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Infectious Disease > Prelim 3 > Flashcards

Prelim 3 Flashcards

1
Q

What is the main goal of epidemiology?

A

To understand the transmission of disease
this can use (genomics or genetic epidemiology
or disease modeling methods)

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2
Q

Epidemiology

A

The study of patterns and determinants in a population

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3
Q

Reservoir of disease

A

Populations (of hosts) or environments in which is pathogen is maintained and can be transmitted to the target population

  • Could include multiple host species
  • Environmental reservoirs

Hosts serving as reservoirs might suffer symptoms or be asymptomatic

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4
Q

Do reservoirs make disease management difficult

A

Reservoirs can make disease management difficult if the target population can always be reinfected from the reservoir

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5
Q

Reservoirs that are able to transmit a pathogen to a vector are called _____

A

Competent

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6
Q

“Crowd Epidemic” Disease

A
  • Acute diseases that effectively transmit between individuals and lead to lasting immunity
  • Such pathogens require large or highly interconnected populations because they will quickly “burn through” susceptible individuals (smallpox, influenza, measles, diphteriia, pertussis)
  • Pathogens may require a critical community size to be maintained
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7
Q

What are the different kinds of population structure?

A

Continuous
Patchy
Mainland island core
Metapopulation* (more representative or our population)
Nonequilibrium

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8
Q

Lyme Disease name

A

Borrelia Burgdorferi
spirochetes that swim like corkscrews

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9
Q

Lyme disease Symptoms

A

Fever, chills, headache, fatigue, muscle and joint aches, and swollen lymph nodes
- Classic erythema migrans rash (bulls-eye)

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10
Q

What is the vector for lyme disease?

A

Ticks

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11
Q

What occurred in connecticut in the 1970s

A

There was a cluster of lyme cases

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12
Q

Is Lyme old?

A

Yes, it has an ancient association with humans

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13
Q

What is the name of the tick for lyme?

A

Ixodes scapularis (black legged tick)

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14
Q

How long is the life cycle of lyme?

A

2 years

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15
Q

Explain the life cycle of the Ixodes Scapularis

A

Egg: The life cycle begins with the hatching of eggs, usually in the spring.

Larva: The larval stage hatches from the egg and feeds on a host, such as a small mammal or bird, during the summer.
(stage in which they get infected from birds and small mammals with Borrelia burgdorferi)

Nymph: After feeding, the larva molts into the nymphal stage. Nymphs are active in the late spring and early summer of the following year.
(stage in which they usually feed on both small and larger animals such as humans and transmit the disease the most)

Adult: After feeding as nymphs, they molt into adults. Adult ticks feed on larger hosts, such as deer or humans, in the fall.

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16
Q

What are the two phases of the Ixodes Scapularis life cycle when it can acquire lyme?

A

In the larva stage or the nymph

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17
Q

Are humans competent host for B. burgdorferi?

A

No

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18
Q

What is the best competent host reservioir for the bacteria?

A

White footed mice

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19
Q

What is the point of mathematical disease moelling?

A
  • For a given pathogen, what factors influence when an outbreak will occur
  • Predicting vaccination effectiveness
  • Preparedness for pandemic outbreaks
  • Pathogens with complex transmission
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20
Q

What is m in the tick mathematical model

A

The number of larval blood meals in the tick population

  • Larvae need a blood meal to molt to the nymph stage. Each larva feeds once, on one host
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21
Q

What is the equation fo predicting the number of nymphs

A

m = NBS

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22
Q

N in tick model

A

Number of hosts for larvae to feed on

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23
Q

B in tick model

A

Number of larval ticks per host (tick burden)

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24
Q

S in tick model

A

Percent of larvae that molt successfully

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25
Q

What equation should you use to determine the number of ticks with different host species

A

m =NBS assumes that there is a single host species

mi- NiBiSi models each species separately, e.g.m for host species i,

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26
Q

How to predict teh number of infected nymphs?

A

I = m C

I- infected nymphs
M - number of nymphs
C - probability of acquiring pathogen as a larvae

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27
Q

How can we predict the number of infected nymphs for different hosts?

A

Ii = miCi
each species is modeled separately

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28
Q

What is the equation for total number of infected nymphs for the entire community

A

I(t) = (sigma)miCi

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29
Q

How can we predict the prevalence of infected nypmphs?

A

To determine prevalence, we need to determine the
number of nymphs NOT infected on each host species
Ui= mi(1-Ci)
Ut = (sigma)mi(1-Ci)

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30
Q

Prevalance of infected nymphs (NIP)

A

NIP = I(t)/(It + Ut)

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31
Q

Epidemic Threshold

A
  • Mathematical term to understand if an epidemic will occur
  • Relates to the transmission rate and aspects of the population

R0=1​
When R0 is greater than 1, the disease has the potential to become endemic or to cause an epidemic, as each infected individual is, on average, infecting more than one other person, leading to sustained transmission

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32
Q

Threshold population size

A

The population size required to reach the epidemic threshold.
- Pathogens need a certain population size to be maintained and not “burn out”
- This size depends on teh pathogen, does it have reservoirs how well does it transmit
- it also depends on how interconnected populations are

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33
Q

What does the threshold population size depend on?

A
  • The pathogen itself
  • How well the pathogen transmits
  • And how interconnected the populations are
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34
Q

SIR Models

A

SIR stands for Susceptibility, Infected, Recovered.

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35
Q

What are some assumptions the SIR model makes?

A
  • The assumption for transmission (direct contact, R0)
  • Individuals are homogeneously mixed within the population (can use networks to overcome this)
  • Infected individuals can transmit immediately and remain infectious (this is not true for every pathogen
  • The assumption for disease dynamics (infected individuals recover a ta rate gamma, and alpha)
36
Q

The assumptions for transmission

A
  • Transmission occurs by DIRECT CONTACT between susceptible and infected individuals; contacts occur randomly as a function of host densities (S and I)
  • Infected individuals transmit the pathogen to susceptible individuals with the rate Beta per contact
37
Q

The Beta SI value is also known as

A

R0, or the reproductive number of a pathogen

It is defined as the number of individuals an infected individual will infect in a given period of time

38
Q

What is (S and I)

A

The host densities

39
Q

How is R0 determined?

A
  • It is determined by traits of the pathogen, but can change depending on the context
40
Q

If R0 becomes less than __, spread will stop

A

1

41
Q

Disease dynamics assumptions

A
  • Infected indivudals recover at a rate gamma
  • Infected indivudals either recover or die. Disease-induced mortaliy can be adjusted with a rate alpha. alpha is sometimes interpreted as a measure of virulence or redcution in host fitness
42
Q

What is alpha a measure of?

A
  • Disease mortality
  • Virulence
  • Reduction in host fitness
43
Q

As you increase B, the transmission rate…

A

The (S) number of susceptible people will decrease a lot while the number of recovered increases a lot. The Infected will peak for a second but then decrease when the amount of recovered increases

44
Q

When you increase recovery rate

A

The amount of susceptible people increase again. However, the amount of infected decreases significantly

45
Q

How would you lower or raise the transmission rate and recovery time to prevent a pathogen from spreading in a population?

A
  • I would ensure that the transmission rate was lower than 1
  • I would make sure that there was a fast recovery period so that people cannot be a source of infection anymore
46
Q

SEIR model

A

Add an E to the SIR model for exposed. This is for individuals who are infected but not able to spread the pathogen yet (essentially, there’s a latency period)

47
Q

What is the special value added between E and I in their SEIR model?

A

alpha in the SEIR model is not about disease mortality, instead i tis about how quickly exposed individuals become infectious (latency)

48
Q

SIRS model

A

Adding the extra S is about losing immunity once you’ve recovered, so you can become infectious once again.
This value is sigma (o looking) which is how long an individual remains resistant before being infected again

49
Q

SEIRS

A

Susceptible, (R0) Exposed, (alpha) Infected, (y) Recovered, (signma o) Susceptible again

50
Q

What happens if you add latency (alpha) between exposed and infection

A

All adding latency does is it creates a delay in the entire process, but it doesn’t change anything else

51
Q

What happens if you add a loss of resistance to the model?

A

Adding a loss of resistance increases the process again and allows for susceptibility to increase again and resistance decreases again

52
Q

Can we produce cycles with this model?

A

To produce cycles, you would need to add a loss of resistance

53
Q

*Vaccination

A

In the SIR model, these become straight lines of 80% resistant and a ver low (20%) straight line of susceptible. There is also no more infection at this stage.

54
Q

*What happens to the SEIRS model if you make it more homoegenous?

A

The suscscpetibility will increase again and the resistance will decrease

55
Q

Disease Spillover

A

refers to the transmission of a disease-causing agent (such as a pathogen or infectious agent) from animals to humans or from one species to another. In the context of zoonotic diseases, spillover occurs when a pathogen that typically infects animals crosses the species barrier and infects humans.

56
Q

Dilution Effect

A

increased biodiversity or species richness in a community is associated with a reduction in the prevalence or impact of certain infectious diseases. The basic idea is that diverse ecosystems, with a greater variety of species, can dilute the abundance or transmission efficiency of disease vectors and hosts, leading to lower disease risk.

57
Q

Is biodiversity always good?

A

No, it depends on the species that make up the community specifically. In the lizard example, getting rid of lizards ended up decreasing the nymph population but leading to more infected ticks

58
Q

humans and diseases meet at…

A

An ecotone is a transitional area or zone where two different ecosystems or biomes meet and interact

59
Q

How can land use change the behavior of wildlife and lead to disease

A

Avian flu outbreaks were positively correlated with rice paddy land areas (agricultural rice fields)

But negatively correlated with the land area of protected bird habitat wetlands

Meaning that humans are creating more outbreaks by changing the land. (there are more outbreaks because they are settling near ecotones where there are vectors and reservoirs)

60
Q

Human encroachment creates ecotones

A

*because humans are settling right in forest or something lol

Human contact complex communities of reservoirs and vector species at ecotones

61
Q

How do humans make Hapanese encephalitis virus worse?

A

Normally, the Wading birds are the reservoir host and the Culex mosquito is the vector. Humans don’t normally contact wading birds so the disease doesn’t spread. However, when humans introduce agriculture and animals like pigs, mosquitos can take the virus from wading birds and infect pigs, which are in closer contact with humans

62
Q

What is a bridge host

A

Bridgehost are another reservoir that amplify the pathogen to the target population because they are in closer contact with them

63
Q

What is the target population

A

The population we care about, it is mainly humans

64
Q

What are teh two reasons JEV has increased

A

Because of rice and pig farming. The rice has attracted mosquitos allowing for an increase of them since they supply water. And the pigs act as a bridge host that are in close contact with people and can spread major disease.

65
Q

What is another reason why agriculture/livestock can spread pathogen quickly?

A

Livestock is usually a genetic monoculture (they share a lot of genetic traits so there isn’t a lot of diversity) so if a livestock picks up a pathogen, it can spread it quickly

66
Q

Is agricultural land use always bad for disease emergence?

A

No, in an experiment done in Kenya comparing cropland, removing wildlife, and pastoral (having some small herbivores), pastoral did the best

67
Q

Hendra and Nipah Viruses

A

Paramyxoviruses, includes measles and mumps

Hendra - Outbreaks in australia
Nipah - Outbreaks across southeast Asia and India
`

68
Q

Why are Hendra and Nipah viruses so virulent?

A

Both are highly virulent and use conserved cell surface proteins as receptors such as ephrin and receptors common across all cell types

They are also able to block IFN and cytokine response to viral infection

69
Q

What are the direct impacts of climate and human health

A
  • Fluctuating global temperatures
  • Higher likelihood of extreme weather events
70
Q

What are the changes to ecology due to the climate change?

A
  • Range, rates, and seasonality will shift as a result
71
Q

El Nino

A

Linked to extreme weather events and natural disasters (severe flooding/drought)
- Disease outbreak like malaria, dengue, and cholera because so much water)

72
Q

Warmer temperatures are affecting…

A

Mosquito range. They are able to travel in a lot more places because of the warmer weather

73
Q

Zika Virus

A

Arbovirus belonging to the Flavivirdae family. Related to Degnue, yellow fever, west nile, JEV.

It was discovered in Africa from monkeys

74
Q

Influence of climate change on Zika Transmission

A

Strong El Nino events are allowing mosquitoes to breed in more areas. Warmer temperature is allowing mosquitos to increase their range

75
Q

Why are so many viruses found in bats

A
  • Bats are social and can share viruses across species
  • Bigger population of susceptibles
  • Bats have longer life spans relative to size than other mammals
  • More time for infection
  • High metabolic rate which means they always have a high temperature and feverish state since they need it for flight. Because they need flight, they have less of an inflammatory response to viruses which allows for them to be infected for very long periods of time which makes it easier for humans to get it.
76
Q

What leads to spillover to humans from bats?

A
  • Bats are wide ranging and can travel long distances
  • They often overlap with humans
77
Q

What about bat ecology leads to spillover?

A

Group size
Population structure
Body size/life span
Reproductive Rate

78
Q

What is a benefit of bats?

A

They are pest control

79
Q

White nose syndrome (WNS)

A

a fungal infection impacting North American bat populations
Caused by Pseudogymnoascus destructans
Proliferates in cave-dwelling bats while they hibernate
Causes bats to wake up more often in the winter, causing them to become underweight

80
Q

European Bats do better than North American Bats

A

Some studies have fond evidence that European bats have coevolved with the fungus. They speculated that the fungus may have been responsible for bat die offs in Europe during the Pleistocene

81
Q

Are tree bats affected?

A

No, only cave bats. Some species are more impacted than others

82
Q

What can make teh WNS infection worse?

A

High humidity and warmer winter temperatures

83
Q

Possible Treatments for WNS

A
  • Stopping spread through education
  • Antifungals (hard to apply and haven’t been successful)
  • Probiotics (bacteria that produce antifungals. has been successful to lower lethal effects of Pd on bats)
84
Q

Chytridiomycosis

A

Caused by Bd Batrachochytrium dendrobatidis which is a fungus

85
Q

Chytrid life cycle

A

Spores swim towards frogs.
Spores burrow under frog skin
Spoures mature into the sporangium
Spores released after 4-5 days

86
Q

Chytrid has consequences

A

Amphibian declines destabilize ecosystems
- Central position in food chain, stabilize populations of insects and predators

87
Q

Not all species are impacted by chytrid

A
  • Bullfrogs dont get sick, but they can spread spore
  • Severe outcomes have been linked to abiotic factors like temperature and humidity
  • Linke dto differences in microbiome
  • Immune system variation in frogs. Linked to habitat fragmenetation and impacts on diversity

Infectious Disease (3 decks)

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