Transmission Routes Flashcards

1
Q

What is virulence?

A

Virulence is non-scalar (relative). It is a quantitative measure of the extent of disease.

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2
Q

How can virulence be measured?

A
  • Amount of fever caused
  • Weightloss
  • Morbidity
  • Mortality
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3
Q

How can pathogens adapt to new environments?

A

By acquiring new mutations

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4
Q

How can genetic variability be increased?

A
  • Random mutation and selection

- Horizontal gene transfer

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5
Q

Random mutation is what type of process?

A

A slow process

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6
Q

Horizontal gene transfer is what type of process?

A

A fast process

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7
Q

What are the different methods of bacterial horizontal gene transfer?

A
  • Transformation
  • Transduction
  • Conjugation
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8
Q

What is bacterial transformation?

A

Taking up genetic material from the external environment

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9
Q

What is bacterial transduction and what can it occur between?

A

Transfer of genetic material by phages

Can only occur between closely related bacteria

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10
Q

Bacterial conjugation is mediated by?

A

Pili

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11
Q

Bacterial conjugation can occur between?

A

Distantly related bacteria

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12
Q

Direct transmission is associated with what virulence?

A

Low virulence

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13
Q

Why do directly transmitted viruses become less virulent overtime?

A

Due to the transmission-mortality tradeoff

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14
Q

Examples of direct transmission and lower virulence?

A

Bacterial and viral STDs
Influenza pandemics
Myxoma virus

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15
Q

Myxoma virus was released when and where?

A

Southern Australia 1950s

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16
Q

Myxoma virus fatality rate over time?

A

Initial fatality rate of 99%
Reduced to 50%
Rabbit population gradually recovered overtime

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17
Q

Bacterial STD?

A

Chlamydia

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18
Q

Waterborne transmission is associated with what type of virulence?

A

Associated with increased virulence

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19
Q

Why can waterborne diseases be more virulent?

A

They do not rely on host motility to be spread

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20
Q

How can enteric diseases be spread?

A
  • Direct contact, human to human
  • Fecal oral
  • Waterborne
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21
Q

Cholera spreads via?

A

Fecal oral route

Waterborne

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22
Q

Cholera infectious dose?

A

10^6

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23
Q

Why is the infectious dose of cholera so high?

A

Not very resistant to the stomach acid

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24
Q

How much diarrhoea is produced by an infected individual?

A

Up to 20L of rice water stool a day

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25
Q

Rice water stool contains how many pathogens?

A

10^7 bacteria per ml

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26
Q

How does vibrio cholerae obtain mutations?

A

Horizontal gene transfer and random mutation

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27
Q

How does cholera ensure horizontal gene transfer?

A

Via the T6SS and competence, transformation

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28
Q

In the aquatic environment where can cholera be found?

A

On the exoskeleton molt of zooplankton. The exoskeleton is rich in chitin

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29
Q

On the chitinous surface the bacteria forms a?

A

Biofilm

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30
Q

What does the chitinous surface trigger?

A

It triggers the developmental programme of natural competence for genetic transformation

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31
Q

What initiates the developmental programme of natural competence?

A

TfoX regulatory protein

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32
Q

What is TfoX?

A

It is a regulatory protein

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33
Q

Competence is required for?

A

Transformation

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34
Q

What increases the availability of external DNA?

A

T6SS

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35
Q

T6SS does what?

A

Injects effectors into other bacterial cells which mediates cell lysis etc…

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36
Q

T6SS activation is controlled by the?

A

The T6SS is part of the competence regulon which is initiated by the TfoX

37
Q

What is the colonisation factor of cholera?

A

TCP

38
Q

What is TCP?

A

Toxin co-regulated protein

A hair like projection on the surface of the bacterial cell

39
Q

What is the hair like protein on the surface of the bacterial cell>

A

TCP

Toxin Co-regulated Protein

40
Q

What is the role of TCP?

A

It is a receptor of the CTX phage
It is the colonisation factor for small intestine colonisation
It is the colonisation factor required for colonisation of planktonic exoskeletons

41
Q

What carbon source does aquatic cholera use?

A

Chitin

42
Q

Cholera colonises the?

A

Small intestine

43
Q

Is cholera internal or external?

A

Non-invasive and external

44
Q

CTX toxin is encoded by the?

A

CTX phage

45
Q

CTX toxin structure?

A

AB5

46
Q

CTX toxin binds to which receptor?

A

GM1 ganglioside receptor

47
Q

When was the most recent plague outbreak?

A

Malaysia 2017

48
Q

What types of plague are there?

A

Bubonic
Pneumonic
Septicemic

49
Q

All types of plague are caused by?

A

Yersinia pestis

50
Q

Bubonic plague is spread by?

A

Arthropod fleas

51
Q

The fleas transmit the bacteria from?

A

Rats to humans

52
Q

Yersinia pestis evolved from?

A

Gut pathogen Yersinia pseudotuberculosis

53
Q

When did Yersinia pestis evolve from Yersinia pseudotuberculosis?

A

1,500 to 20,000 years ago

54
Q

Yersinia pseudotuberculosis is spread via?

A

The fecal oral route

55
Q

Is Yersinia pseudotuberculosis very virulent?

A

No

56
Q

Yersinia pseudotuberculosis is a bacterium of the?

A

Gut

57
Q

In order for Yersinia pestis to have evolved from Yersinia pseudotuberculosis?

A

It needed to acquire various mutations

58
Q

What allowed survival of Yersinia pestis in fleas?

A

pFra plasmid

59
Q

How does the pFra plasmid allow survival in fleas?

A

Yersinia murine toxin

60
Q

What does Yersinia murine toxin allow?

A

Survival in the flea midgut, resistance to antibacterial agents in the flea midgut

61
Q

What allows Yersinia pestis to form a biofilm in the flea?

A

hma gene

62
Q

Biofilm prevents the flea from?

A

Taking meals up, leads to regurgitation, the fleas starve and bite more frequently

63
Q

What encodes the T3SS in Yersinia pestis?

A

pYv plasmid

64
Q

Which plasmid encodes the T3SS?

A

pYv plasmid

65
Q

Which plasmid encodes Yersinia murine toxin?

A

pFra

66
Q

Which plasmid allows dissemination from the bite site, to the lymph nodes etc…?

A

pPst

67
Q

What does pPst encode?

A

Pla plasminogen activator

68
Q

Plasminogen activator allows the bacteria to do what?

A

Infect macrophages and reach the lymph nodes

69
Q

Which plasmids were acquired by Yersinia pestis?

A

pPst
pFra
pYv

70
Q

pYv plasmid encodes?

A

T3SS

71
Q

pFra plasmid encodes?

A

Yersinia murine toxin

72
Q

pPst plasmid encodes?

A

Pla plasminogen activator

73
Q

Why is Yersinia pestis so virulent?

A

1- Poor vector competence… need high bacteremia to infect the vector
2- Host seeking behaviour of the vector: Vector tends to stay on the host. Inducing death in the host causes the vector to move
3- Humans are not the natural host of the disease, no co-evolution over time
4- Vector density, lots of fleas present on the host so even if the host dies there is a high likelihood of transmission

74
Q

What bacteria causes anthrax?

A

Bacillus anthracis

75
Q

Spore germination occurs?

A

Within macrophages

76
Q

Where do spores form?

A

In the environment

77
Q

Why might incidence with anthrax increase?

A

Due to global warming and thawing

78
Q

What causes death by anthrax?

A

The toxins produced

79
Q

The virulence factors are encoded on?

A

Two plasmids

80
Q

What are the two plasmids of anthrax?

A

pXO1

pXO2

81
Q

pXO2 produces?

A

Capsule proteins
Forms a protective coat
Inhibits phagocytosis

82
Q

PXO1 produces?

A

The exotoxins

83
Q

What are the exotoxins?

A

Edema and lethal toxin

84
Q

What does edema toxin do?

A

Causes large swellings of pus and blood to form

85
Q

What does lethal toxin do?

A

Leads to host death

86
Q

How do the two exotoxins facilitate spread of anthrax?

A

The edema toxin causes infected large swellings of pus and blood to form. The lethal toxin causes septic shock and results in death. The edemas rupture to release the bacteria into the environment.

87
Q

The two exotoxins are encoded by?

A

pXO1

88
Q

What contributes to the high virulence of anthrax?

A

Environmentally transmitted by sit and wait transmission. This increases its virulence as it does not need to rely on the host motility for transmission. Relies on the motility of the uninfected and its ability to form spores in the environment.