Bacterial Pathogenesis

Question 1

Define the terms:

• commensal
• symbiont
• pathogen
• opportunity pathogen
• primary pathogen
• virulence
• avirulent
• infective dose

Answer 1

Lecture 3, slide 3

Question 2

What does the outcome of a bacterial infection depend on? What is the meaning of the term pathobionts?

Answer 2

Lecture 3, slide 5

-outcome does not only depend on the bacterium

Question 3

What are some pathogen and host factors that affect bacterial infection outcome?

Answer 3

-Lecture 3, slide 6

Question 4

What are the key attributes of a pathogen? What are pathogenicity islands?

Answer 4

• Lecture 3, slide 12-13

- pathogenicity islands: clusters of virulence genes

Question 5

What is the criteria for a pathogen?

Answer 5

Lecture 3, slide 15

Question 6

What are some potential routes/sources of infection?

Answer 6

Lecture 3, slide 17

Question 7

What is the structure of Vibrio cholerae? What are the symptoms and treatment for the disease it causes?

Answer 7

Lecture 3, slide 20-21

Question 8

What is the structure and role of cholera toxin?

Answer 8

Lecture 3, slide 22

Question 9

How does Vibrio cholerae cause diarrhoea?

Answer 9

Lecture 3, slide 23-24

Question 10

How did Vibrio cholerae acquire its toxin?

Answer 10

Lecture 3, slide 27

Question 11

What is Clostridium difficle? What disease does it cause?

Answer 11

Lecture 3, slide 28-29

Question 12

What are the two toxins Clostridium difficle releases?

Answer 12

Lecture 3, slide 30

Question 13

How do Clostridium difficle toxins cause disease?

Answer 13

Lecture 3, slide 31

• glycosylation of Rho-GTPases results in the inactivation of Rho proteins.
• Rho proteins are the key members in many biological processes and signalling pathways, inactivation of which leads to cytopathic and cytotoxic effects and immune responses of the host cells

Question 14

How does Staphylococcus aureus confer tropism?

Answer 14

Lecture 3, slides 33-34, 37

Question 15

How does Staphylococcus aureus evade the immune system?

Answer 15

Lecture 3, slide 34, 38

Question 16

What are some Staphyloccocus aureus exotoxins? What diseases do they cause?

Answer 16

Lecture 3, slide 39

-correction: exfoliation toxin is not a superantigen

Question 17

What are superantigens?

Answer 17

Lecture 3, slide 40

Question 18

What Gram type of Neisseria meningitidis?

Answer 18

Gram-negative

Question 19

How does its capsule allow Neisseria meningitidis to evade the immune system and vaccine development?

Answer 19

Lecture 3, slide 43-44

Question 20

How does Neisseria meningitidis evade complement-mediated lysis?

Answer 20

Lecture 3, slides 42, 45-46

• factor H is a negative regulator of complement, so they recruit it to prevent complement
• capsule

Question 21

How does Neisseria meningitidis control the expression of virulence factors depending on temperature?

Answer 21

Lecture 3, slide 47

Question 22

Give some examples of intracellular bacteria.

Answer 22

Lecture 4, slide 2

Question 23

Name three methods of immune evasion for intracellular pathogens.

Answer 23

Lecture 4, slide 5

Question 24

What is the inflammasome/its components? What is pyroptosis?

Answer 24

Lecture 4, slide 6-7

Question 25

What is the pathogenesis of Shigella and Salmonella?

Answer 25

Lecture 4, slide 8, 13

Question 26

How does Shilgella enter epithelial cells?

Answer 26

Lecture 4, slides 11-12

Question 27

What are the roles of Salmonella's T3SS

Answer 27

Lecture 4, slides 14

Question 28

What is the zipper mechanism of bacterial entry?

Answer 28

Lecture 4, slide 17

Question 29

What are core genes, accessory genes and the pangenome?

Answer 29

Lecture 4, slide 21

Question 30

What are the three main mechanisms of horizontal gene transfer?

Answer 30

Lecture 4, slide 22 | -there is evidence that our own microbiota is a major source of antibiotic-resistant genes in pathogens

Question 31

What is the process of conjugation?

Answer 31

Lecture 4, slide 23

Question 32

What is the process of transformation?

Answer 32

Lecture 4, slide 24

Question 33

What is the process of transduction?

Answer 33

Lecture 4, slide 25

Question 34

How do bacteria prevent horizontal gene transfer?

Answer 34

Lecture 4, slide 27-28

Question 35

What is intragenomic variation in bacteria? What are the different types?

Answer 35

Lecture 4, slide 30

Question 36

What is phase variation?

Answer 36

Lecture 4, slide 31

Question 37

Give Type I pili as an example of phase variation. Explain the process.

Answer 37

Lecture 4, slide 32-33

Question 38

Give PorA (a porin) as an example of phase variation. Explain the process.

Answer 38

Lecture 4, slide 34-35 | -OMP: outer membrane protein

Question 39

Give PorA (a porin) as an example of antigenic variation. Explain the process.

Answer 39

Lecture 4, slide 36 | -OMP: outer membrane protein

Question 40

What is localised hypermutation?

Answer 40

Some DNA sequences are a substrate for higher rates of mutation when compared with the rest of the genome.

Question 41

What would intragenomic mutation of restriction/modification systems lead to?

Answer 41

Lecture 4, slide 38 | -restriction/modification systems are products of/encoded by repeat-associated genes

Question 42

Give Tfp as an example of antigenic variation. Explain the process.

Answer 42

Lecture 4, slide 39, 41

Question 43

What is sense environment? What are the two causes of genetic variation/gene regulation in bacteria?

Answer 43

Lecture 4, slide 43-44 | -quorum sensing regulates virulence gene expression in many bacterial pathogens.

Question 44

What is quorum sensing?

Answer 44

Quorum sensing is the ability to detect and respond to cell population density by gene regulation.

Question 45

How does the microbiota protect us from bacteria that can sense their environment?

Answer 45

Lecture 4, slide 47

Question 46

What is the two component system?

Answer 46

Lecture 3, slide 48