubiquitous surface proteins (UspA1 and UspA2) contribute to adherence

22
Q

how do UspA Proteins Mediate Complement Resistance

A

+ UspA1 (88-kDa), UspA2 (62-kDa) and UspA2H (92-kDa)
+ UspA1 and UspA2 are 43% identical but share a 140 amino acid domain (93%)
+ UspA1/UspA2 bind C3 and C4b and prevent activation of classical and alternative pathways
+ UspA2 binds vitronectin preventing MAC activation

23
Q

how do we know M. catarrhalis is Resistant to the Classical and Alternative Complement Pathways?

A

EGTA inhibits classical pathway (C4b2b)
EDTA inhibits both pathways
Alternative (C3bBb)

24
Q

what does C4BP do?

A

Regulates Complement Activation and is recruited by UspA Proteins

25
Q

how does UspA2 Bind C3 and Inhibit Complement Activation

A

+ C3, ~1 mg/ml in serum
+ Attaches to bacterial surface in absence of Ab
+ Cleave to release C3b
+ Activates alternative complement pathway
+ C3 bound non- covalently by UspA2 preventing cleavage to C3b

26
Q

how does Vitronection Inhibits Assembly of MAC?

A

Vitronectin prevents assembly of MAC by binding to the membrane binding domain of the C5 convertase or by inhibiting polymerisation of C9 stopping pore formation

27
Q

whats the affect of UspA2 of M. catarrhalis Binding to Vitronectin

A

prevents MAC assembly imparting serum resistance to M. catarrhalis

28
Q

how does Factor H Control Complement Activation

A

C3bBb binds fH inactivating iC3b

29
Q

how does Neisseria meningitidis Recruit fH?

A
  • A 36-kDa surface-located lipoprotein, fHBP, binds fH and prevents formation of or inactivates the C3 convertase of the alternative pathway. This protein is fully active in encapsulated meningococcal cell.
30
Q

whats the action of fHBP

A
  • Mediates Serum Resistance

- fHBP and NspA have fH Binding Activity

31
Q

what are the N. meningitidis Variations in Presence of fHBP and NspA

A

+ fHBP and NspA prevent deposition of C3 and activation of AP
+ Strains exhibit variations in expression of fHBP and NspA
+ Expression of fHBP controlled by regulator, FNR, resulting in induction of fHBP expression at low oxygen levels
+ Strain-to-strain variations in fHBP due to differences in FNR expression
+ fHBP is a major vaccine candidate

32
Q

name 3 microbes and their Complement Evasion Strategies

A

N. gonorrhoeae- BP PorB + PilC - C4BP
N. meningitidis- PorA + Opc - C4BP and Vitronectin
S. pyogenes- M proteins + Fba - C4BP, fH

33
Q

Complement Resistance Summary

A
  1.  Bacteria recruit host regulatory proteins and prevent activation of the complement pathways
  2.  Bacteria encode surface proteins for binding of fH, C4BP and vitronectin
  3.  Bacterial pathogens often exhibit multiple ways of inhibiting complement activation

Infection And Immunity (16 decks)

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