Transmission Routes Flashcards

(88 cards)

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
Rice water stool contains how many pathogens?
10^7 bacteria per ml
26
How does vibrio cholerae obtain mutations?
Horizontal gene transfer and random mutation
27
How does cholera ensure horizontal gene transfer?
Via the T6SS and competence, transformation
28
In the aquatic environment where can cholera be found?
On the exoskeleton molt of zooplankton. The exoskeleton is rich in chitin
29
On the chitinous surface the bacteria forms a?
Biofilm
30
What does the chitinous surface trigger?
It triggers the developmental programme of natural competence for genetic transformation
31
What initiates the developmental programme of natural competence?
TfoX regulatory protein
32
What is TfoX?
It is a regulatory protein
33
Competence is required for?
Transformation
34
What increases the availability of external DNA?
T6SS
35
T6SS does what?
Injects effectors into other bacterial cells which mediates cell lysis etc...
36
T6SS activation is controlled by the?
The T6SS is part of the competence regulon which is initiated by the TfoX
37
What is the colonisation factor of cholera?
TCP
38
What is TCP?
Toxin co-regulated protein | A hair like projection on the surface of the bacterial cell
39
What is the hair like protein on the surface of the bacterial cell>
TCP | Toxin Co-regulated Protein
40
What is the role of TCP?
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
What carbon source does aquatic cholera use?
Chitin
42
Cholera colonises the?
Small intestine
43
Is cholera internal or external?
Non-invasive and external
44
CTX toxin is encoded by the?
CTX phage
45
CTX toxin structure?
AB5
46
CTX toxin binds to which receptor?
GM1 ganglioside receptor
47
When was the most recent plague outbreak?
Malaysia 2017
48
What types of plague are there?
Bubonic Pneumonic Septicemic
49
All types of plague are caused by?
Yersinia pestis
50
Bubonic plague is spread by?
Arthropod fleas
51
The fleas transmit the bacteria from?
Rats to humans
52
Yersinia pestis evolved from?
Gut pathogen Yersinia pseudotuberculosis
53
When did Yersinia pestis evolve from Yersinia pseudotuberculosis?
1,500 to 20,000 years ago
54
Yersinia pseudotuberculosis is spread via?
The fecal oral route
55
Is Yersinia pseudotuberculosis very virulent?
No
56
Yersinia pseudotuberculosis is a bacterium of the?
Gut
57
In order for Yersinia pestis to have evolved from Yersinia pseudotuberculosis?
It needed to acquire various mutations
58
What allowed survival of Yersinia pestis in fleas?
pFra plasmid
59
How does the pFra plasmid allow survival in fleas?
Yersinia murine toxin
60
What does Yersinia murine toxin allow?
Survival in the flea midgut, resistance to antibacterial agents in the flea midgut
61
What allows Yersinia pestis to form a biofilm in the flea?
hma gene
62
Biofilm prevents the flea from?
Taking meals up, leads to regurgitation, the fleas starve and bite more frequently
63
What encodes the T3SS in Yersinia pestis?
pYv plasmid
64
Which plasmid encodes the T3SS?
pYv plasmid
65
Which plasmid encodes Yersinia murine toxin?
pFra
66
Which plasmid allows dissemination from the bite site, to the lymph nodes etc...?
pPst
67
What does pPst encode?
Pla plasminogen activator
68
Plasminogen activator allows the bacteria to do what?
Infect macrophages and reach the lymph nodes
69
Which plasmids were acquired by Yersinia pestis?
pPst pFra pYv
70
pYv plasmid encodes?
T3SS
71
pFra plasmid encodes?
Yersinia murine toxin
72
pPst plasmid encodes?
Pla plasminogen activator
73
Why is Yersinia pestis so virulent?
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
What bacteria causes anthrax?
Bacillus anthracis
75
Spore germination occurs?
Within macrophages
76
Where do spores form?
In the environment
77
Why might incidence with anthrax increase?
Due to global warming and thawing
78
What causes death by anthrax?
The toxins produced
79
The virulence factors are encoded on?
Two plasmids
80
What are the two plasmids of anthrax?
pXO1 | pXO2
81
pXO2 produces?
Capsule proteins Forms a protective coat Inhibits phagocytosis
82
PXO1 produces?
The exotoxins
83
What are the exotoxins?
Edema and lethal toxin
84
What does edema toxin do?
Causes large swellings of pus and blood to form
85
What does lethal toxin do?
Leads to host death
86
How do the two exotoxins facilitate spread of anthrax?
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
The two exotoxins are encoded by?
pXO1
88
What contributes to the high virulence of anthrax?
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.