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Bacteriology > Bacterial Pathogenesis > Flashcards

Bacterial Pathogenesis Flashcards

1
Q

Define the terms:

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

Lecture 3, slide 3

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2
Q

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

A

Lecture 3, slide 5

-outcome does not only depend on the bacterium

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3
Q

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

A

-Lecture 3, slide 6

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4
Q

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

A
  • Lecture 3, slide 12-13

- pathogenicity islands: clusters of virulence genes

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5
Q

What is the criteria for a pathogen?

A

Lecture 3, slide 15

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6
Q

What are some potential routes/sources of infection?

A

Lecture 3, slide 17

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7
Q

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

A

Lecture 3, slide 20-21

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8
Q

What is the structure and role of cholera toxin?

A

Lecture 3, slide 22

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9
Q

How does Vibrio cholerae cause diarrhoea?

A

Lecture 3, slide 23-24

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10
Q

How did Vibrio cholerae acquire its toxin?

A

Lecture 3, slide 27

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11
Q

What is Clostridium difficle? What disease does it cause?

A

Lecture 3, slide 28-29

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12
Q

What are the two toxins Clostridium difficle releases?

A

Lecture 3, slide 30

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13
Q

How do Clostridium difficle toxins cause disease?

A

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
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14
Q

How does Staphylococcus aureus confer tropism?

A

Lecture 3, slides 33-34, 37

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15
Q

How does Staphylococcus aureus evade the immune system?

A

Lecture 3, slide 34, 38

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16
Q

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

A

Lecture 3, slide 39

-correction: exfoliation toxin is not a superantigen

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17
Q

What are superantigens?

A

Lecture 3, slide 40

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18
Q

What Gram type of Neisseria meningitidis?

A

Gram-negative

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19
Q

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

A

Lecture 3, slide 43-44

20
Q

How does Neisseria meningitidis evade complement-mediated lysis?

A

Lecture 3, slides 42, 45-46

  • factor H is a negative regulator of complement, so they recruit it to prevent complement
  • capsule
21
Q

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

A

Lecture 3, slide 47

22
Q

Give some examples of intracellular bacteria.

A

Lecture 4, slide 2

23
Q

Name three methods of immune evasion for intracellular pathogens.

A

Lecture 4, slide 5

24
Q

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

A

Lecture 4, slide 6-7

25
Q

What is the pathogenesis of Shigella and Salmonella?

A

Lecture 4, slide 8, 13

26
Q

How does Shilgella enter epithelial cells?

A

Lecture 4, slides 11-12

27
Q

What are the roles of Salmonella’s T3SS

A

Lecture 4, slides 14

28
Q

What is the zipper mechanism of bacterial entry?

A

Lecture 4, slide 17

29
Q

What are core genes, accessory genes and the pangenome?

A

Lecture 4, slide 21

30
Q

What are the three main mechanisms of horizontal gene transfer?

A

Lecture 4, slide 22

-there is evidence that our own microbiota is a major source of antibiotic-resistant genes in pathogens

31
Q

What is the process of conjugation?

A

Lecture 4, slide 23

32
Q

What is the process of transformation?

A

Lecture 4, slide 24

33
Q

What is the process of transduction?

A

Lecture 4, slide 25

34
Q

How do bacteria prevent horizontal gene transfer?

A

Lecture 4, slide 27-28

35
Q

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

A

Lecture 4, slide 30

36
Q

What is phase variation?

A

Lecture 4, slide 31

37
Q

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

A

Lecture 4, slide 32-33

38
Q

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

A

Lecture 4, slide 34-35

-OMP: outer membrane protein

39
Q

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

A

Lecture 4, slide 36

-OMP: outer membrane protein

40
Q

What is localised hypermutation?

A

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

41
Q

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

A

Lecture 4, slide 38

-restriction/modification systems are products of/encoded by repeat-associated genes

42
Q

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

A

Lecture 4, slide 39, 41

43
Q

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

A

Lecture 4, slide 43-44

-quorum sensing regulates virulence gene expression in many bacterial pathogens.

44
Q

What is quorum sensing?

A

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

45
Q

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

A

Lecture 4, slide 47

46
Q

What is the two component system?

A

Lecture 3, slide 48

Bacteriology (3 decks)

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