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APS 276- Symbiosis > 4 + 5: animal parasitism > Flashcards

4 + 5: animal parasitism Flashcards

1
Q

give 2 examples of tapeworms as human parasites?

A

beef tapeworm: T.saginata

pork tapeworm: T.solium

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2
Q

a) what can T.solium cause?

b) what are the definitive and intermediate hosts of the tapeworms

A

a) cysticercosis which can cause seizures

b) humans , pigs or cattle

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3
Q

give the steps of the basic lifecycle of tapeworms (7)

A
  1. vegetation contaminated with eggs eaten by pigs or cattle
  2. oncospheres hatch in intestine and invade intestine wall
  3. develop into cysticerci in muscle wall
  4. raw/uncooked meat ingested
  5. develop into adults in human intestine
  6. adults attach to small intestine with scolex
  7. migrate to anus and pass in stool
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4
Q

in broad terms what is a parasite?

- if using this definition what % of animal species are parasites?

A

an obligate feeding on a living organism without death to the host
- 50%

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5
Q

in the Poulan study 2000 what did he study and discover about parasite body size and diversity?

A

flatworm ectoparasites on fish

  • often parasite is smaller than its host
  • as body length decreases, species diversity increases
  • small body size favoured
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6
Q

what did Poulan discover in terms of temperature?

A
  • endoparasitic helminths from 55 marine fish species
  • more vectors and insects in warmer environments
  • warmer and moist conditions favourable to parasites
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7
Q

what did Poulan discover in terms of water?

A
  • intestinal helminths in vertebrates

- more parasites where vertebrates in contact with water as is an ease of transmission

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8
Q

a) what have parasites evolved from?

b) what do phylogenetic analyses indicate?

A

a) free living ancestors

b) about 60 metazoan transitions to parasitism

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9
Q

what is the difference between the definitive host and the intermediate host?

A 
definitive= parasite reaches maturity and reproduces here
intermediate= asexual parasitic stage and can be used as a resource to multiply asexually
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10
Q

life cycles can increase or decrease in complexity- can hosts be added in parallel?

A

yes

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11
Q

when transitioning from one host to two hosts what is the upwards incorporation? (5)

A
  • host in initial life cycle is ingested increasingly frequently by potential host 2
  • parasites reproduce in both hosts
  • reproduction suppressed in host 1 and host 2 intermediate
  • eggs exit host 1 and 2 at different trophic levels
  • not damaging to loose host 1 link to eggs as intermediate host useful to multiply asexually
  • eggs pass to host 1 and then host 2 and only eggs produced from host 2
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12
Q

when transitioning from one host to two hosts what is the downwards incorporation?

A
  • propagules enter prey host 2 from host 1
  • eggs passed to both hosts directly as well as from host 2 to 1
  • eggs dont exit host 2
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13
Q

in complex life cycles hosts are added in series but how may hosts also be added?

A

in parallel

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14
Q

what is host specificity?

A

the extent to which a parasite species is restricted in the number of host species used at a given stage in the life cycle

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15
Q

how may host specificity vary?

A
  • some highly host specific limited to single host species or population
  • others specific to genus or family
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16
Q

how can host specificity be measured but what may be a downside?

A
  • count number of different host species parasite uses
  • go through published records of parasite occurrence
    BUT: more research means an increase in the known host species
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17
Q

what are the 4 main levels of host specificity?

A

genotype
population
species
higher taxon

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18
Q

give 11 points about Schistosoma mansoni

A
  • 200 million infected
  • only digenea living in blood
  • mainly infects those in central Africa
  • causes bilharziasis
  • control via intermediate host freshwater snail
  • disease described 1860s
  • life cycle described 1906
  • control achieved by targeting snail population (chemically with gopo berries or biologically with crayfish)
  • first vaccine 2006
  • annual dose of praziquantel
  • utilises human behaviour as humans are drawn to water to wash and drink
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19
Q

what does knowing the life cycle of a parasite help with?

A

can tackle it to determine its vulnerable stage

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20
Q

what is the life cycle of Schistosoma mansoni? (7)

A
  • free living cercaria released from intermediate water living snail host
  • enter skin in minutes of contact
  • snails lose their tails and move by suckers in portal vein
  • mate here and eggs laid in smaller vessels around gut or urethra
  • pass through walls of vessels and released into water by faeces or urine
  • hatch into miracidia that swim to snails by chemotaxis
  • develop into adult sporocyst in snail and releases thousands of cercaria
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21
Q

how is specificity maintained in Schistosoma?

A

temporal adaptation in emergence of cercaria

- cercaria emerge at the same time as the host visits the water

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22
Q

what are the 3 main drivers/ theories for host parasite coevolution?

A
  1. virulence transmission trade off
  2. red queen hypothesis
  3. geographic mosaic
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23
Q

what is virulence and what is transmision?

A 
virulence= parasite induced host mortality
transmission= ability to pass from host to host (density dependent)
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24
Q

what is the virulence transmission trade off?

A

higher virulence=

  • increase production of parasite offspring
  • kill the host sooner so reduce transmission
  • host evolution responds strongly as high virulence strongly selects for resistance genes
  • parasite evolution sensitive to the trade off
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25
Q

what is the virulence and transmission like for the common cold?

A

low virulence

high transmission

26
Q

what is the red queen hypothesis?

A

host parasite arms race

  • parasite evolves strategies to overcome host defences
  • host evolves to resist new parasite strategies
  • host and parasite locked into coevolutionary cycle
27
Q

what is the geographic mosaic driver for coevolution? (5)

A
  • host populations form geographic mosaic where populations are separated by different degrees, interact to different degrees
  • complete separation means no interaction
  • red queen and virulence transmission occur in this mosaic
  • results in coevolution
  • may result in cospeciation
28
Q

what is the Australia rabbit population example of a geographic mosaic?

A
  • myxomatosis virus introduced in 1950 as biological control
  • 1950/51 high virulence and mortality
  • resistance gene spread so some of the pop survive and result in a more resistant pop
  • limit to how much genes can spread and equilibrium reached
  • swings back and virulent outbreak again
29
Q

what is cospeciation?

A

one species speciates in response to another species

30
Q

what is congruent phylogenies that may result from host parasite cospeciation and what is the rule applied?

A

parasite speciates at the same time as the host

- fahrenholz rule: parasite phylogeny mirrors host phylogeny

31
Q

how may incongruent cospeciation arise and why?

A
  • parasites can switch to another host
  • can add a new host
  • can die out (sorting event)
  • can speciate (duplication)
  • greater effect on mobile hosts as easier for parasite to disperse and find new hosts
  • occur due to sorting events leaving hosts free for host switch event
32
Q

explain the phylogeny and level of congruence in birds and feather lice (9)

A
  • host switch clearly seen
  • feather lice mobile with high congruence as is a positive relationship between host and parasite body size
  • lice need to be the right size for host
  • lice that fit perfectly between bird feather barbs are well protected from preening
  • pigeons try to preen feathers to remove lice
  • bill runs over barbs not between them
  • larger lice selected against as cant fit between barbs
  • barb size increases with pigeon size so have larger lice
  • large lice cant thrive on a smaller pigeon host
33
Q

lice and human evolution are very congruent but are some differences - what are the 2 hypotheses as to why humans have 2 rather than 1 lice?

A
  1. recent host switch

2. pair of lice lost

34
Q

what is the recent host switch hypothesis? (3)

A
  • perfect cospeciation between primates and lice
  • pediculus going one way and Pthirus going the other
  • at a later point a single host switch occurred where pubic lice moved from gorillas to humans
35
Q

what is the pair of lice lost hypothesis? (6)

A
  • duplication event may have happened on ancestors of gorillas, humans, chimps creating lineages leading to these 2 current genera
  • divergence between Pthirus pubis and Pthirus gorillae occured at same time as hosts diverged
  • humans retained both genera
  • chimps lost Pthirus species
  • gorillas lost Pediculus species
  • sorting event
36
Q

what was likely the reason for the lice and human evolution slight incongruence and give 5 points?

A

combination of both hypotheses

  • divergence estimates suggest Pthirus and Pediculus diverged in duplication event on ancestor of chimp, human, gorilla 13mya
  • each genus had potential to co-speciate with all descendent hosts
  • only gorillas retained Pthrius and only humans retained Pediculus
  • 2 resulting Pediculus species diverged in tandem with hosts 6mya
  • 3-4mya Pthrius species switched from gorilla lineage leading to modern humans
37
Q

give 5 points about the lice and human evolution link in terms of ancient lineages

A
  • Pediculus humanus composed of 2 ancient lineages
  • origin of lineages 1.18my before modern humans
  • one lineage has worldwide distribution and undergone bottleneck 100,000 ya
  • about the same time homo sapiens went through bottleneck
  • another lineage less common and is in Americas, thought to have evolved on homo erectus which remained isolated from ancestors for about 1my
38
Q

if parasites are better adapted to local host genotypes what would you expect?

A

them to be fitter in combination with local hosts rather than foreign hosts

39
Q

in terms of host and parasite where does genetic variation exist and what is this variation pre-requisite for?

A
  • in host resistance
  • in parasite success
    pre-requisite for host parasite coevolution and eventually cospeciation
40
Q

in order to exploit a host what 3 things must be done?

A

find, get resources from and manipulate the host

41
Q

what is R0 and define

A

basic reproductive rate

- number of secondary infections that each primary infection produces in a susceptible population

42
Q

what is R0 key for and what does it mean if it is > or < 1

A

to understand disease dynamics
R0>1 invasion
R0<1 no invasion as not enough susceptibles

43
Q

as generations go on what happens to the number infected by disease?

A

fewer and fewer infected as more become immune

44
Q

what is herd immunity?

A

parasite cant find individuals if protected by this immunity even if not immune yourself
- rely on fact disease no common in community due to this immunity

45
Q

what is R?

A

actual reproductive rate taking into account population may not be susceptible

46
Q

a) what happens if number of susceptibles goes down?

b) what happens to number of infections of R<1 ?

A

a) reduced effective rate of R (R0)

b) decrease in number of infections and epidemic dies out

47
Q

what are the 2 main subcomponents of R0?

A

transmission rate

virulence

48
Q

what is the equation for R0? and what does each part mean

A

β (N) / μ + α + v

transmission / mortality 
β= transmission rate
μ = mortality of parasite free host
α= virulence 
v= host recovery rate
49
Q

linked to what are transmission and virulence a trade off?

  • with low V what is there?
  • with high V what is there?
A

exploitation

  • low V high T low E
  • high V low T high E
50
Q

give 5 points on the 1928 flu pandemic

A
  • killed 50-100 million people worldwide
  • avian derived pandemic
  • H1N1 strain of avian ancestry (usually in waterfowl guts)
  • kills young and old the most
  • but all range of ages of people died
51
Q

what did Morens et al discover in 2007 about the 1918 flu pandemic?

A
  • first wave divided into 3 waves with post pandemic recurrence each year
  • as well as young and old mortality high in 20-30 year olds so not a protection to be young and healthy
  • lots of fluid produced in lungs
  • likely 20-30 infected due to overactive immune system
52
Q

what is the water mite parasitism of host mayflies as ectoparasites? (5)

A
  • water mites hatch on water bed and migrate to surface
  • attach to mayfly larvae
  • female mayflies return to water to lay eggs
  • mites live on M and F mayflies and complete life cycle in water
  • can jump from M to F host during mating
53
Q

what is the water mite parasitism of host mayflies as endoparasites? (3)

A
  • manipulate metabolism of M so take on shape and behaviour of females in an intersex morph
  • genetically still M and F but no eggs, ovaries, tsetses
  • parasitised mayflies all fly upstream as females do to oviposit and both M and F show oviposition behaviour even though no eggs to lay
54
Q

what are the 9 main life cycle stages of the Lancet liver fluke Dicrocoelium dendriticum?

A
  1. after infection metacercariae move to ganglion under oesophagus
  2. ant vector actions taken control of with manipulating information relayed by nerve cells
  3. when evening/cool ant leaves colony to climb to grass tips and clamp here with mandibles remaining here until dawn so susceptible to being eaten by host
  4. in daytime parasite released them from control and ants return to normal to avoid dessication from midday sun
  5. eaten by host and metacercariae develop in small intestine
  6. worms mature sexually in bile duct and produce eggs
  7. eggs passed to host faeces and eaten by snails
  8. eggs hatch in snal and parasite produces cercariae
  9. passed from snails in slime balls which are eaten by ants
55
Q

give points about Toxoplasma gondii

A
  • parasitic protozoa
  • definitive host =cat
  • asexual part of life cycle completed in warm blooded intermediate such as rats and birds
  • parasite transmitted when cat eats intermediate
  • manipulate rat to be more risky
  • estimated 1/3 humans infected
  • can cause mental illness such as depression and schizophrenia in humans
  • initiates risky behaviour
  • react to antipsychotic drugs and rats will reduce risky behavior if exposed
56
Q

what is the oystercatcher example of host manipulation? (4)

A
  • oystercatcher definitive
  • cockles intermediate and burrow in sand
  • could be coincidence
  • parasite trematode cercariae accumulate in cockle foot so it cant burrow
57
Q

what is the bumblebee and conopid fly example of host manipulation? (5)

A
  • conopid flies wait on flowers and inject eggs into bees that visit
  • egg grows inside bee body cavity
  • egg hatch and larvae feed on abdominal contents, killing bee
  • infected bee avoids hive and colony, spends more time in cold outside of nest
  • bees do this to minimise effect of parasitism as host lifespan longer in cold so will reduce parasite size and growth rate
58
Q

in some cases the parasite may be larger than the host- what is the manipulation example for this

A
  • reed warbler hosts are manipulated to accept parasite cuckoo eggs as their own
  • cuckoo chicks have large gapes so fed more than other chicks
  • cuckoo chicks make sound similar to the whole brood of host birds
59
Q

what is parasite manipulation of host phenotype a paradigm of?

A

the evolutionary biology of host parasite infections

60
Q

what is meta analysis and effect size?

A 
MA= statistical method to compare published data
ES= measure of magnitude of trait difference under study
61
Q

over the years what has happened to effect size in publications?

A

decreased- no longer need to just prove hypothesis, more likely published if counter theory argument

62
Q

what are 4 examples of adaptive manipulation of host behaviour to increase transmission success?

A
  • decrease in stamina
  • increase in conspicuousness
  • disorientation
  • altered response to environmental stimuli

APS 276- Symbiosis (29 decks)

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