Bacterial Survival Mechanisms

Question 1

Outline using specific examples how Type 3 secretion systems play a role in pathology.

quiz

Answer 1

-Shigella spp or Yersinia pestis
-Virulence plasmids encoding genes necessary for the Type 3 secretion system machinery.
-Expression of these genes are conditional and in response to the environment e.g. temperature, osmolarity, interaction with the host.
-Gene expression changes then result in the production of genes and proteins which result in the assembly of T3SS.
-This is also matched by the production of specific effectors which are able to cause cellular damage. (Here the answer should reflect the specific example and relevant host-pathogen interactions)
-Can you think of more examples?

Question 2

How does the host distinguish between a commensal and a pathogen? How can a commensal become a pathogen?

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Answer 2

-Refer to the example of the commensal and pathogenic EHEC strains
-Gene acquisition of mobile genetic elements facilitate the transfer of resistance. In the case of E. coli, this can occur as a result of the acquisition of the lambdoid phages carrying the Shigatoxin genes.
-Can you think of more examples?

Question 3

Describe how secretion systems can facilitate host adaptation?

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Answer 3

-Bordetella pertussis adaptation with diversity in secretion systems
-Facilitate commensal and pathogen lifestyle as in E. coli.
-Can you identify any further examples in the literature?

Question 4

How do toxins cause pathology?

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Answer 4

-Multiple detailed examples provided within the lecture e.g. Vibrio cholera, Shigella spp. and Yersinia pestis.
-What triggers toxin release from any of these pathogens?
-When toxin is released, how is it taken up by the cell?
-How does this uptake, interact with the immune response to cause pathology?

Question 5

How do Type 3 secretion systems play a role in pathology?

Answer 5

• Can span multiple membranes (important for toxin release)
• Dampen host release of pro-inflammatory cytokines
• proliferates intraphagosomally
• releases toxins/ effectors into host
• Avoid immune response (altering LPS structure and effector release via T3SS)

Question 6

Do commensals harbour virulence factors? Eg. Toxin production, Type 3 secretion systems

Answer 6

No they dont. For example, some E. coli do not have T3SS or produce toxins and these bacteria do NOT cause gastrointestional damage as opposed to other E. coli that have these features. This shows that genetic variation is a key driver in pathogenesis

Question 7

Describe how secretion systems can facilitate host adaptation?

Answer 7

• T3SS can downregulate host immune response genes
• Cholera toxin allows survival in macrophage by limiting effector mechanisms

They may change depending on the host. For example, whooping cough (Bordetella pertussis) is found in sheep and humans. Except the T6SS is lost in sheep and also does NOT work in sheep cells

Question 8

How does the host distinguish between a commensal and a pathogen? How can a commensal become a pathogen?

Answer 8

Gene acquisition of mobile genetic elements facilitate the transfer of resistance.
In the case of E. coli, this can occur as a result of the acquisition of the lambdoid phages carrying the Shigatoxin genes

Question 9

How does Shigella toxin cause pathology?

Answer 9

Its production is encoded by a bacteriophage, if bacteria acquires bacteriophage then it becomes a pathogen.
Shigella spp has T3SS

Question 10

How does Vibrio cholerae play a role in pathology?

Answer 10

• TCP pillin (facilitate adhesion)
• Has enzymes (mucinase and neuroidinase) that degrade
• Releases enterotoxin

Question 11

How does Yersinia pestis cause disease?

Answer 11

• Has T3SS
• Carrys loads of different plasmids that carry virulence factors
• flea to human there is temp change, which activates virulence genes
• Has effector YopJ that induces macrophage apoptosis