Pandemics Flashcards

(40 cards)

1
Q

What type of genetic change causes a pnademic

A

large shift in the influenza virus (genetic shift).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

WHat animals are involved in a pandemic and how?

A

Swine mixes viruses from humans, avians and swine, (all three can infect the swine.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Once in the popualtion, what happens to the pandemic virus

A

gwenetic drift in order to change enough to infect and spread. Becomes less pathogenic over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What makes a pandemic strain of influenza? (6)

A
  1. Little prior immunity in the population
  2. High replication of the virus
  3. Efficient infection of the upper and lower respiratory tract
  4. Wide scale destruction of epithelial cells in the respiratory tract
  5. Cytokine storm leading to more damage to the lungs and lots of infiltrating cells
  6. Good conditions for bacterial growth (dead cells and edema provide bacterial nutrients)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What linkage does a normal human viral HA bind on a human cell?

A

sialic acid α2-6 linkages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What linkage does a pandemic viral HA bind on a human cell

A

both the α2-3 linkage and α2-6 linkage of sialic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What linkages are found in the LRT? URT?

A

α2-3 linkage of sialic acid is found in the LRT

α2-6 linkage in URT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What needs to happen for an influenza virus to be Infectious?

A

viral HA needs to be cleaved by cellular proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How did the 1918 virus make itself more infectious through mutations

A

allowed more proteases to cleave the HA

allowed for more efficient cleavage of HA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What role does low glycosylation of HA have on a strain’s pathogenesis

A

low glycosylation = less binding by antimicrobials (like surfactant protein D)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What role does high glycosylation of HA have on a strain’s pathogenesis

A

high glycosylation = masks HA from neutralizing antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Did the 1918 flu have low or high glycosylation

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is, and what does PB1-F2 do? (3)

A

it is a vrulence factor that

  1. cuases CD8 and alveolar macrophage apoptosis
  2. inflammatory increase (cytokine storm)
  3. Increases infiltrates of lung airways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Did 1918 and 2009 have PB1-F2

A

only 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What two general things made the 1918 starin so virulent

A

1918 was able to

1. replicate very efficiently-produce high levels of virus 2. infect both the upper and lower respiratory tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

why is URT and LRT infection important to a virus

A
URT = efficient spread
LRT = destroys epithelial cells to allow secondary bacterial infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does HPAI, LPAI mean?

A

High/Low Pathogenic Avian Influenza- based on ability to kill chickens- has nothing to do with humans

18
Q

What is the mortality rate of H5N1 avian flu

A

53% case fatality rate

19
Q

Is H5N1 HPAI or LPAI

20
Q

What is case fatality rate of H7N9

21
Q

is H7N9 HPAI or LPAI

A

LPAI- doesn’t cuase a lot of death in birds but does in humans

22
Q

What two mutations allow avian influenza to be transmissible from human to human

A
  1. avian NA needs to be able to cleave the alpha 2-6 sialic acid linkage
  2. PB2-polymerase needs to replicate better at colder temps (birds have higher body temps than humans
23
Q

MERS Case fatality rate

24
Q

SARS cFR

25
What population had the highest rate of morbidity with SARS
Older people died at a much higher rate
26
what are the complications arising with SARS infx (4)
1. 20% Diarrhea, 2. abnormal liver function (70-90%), 3. Lymphopenia 70-95% (reduction in CD4 and CD8 T cells) 4. Severe Respiratory Distress (20-30% require intensive care and ventilation)
27
What animal did the SARS virus originate
Infected animals at a Chinese Wet Market: Palm Civets, Raccoon dogs
28
How is SARS tranmistted (2)
Mostly took prolonged close contact and spread respiratory droplets. Some super spreaders who aerosolized (high virus titer)
29
what measure prevents the spread of SARS
N95 respirators
30
What are potential aerosolizers for the virus? (6)
``` Cough-generating procedures Bronchoscopy Sputum induction Intubation and extubation Cardiopulmonary resuscitation Open suctioning of airways ```
31
Transmission of MERS (3)
droplet, contact (vomit, feces, urine), Airborne
32
What complications are there with MERS
ARDS, renal failure, multi-organ failure
33
What population most infected with MERS.
Most infections in adults median age 50,
34
What population most hospitalized with MERS
hospitalizations mostly with people who have chronic comorbidities
35
How is MERS transmitted (3)
bats, camels, super spreading events in health care setting.
36
what animals can be involved in spread of Nipah
pigs, bats, horses,
37
WHat two things diseases does Nipah cause
Causes encephalitis, and sometimes respiratory symptoms
38
Case fatality rate of Nipah
74% CFR
39
What is the unique vector of transmission in Nipah
Bats spread-raw date palm sap (palm wine), to pigs, 50% cases person to person spread
40
MERS: stands for, is what family
Middle East Resp Syndrome, CoV