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DISEASE E&E Final Exam > 17. Host Diversity and Multi-Host Pathogens. > Flashcards

17. Host Diversity and Multi-Host Pathogens. Flashcards

1
Q

Multi-host pathogens:

A

-infect multiple hosts
>hosts differ in their reservoir competence

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2
Q

Host community:

A

-will influence epidemiology of multi-host pathogens
Ex. bird hosts and WNV, vertebrate hosts and Lyme disease

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3
Q

Dilution hypothesis: simple

A

-host diversity can dilute risk of infectious disease
>negative relationship between disease risk and host diversity

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4
Q

Amplification hypothesis: simple

A

-host diversity can increase risk of infectious disease

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5
Q

Reservoir competence:

A

-ability of animal species to be a host for a pathogen
*perspective of host rather than pathogen
-all host traits that are important for the life cycle of the pathogen

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6
Q

Host traits that are important for the life cycle of the pathogen:

A

-susceptibility
-pathogen abundance in tissues
-clearance
-transmission

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7
Q

What host features will help determine the host’s contribution to the R0 of the pathogen?

A

-host reservoir competence
-host abundance/density

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8
Q

Composition of the host community:

A

-will affect the prevalence and incidence of multi-host pathogens

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9
Q

WNV and reservoir hosts:

A

-cycles between mosquitoes and birds
-some birds, develop high viremia
>high viremia: facilitates virus transmission to feeding mosquitoes (reservoir host)
-mammals have low viremia (incompetent dead-end host)
*vary in symptoms and disease

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10
Q

Viremia profiles in 10 orders of birds: WNV

A

-infected with WNV and had repeated blood samples
-songbirds and shore birds: highest viremia and longest duration
-parrots and fowl: lowest viremias of short duration

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11
Q

Which birds do we expect to be the most competent reservoir hosts?

A

-birds with high viremias of long duration

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12
Q

Reservoir competence (WNV) requires:

A
  1. Susceptibility (s)
  2. Infectiousness to mosquitoes (i)
  3. Duration of viremia (d)
    *product of all 3
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13
Q

Susceptibility, WNV:

A

-ability of bird to acquire WNV infection
>WNV must be able to infect the bird

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14
Q

Infectiousness, WNV:

A

-depends on viremia
-hosts with higher viremia=have higher host-to-mosquito transmission success of WNV

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15
Q

Duration of viremia:

A

-duration of infectious period
-host with longer duration=can infect mosquitoes over a longer period of time

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16
Q

Study showed the most important reservoir hosts for WNV are:

A

-blue jay
-common grackle
-house finch
-American crow
-house sparrow

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17
Q

WNV transmitted among bird species by:

A

-mosquitoes belonging to genus Culex

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18
Q

If mosquitoes have no feeding preferences:

A

-should feed on birds in proportion to their abundance

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19
Q

Feeding preferences of mosquitoes: study, what you ‘should’ see

A

-population size of host bird A, 80 birds, and host bird B, 20 birds
>80% of blood meals should be from A
>20% of blood meals should be from B

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20
Q

Most common bird species: study

A

-house sparrow
-rock dove
-European starling

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21
Q

Blood meal in Culex mosquitoes: study

A

*mosquitoes do NOT feed on birds in proportion to their abundance
*robins were most common (16.7x)
-house sparrows are less important (7.9x)

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22
Q

How do you estimate the fraction of WNV-infected mosquitoes produced by each bird species?

A

Multiply:
-relative abundance of each bird species
-mosquito feeding preference
-reservoir competence of host

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23
Q

Fraction of WNV-infected mosquitoes produced by each bird species: robins

A

-less than 4% of the birds
-produce ~60% of WNV-infected mosquitoes

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24
Q

Fraction of WNV-infected mosquitoes produced by each bird species: sparrows

A

-56% of the birds
-~24% of WNV-infected mosquitoes

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25
Q

Mosquitoes feeding preferences:

A

-are important for which bird species contribute to WNV epidemiology

26
Q

host heterogeneity factors:

A

-abundance
-reservoir competence
-vector preferences (for VBPs)

27
Q

Abundance:

A

-some host species more common than others

28
Q

Reservoir competence:

A

-some host species have higher viremia and/or longer duration of infectious period

29
Q

Vector preferences:

A

-arthropod vectors prefer some hosts over others
*influenced the contributions of robins and sparrows to the production of WNV-infected mosquitoes

30
Q

Lyme disease:

A

-caused by Bbss (a tick-borne bacterium)
-black legged tick (I. scapularis) is the vector
>generalist tick: feeds on dozens of vertebrates
-transmitted between vertebrate hosts by ticks during blood meal
-both Bbss and I scapularis are mulit-host pathogens/parasites

31
Q

Risk of Lyme disease:

A

-depends on nymphal infection prevalence (NIP)

32
Q

Nymphal infection prevalence (NIP):

A

-% of nymphs infected with Bbss
>more nymphs=greater risk of disease

33
Q

Variation in reservoir competence for Bbss: factors

A

-body burden
-moulting percentage
-reservoir competence
-host density
*all contribute to R0 of Bbss

34
Q

Body burden: Bbss

A

-number of ticks per host
Ex. 1 deer feeds more ticks than 1 white-footed mouse

35
Q

Moulting percentage: Bbss

A

-% of engorged larvae that become nymphs
Ex. higher in skunks than birds

36
Q

Reservoir competence: Bbss

A

-susceptibility, duration of infection and transmission
Ex. higher for white-footed mouse than deer

37
Q

Density: Bbss

A

-number of individuals per hectare
Ex. density of deer is lower than white-footed mouse

38
Q

Reservoir hosts for Bbss

A

-white-footed mouse=good reservoir host
-possums and deer=poor reservoir hosts

39
Q

Host community and risk for Lyme disease:

A

-high biodiversity: NIP is low
-low biodiversity: only white-footed mice=NIP is high
*assuming that density of infected nymphs (DIP) is equal in both communities

40
Q

NIP vs. diversity of host community:

A

-started with a community of only mice and continued to add hosts with low RC
>adding hosts with low RC reduces NIP

41
Q

Forest fragmentation and Lyme disease risk:

A

-biodiversity of vertebrate host is low in smaller forest fragment
>white-footed mice do well here (density of them increases)
*mouse density decreases with increasing size of woodland patch (will encounter more predators)

42
Q

NIP and forest habitat fragmentation:

A

-NIP will decrease with area of forest patch
-highest NIP in highly fragmented habitats with a small patch area
-density of infected nymphs (DIN) also had a negative relationship with patch area

43
Q

DIN:

A

-density of infected nymphs
*best predictor for Lyme disease

44
Q

Important assumptions for dilution hypothesis:

A

-vector and pathogen are both generalists
-vertebrate hosts vary in RC for the pathogen
-competent hosts achieve higher relative abundance in species poor habitat
-increasing biodiversity favours noncompetent hosts
-no increase in tick density with the addition of non-competent hosts

45
Q

Conclusions on biodiversity and Lyme disease risk:

A

-white footed mice are highly competent reservoir hosts
-low diversity habitats=higher risk of LD
-high diversity habitats=lower risk of LD
-highly fragmented forests=high density or mice and high NIP
*habitat conservation and biodiversity preservation can reduce LD risk

46
Q

Dilution hypothesis suggests:

A

-that preserving biodiversity will reduce risk of zoonotic disease to human

47
Q

Leishmaniasis:

A

-a VBD
-protozoan parasite
-transmitted by sand flies
-“chiclero’s ulcer”
>cichleros are people whole collect chicle (latex produced by sapodilla tress)
-infects humans who live and work in intact rain forests

48
Q

Summary of Leishmaniasis:

A

-time spent in biodiverse rain forests in Central America, increases risk of contracting Leishmaniasis
*example of amplification hypothesis

49
Q

Effects of biodiversity of 70 common human parasites:

A

-many cases showed that biodiversity will increase the disease risk for humans (amplification effect)
-many showed that biodiversity does not increase nor decrease the risk
-minority showed that biodiversity will reduce disease risk (dilution effect)

50
Q

Bovine tuberculosis (BTB) in UK

A

-caused by mycobacterium bovis
>multi-host pathogen (effects cattle and wildlife)
-considerable economic losses to farmers

51
Q

European badger:

A

-a wildlife host for M. bovis
-protected wildlife species in UK
-beloved animal to the public

52
Q

Incidence of BTB in UK:

A

-increased from 1986 to 2010
-cattle are routinely tested
>positive ones are slaughtered
>farmer loses official TB free status (restrictions on sales and movement of cattle)

53
Q

Randomized badger culling trial:

A

-famers think badgers are the culprit to the spread of BTB
-previously studies found opposite effects of culling
-at 10 locations badgers were pro-actively culled or left alone
>measure the incidence of BTB in nearby cattle populations

54
Q

Results from randomized badger culling trial:

A

-culling area: 26% reduced incidence in BTB in cattle
-during the trail zone surrounding cull area: increased incidence of BTB by 25%
-after the trail zone surrounding cull area: decreased incidence of BTB by 4%
*culling is effective inside the proactive culling area, but seems to increase incidence of BTB in cattle in surrounding areas

55
Q

Perturbation hypothesis:

A

-culling disrupted social structure of badgers
Badgers moved in between culled and non-culled areas
*movement of infected badgers increased exposure of cattle to TB in areas outside the culling zone
-effective TB control would require culling badgers on very large scale

56
Q

Vaccine against TB: humans

A

-BCG vaccine was developed to protect against TB
>attenuated form of M. bovis
-given as a single dose to children in TB-endemic areas
-routine vaccines in Canada were discontinued in Canada in 1970s

57
Q

Efficacy of TB vaccine:

A

-prevents 20% of kids from getting infected
-subset that gets infected, prevents 50% from developing disease

58
Q

Vaccine trails for TB found that:

A

-BCG protects against M. bovis in:
>mice
>possums
>badgers
>white-tailed deer
>cattle

59
Q

Vaccinate badgers with BCG:

A

-zone A: placebo
-zone B: 50/50 placebo and BCG
-zone C: BCG
-over 4 years, performed 7 sweeps of area
-tested badger serum for antibodies to BTB antigens
-badgers that seroconvert are classified as infected

60
Q

Seroconversion of badgers over time:

A

-non-vaccinated badgers seroconverted more quickly than vaccinated badgers
-vaccine efficacy increased over study
>26% to 84%
-prevalence of lesions was 26% in placebo and 9% in vaccine group

61
Q

Summary of badgers and bovine BTB:

A

-multi-host pathogens
-badgers are reservoirs
-culling must be done at large scale to be effective
*conflict between agriculture and conservation
-vaccination of badgers with BCG reduced prevalence of BTB in Ireland
>not known if it would help reduce BTB in cattle

62
Q

Why not vaccinate cattle directly?

A

-wouldn’t be able to tell if they have TB or if it was the vaccine
>can’t show other countries are TB free

DISEASE E&E Final Exam (11 decks)

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