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Pseudomonas aeruginosa > Chronic Infection > Flashcards

Chronic Infection Flashcards

1
Q

P.aeruginosa can form biofilms where?

A

On abiotic surfaces or on biotic surfaces

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2
Q

What regulatory switches control biofilm production?

A

Gac/Rsm cascade

c-di-GMP signalling- high c-di-GMP

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3
Q

What are the features of chronic infection?

A 
T6SS highly active
Sessile
T3SS not very active
Exopolysaccharide production
Not many virulence factors being produced
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4
Q

What is required for biofilm formation?

A

Flagella, Type IV pili, cup fimbriae and adhesins

Production of exopolysaccharide

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5
Q

What is needed for biofilm attachment to surfaces?

A

Flagella, type IV pili, cup fimbriae, adhesins

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6
Q

What exopolysaccharide is produced in the mucoid biofilm phenotype?

A

Alginate

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7
Q

What exopolysaccharides are produced in the non-mucoid biofilm phenotype?

A

Pel

Psl

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8
Q

What dye binds to exopolysaccharides?

A

Congo red

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9
Q

What is the process of biofilm formation?

A

1) Transport to the biotic/abiotic surface via flagella
2) Attachment to the biotic/abiotic surface via flagella, type IV pili, adhesins, cup fimbriae
3) Motility on the surface and mushroom formation via type IV pili
4) Biofilm maturation via exopolysaccharide production: Production of alginate, psl, pel, eDNA
4) Dispersal: Breaking down the exopolysaccharides and cleavage of adhesins… glycoside hydrolase and alginate lyase

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10
Q

What is needed for mushroom formation?

A

Type IV pili

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11
Q

What is needed for breaking down of the exopolysaccharide?

A

Enzymes
Alginate lysase
Glycoside hydrolase

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12
Q

What is needed to break down alginate?

A

Alginate lyase

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13
Q

What is needed to break down pel/psl?

A

Glycoside hydrolase

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14
Q

How do biofilms protect the bacteria?

A

Makes them much more antibiotic resistant as it is harder for antibiotics to penetrate the biofilm
Makes it harder for the bacteria to become phagocytosed

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15
Q

Exopolysaccharide associated with mucoidy?

A

Alginate

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16
Q

What exopolysaccharide is primarily produced by P.aeruginosa in CF patients?

A

Mucoidy biofilm phenotype- alginate

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17
Q

What is the importance of the T6SS with relation to biofilms?

A

During biofilm formation is is possible that other bacterial species may enter the biofilm and benefit from its protective environment. The T6SS is therefore beneficial in killing these cells which may compete for nutrients etc

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18
Q

How does the T6SS work?

A

There is a contractile sheath which reveals a nanotube- able to penetrate the target bacterium

19
Q

In acute infection how does the input environmental strain compare to the output strain?

A

Not many differences
There are hardly any genetic differences
There was no time for differences to be accumulated as there is no persistence

20
Q

In chronic infection how does the input environmental strain compare to the output strain?

A

There are may genetic differences
The bacteria are persisting in chronic infection and have therefore had time to evolve and develop mutations that have been selected for
They acquire pathoadaptive mutations which help them to survive in the environment

21
Q

Chronic infection is very common in?

A

CF patients

22
Q

What are the typical types of pathoadaptive mutations acquired in chronic infection?

A
  • Loss of motility
  • Increase in mucoidy
  • Loss of T3SS
  • Increase in T6SS
  • Loss of virulence effectors
  • Loss of QS
  • Increased antibiotic resistance
23
Q

What mutation leads to sessility?

A

Mutations in rpoN

24
Q

What mutation increases antibiotic resistance?

A

Mutations in muxZ

25
Q

What is MuxZ?

A

Negative regulator of an efflux pump

26
Q

How do mutations in muxZ increase antibiotic resistance?

A

MuxZ is a negative regulator of an efflux pump
Therefore, mutation in muxZ will increase the capacity of the bacteria to expel any drugs or antibiotics that enter
Increased antibiotic resistance

27
Q

What is mucA

A

Anti-sigma factor

28
Q

Mutations in mucA lead to?

A

Increased alginate production and mucoidy

29
Q

Mutations in mucA are typically?

A

Loss of function mutations

30
Q

How does a mutation in mucA increase alginate production?

A

AlgU leads to alginate production
MucA is able to sequester AlgU and reduce the amount of alginate produced
Therefore mutations in mucA increase alginate production

31
Q

What is algU?

A

Alternative sigma factor

32
Q

What do mutations in retS cause?

A

Hyperbiofilm phenotype

Increased c-di-GMP levels

33
Q

What is RetS?

A

Negative regulator of Gac/Rsm signalling

34
Q

What do mutations in lasR result in?

A

Loss of QS system

35
Q

What is LasR?

A

Transcriptional regulator

The master quorum sensing regulator

36
Q

What is rpoN?

A

Alternative sigma factor

37
Q

Summary of all the mutations?

A 
mucA loss of function
retS loss of function
rpoN mutations
mexZ mutations
lasR mutations
38
Q

Why do contingency mutations arise?

A

Mutations often have a cost involved. Contingency mutations allow the phenotype/effect of a prior mutation to be reverted

39
Q

Why might a contingency mutation for increased alginate production occur?

A

As increased alginate production is a very energy costly process

40
Q

What is the contingency mutation to the loss of function mucA?

A

Mutations in algU

41
Q

What contingency mutations are there to the retS mutation?

A

Mutations in gacA, gacS, rsmA

42
Q

How can strains evolve quickly?

A

Mutations in mutS and mutL

43
Q

What are mutS and mutL involved in?

A

They are involved in mismatch repair

44
Q

Mutations in mutL and mutS result in?

A

The incorperation of more mutations as fewer mutations are fixed/resolved

Pseudomonas aeruginosa (8 decks)

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