Disease Modeling Flashcards

(52 cards)

1
Q

What are the arguments against studying wildlife disease?

A
  1. Disease is natural.
  2. Population control.
  3. Disease mortality is compensatory.
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2
Q

What are the arguments for studying wildlife disease?

A
  1. Economic implications.
  2. Public health issue.
  3. Human caused changes.
  4. Human actions are impairing wildlife habitat repair.
  5. Toll of disease has undermined conservation efforts.
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3
Q

What is the triangulation approach?

A
  1. Questions.
  2. Field research.
  3. Laboratory investigations.
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4
Q

Why rely on modeling?

A
  1. Different hosts play different roles.
  2. It is never just one pathogen impacting the host.
  3. Biology of the host and biology of the pathogen impact this pathogen’s pattern in the host.
  4. Allows for an analytical approach to complex systems.
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5
Q

What are the reasons we do disease modeling?

A
  1. Better understanding of how disease systems work.
  2. Prioritize research and data collection.
  3. Assess and quantify threats posed by wildlife disease systems.
  4. Understand how the disease system will respond to management interventions.
  5. Communicate analytical insights and facilitate responsible stakeholder engagement.
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6
Q

How should mathematical models of disease be used?

A

To gain insights into how a disease is spreading through a population and what it will likely do next.
*Predictive. Not for broad generalization, no certainty.

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7
Q

What is something that you cannot control, even with the strictest parameters?

A

The behavior of a population.

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8
Q

What are the 3 engines of transmission?

A
  1. Host movements.
  2. Contact patterns.
  3. Interactions.
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9
Q

Who was the first disease modeler? What did he model?

A

a. Daniel Bernoulli.
b. The benefits of smallpox inoculation.
*Done 300 years ago, before germ theory.

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10
Q

Who was Sir Ronald Ross? What disease did he model?

A

a. A Nobel Prize winning scientist that developed the first disease dynamics model.
b. Malaria parasite lifecycle.
c. Developed a quantitative approach to explain emergence and persistence.

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11
Q

Who was Hilda Phoebe Hudson?

A

Collaborator and coauthor of Sir Ronald Ross. Accomplished mathematician.

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12
Q

What did Kermack and McKendrick develop?

A

The Kermack-McKendrick model, which describes the dynamics of disease transmission in terms of a system of differential equations.
*SIR model.

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13
Q

What did Anderson and May discover?

A

That epidemiological patterns could be observed w/o concentrating on any one infectious agent. Also incorporated the study of disease into population ecology.

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14
Q

What are the 5 compartmental models?

A
  1. SI model.
  2. SIR model.
  3. SIRV model.
  4. SEIR/SLIR.
  5. SLIV.
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15
Q

What is the basic rules of compartmentalized models?

A
  1. Each category is mutually exclusive.
  2. Closed population (No modification of the population size through birth, death, or disease).
  3. Mixing in the pop. is homogenous.
  4. Infection does not equal mortality.
  5. Infected hosts are immediately infectious.
  6. Recovered individuals are immune for life.
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16
Q

What two compartments does the SI model involve?

A
  1. Susceptible.
  2. Infected/Infectious.
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17
Q

What three compartments does the SIR model involve?

A
  1. Susceptible.
    B
  2. Infected/Infectious.
    Y
  3. Recovered.
    *N= S+I+R.
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18
Q

What four compartments does the
SIRV model involve?

A
  1. Susceptible.
  2. Vaccinated.
  3. Infected/Infectious.
  4. Recovered.
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19
Q

What four compartments does the SEIR/SLIR model involve?

A
  1. Susceptible.
  2. Exposed/Latent.
  3. Infected.
  4. Recovered.
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20
Q

What four compartments does the
SLIV model involve?

A
  1. Susceptible.
  2. Latent
  3. Infected.
  4. Vaccinated.
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21
Q

What does B stand for in the SIR model?

A

Average rate at which an infected individual can infect a susceptible individual. Transmission coefficient.
*Contact rate *Probability of transmission given a contact.

22
Q

What does Y stand for in the SIR model?

A

Average rate at which an infected individual recovers. Recovery rate.
*1/Infectious period

23
Q

How is the infectious period calculated using the Y value?

24
Q

What is the SIR model used for?

A

Understanding, interpreting, and forecasting a disease and how it is interacting in a population. Helps with decision making and selecting the best course of action.

25
In a population of 100, how many will be susceptible?
99. This population will progressively fall to a plateau.
26
In a population of 100, how many will be infectious?
1. This population will progressively rise to a plateau.
27
In a population of 100, how many will be recovered?
0. Progressive rise then plateau.
28
What happens in an SIR model when treatment of the disease occurs?
1. The I population spikes earlier. 2. More members of the overall population stay in S.
29
What is R0?
The average # of new infections caused by a single infected organism in a fully susceptible population. *Basic reproductive rate.
30
How is R0 calculated?
B/Y.
31
What does R0 depend on other than constants?
1. Population behavior (Solitary or Gregarious?). 2. Pathogenicity, Infectivity of pathogen.
32
What is R0 a metric of?
Potential transmissibility of an infectious agent.
33
What is R0 not a measure of?
Virulence or pathogenicity, just how many cases to expect.
34
What is Reff?
The avg. # of new infections caused by a single infected individual at a time (t) in a partially infected population.
35
How is Reff calculated?
R0*(S/N).
36
Force of infection(FOI)?
Per capita rate at which susceptible individuals get infected.
37
How is FOI (lambda) determined?
Deduced from epidemiological data.
38
How is FOI (lambda) calculated?
Lambda = B*(I/A).
39
What are 2 ways a pathogen can be classified based on how it interacts with a population?
1. Density dependent. 2. Frequency dependent.
40
What is the relationship between disease and population for a density dependent pathogen?
FOI increases linearly with the density of the infected in the population.
41
How is the spread of a density dependent pathogen stopped?
Decrease the density of the host population, normally through mass culling.
42
What kind of pathogens are normally density dependent?
Pathogens that require direct contact to spread, so ones that cause contagious diseases.
43
What is the relationship between disease and population for a frequency dependent pathogen?
FOI increase with infection prevalence.
44
How is the spread of a frequency dependent pathogen stopped?
Culling only the infected members of the population.
45
What kind of pathogens are normally frequency dependent?
1. Vector borne. 2. Venereal.
46
Where are most pathogens found when it comes to density or frequency dependent?
Between the two on a continuum.
47
What is the minimum requirement for an outbreak to occur?
dI/dt is > 0 to the point where at least 1 new infected individual is produced every time.
48
What is the simplified version of: dI/dt = B*S*I - YI > 0?
a. I (B*S - Y) > 0. b. BS > Y. c. S > (Y/B) or S> 1/R0.
49
How is vx threshold calculated?
1 - 1/R0.
50
What is Vc?
The critical minimum proportion of the population that must be vaccinated to prevent an outbreak.
51
Why is it impossible to have 100% vx coverage?
1. Immunocompromised members of the population. 2. Belief systems (Religious and personal). 3. Access (especially in developing countries).
52
Herd immunity?
When a collective host population achieves "collective immunity", resulting in lowering of the rate at which the disease spreads through the population.