15. Host Population Ecology and Infectious Disease

Question 1

Macroparasites example on regulating host populations in DD manner:

Answer 1

-red grouse: lives in UK
-macroparasite: grouse worm (Trichostrongylus tenuis)
>directly transmitted nematode parasite

Question 2

Red grouse populations cycle:

Answer 2

-number of birds shot by hunters is a good indicator of red grouse abundance
-show that 77% of red grouse populations cycle with a period between 4 and 8 years
-grouse parasite is believed to cause cycles

Question 3

Number of birds shot by hunters is a good indicator:

Answer 3

-similarity between red grouse counted per square km prior to hunting season by biologists and the ones hunted

Question 4

Life cycle of the grouse worm:

Answer 4

*nematode parasite, direct lifecycle
1. Infected grouse release eggs into environment with fecal material
2. Larvae go through several free-living stages to reach infective ‘L3’ stage
3. Infective ‘L3’ stage wait on heather buds to be eaten by their red grouse host
4. Ingested larvae develop into adult worms in caecum (part of large intestine) of red grouse

Question 5

If red grouse is infected in the autumn:

Answer 5

-can arrest their development over the winter and resume development in spring
-parasites don’t want to produce eggs in wintertime because they will not result in transmission to new grouse hosts

Question 6

Pathology of grouse worm:

Answer 6

-damage mucosa of large intestine
-grouse tolerates worms in high numbers, but counts over 4000 are associated with intestinal damage (*dose-dependent effect)
*very common in red grouse but not in other game birds (a lot easier to study)

Question 7

Pathology of grouse worms results in:

Answer 7

-weight loss
-lower reproductive success
-higher mortality (virulence)

Question 8

rt of red grouse:

Answer 8

-per capita rate of increase of the red grouse at time, t
>host population already occupies a fraction of the carry capacity
*negatively related to intensity of worm infection in adult grouse
*crashes in population size are associated with high parasite intensities
>grouse worm might be regulating N of its host

Question 9

Does the previous data prove that nematodes CAUSE the grouse population dynamics?

Answer 9

-NO
*correlation is not causation

Question 10

Correlation is not causation: alternative explanation

Answer 10

-food availability is what is regulating grouse abundance
>food is limiting=birds reduce investment in immune system
>malnourished birds are more susceptible to worm parasites
-worms are not the cause of population cycles, they are consequences of the birds being malnourished
*need to do something to prove that parasites drive the population cycles

Question 11

Experimentally reduce parasite burdens in grouse:

Answer 11

-captured and treated with antihelmintic levamisole hydrochloride
-2 control populations not treated
-2 populations treated twice
-treated 15%-50% of adult breed population
*theoretical model predicted 1989 and 1993 as crash years: treated them in those years

Question 12

Shot treated and untreated to compare worm burden:

Answer 12

-experiment confirmed that the anthelmintic treatment was effective at reducing the worm burden in the red grouse

Question 13

Why a small population crash in 1993 in one of the treated populations?

Answer 13

-it’s a wild population, hard to catch them all

Question 14

Population of one host-one parasite systems: virulent parasites can

Answer 14

-regulate host population size via DD effects on host vital rates
-microparasites: can control host population size in nature (ex. rabies in red fox in Europe)
-macroparasites: can control host population size in nature (grouse worm in red grouse populations in UK)

Question 15

Parasitism and other ecological interactions:

Answer 15

-host-parasite systems interact with other ecological interactions
-host organism might be prey item for a predator
>parasite might make infected host more susceptible to predation
-host might be in competition with another host species
-parasite might change outcome of competition between two host species

Question 16

Snowshoe hares:

Answer 16

-investigate effect of a directly transmitted nematode parasite on the predation rates of snowshoe hares

Question 17

3 main predators of snowshoe hares:

Answer 17

-coyote
-great-horned owl
-red-tailed hawk

Question 18

Nematode parasites of snowshoe hares:

Answer 18

-5 different nematode parasites
*Obeliscoides cuniculi: most abundant, lives in STOMACH
-3/5 have direct life cycles
-2/5 have indirect life cycles with hares as final host
*not adaptive for any of the nematode species to increase susceptibility of their hare host to predation

Question 19

Ivermectin treatment to kill parasitic nematodes:

Answer 19

-hares were treated to reduce burden of parasitic worms
>reduced burdens of 4 nematode species by 38-88% for 50days post-treatment
-untreated: parasite-normal group
-ivermectin-treated group: parasite-reduced group

Question 20

Radio-collared snowshoe hares:

Answer 20

-612 snowshoe hares were radio-collared
-allowed determination of cause of death
-318 radio-collared animals died of natural causes
>95% were killed by predators
*compare predation risk between parasite-reduced hares and parasite-normal hares

Question 21

Survival of treated vs. parasite-normal snowshoe hares:

Answer 21

*parasite-reduced hares had higher survival than parasite-normal hares (2.4x higher)
-parasite-reduced: 74.4% survivorship
-parasite-normal: 31% survivorship

Question 22

Summary of hosts, parasites, and predators:

Answer 22

-survival of parasite-reduced hares was 2.4x higher
-nematode parasites increased risk of predation
-predation is NOT adaptive for these parasitic nematodes
-parasites and predators interact to control the density of the host/prey species of interest
*indirect effects of parasitism

Question 23

Indirect effects of parasitism:

Answer 23

-nematode parasites made snowshoe hares MORE VULNERABLE to predation

Question 24

Complex lifecycle of Euhaplorchis californiensis: (trematode parasite)

Answer 24

-marine birds are final host for adult trematode parasites
1. Trematode eggs are released in bird droppings
2. Marine snails (intermediate host 1) ingest eggs that develop into infective cercariae
3. Snail releases infective cercariae and they infect killifish (intermediate host 2)
4. Trematode parasites encyst as metacercariae in brain of killifish
5. Avian predators eat infected killifish to complete the life cycle

Question 25

Euhaplorchis californiensis similar to:

Answer 25

-common liver fluke (Fasciola hepatica)
>causes fasciolosis in cattle and sheep
>only one intermediate host (snail)
>snail releases motile cercariae in water that encyst on vegetation at shoreline

Question 26

Trematode parasites cause:

Answer 26

-conspicuous (strange) behaviours in killifish (intermediate host 2)
-show their lateral and ventral surfaces far more frequently
>light coloured surfaces make them more conspicuous to avian predators
-spend more time at the surface of the water
>makes them easier target

Question 27

Conspicuous behaviours in killifish:

Answer 27

-surfacing
-flashing
-contorting
-shimmying
-jerking

Question 28

Intensity of infection and killifish behaviour:

Answer 28

-intensity is positively correlated with frequency of conspicuous behaviours
-trematode parasites increased behaviours by a factor of 4
*those with lots of parasites have more behaviours compared to hosts with few parasites
*DOSE-DEPENDANT EFECTS

Question 29

Parasites target brain of killifish host:

Answer 29

-metacercaria stage of parasite
>cause weird behaviours of killifish
*parasites can influence NT in intermediate hosts to manipulate behaviour

Question 30

Infection intensity and predation risk:

Answer 30

-pens protected and not protected
-fish with lots of parasites were missing from open pens
>those with heavy parasite loads were more likely to be eaten by birds
-uninfected fish: no difference in predation rates between open and closed pen

Question 31

Over 1400 cysts:

Answer 31

-30x more susceptible to predation than unparasitized fish

Question 32

Parasitic manipulation:

Answer 32

-increased frequency of conspicuous behaviours by 4-fold
*small changes in behaviour can drive large changes in predation rates (30-fold)

Question 33

Conclusions of killifish study:

Answer 33

-heavily parasitized fish were 30x more susceptible to predation
>snowshoe study it was increased 2.4x
*importance of behaviour (small changes can drive big changes in predation)

Question 34

Manipulation of killifish behaviour to enhance predation by birds is:

Answer 34

-an adaptive strategy by the trematode parasite
*parasites facilitate predation and are important component of food webs in ecosystems

Question 35

Rinderpest:

Answer 35

-introduced to Africa in 1880
-1957: invention of vaccine
-2011: eliminated from world
*vaccination of domestic ungulates allowed wildebeest populations to recover
>keystone species

Question 36

Crash and recovery of wildebeest populations had:

Answer 36

-dramatic consequences for Serengeti ecosystem

Question 37

Rinderpest comes to Africa:

Answer 37

-Italy was trying to conquer Ethiopia (1880s)
>supplied armies with Indian cattle for food and labor
>had rinderpest (highly contagious viral disease)
-spread rapidly
-killed more than 90% of domestic cattle and wild ungulates
*mass mortality of domestic and wild ungulates caused 1/3 Ethiopians and 2/3 of Maasai in Tanzania to STARVE TO DEATH

Question 38

Walter Plowright (1923-2010):

Answer 38

-English vet scientist
-devoted career to eradication of rinderpest
*developed tissue culture rinderpest vaccine (TCRV)
-rinderpest was the first animal disease to be eliminated worldwide
-awarded 1999 World Food Prize

Question 39

TCRV:

Answer 39

-tissue culture rinderpest vaccine
-live
-attenuated (non-pathogenic) virus (non-virulent)
>could be transmitted to another animal (producing lifelong immunity)
*critical for rinderpest elimination

Question 40

Wildebeest populations recovered:

Answer 40

-important grazers in Serengeti ecosystem
-rinderpest epidemic reduced wildebeest population from over 1 million to 250,000
-vaccination eradicated it from domestic cattle
>prevented transmission to wild ungulates
*recovered dramatically from 1960 onwards
>abundance of top predators, lions and hyenas increased

Question 41

Carry capacity of wildebeest population:

Answer 41

-around 1.2 million animals
-seems to follow a logistic growth curve

Question 42

Rinderpest, wildebeests, and woodlands:

Answer 42

-reduced wildebeests=reduced grazing pressure
>caused grasses and shrubs to grow out of control
-frequent and intense wildfires burned down young tees
-1980s: many former woodland areas were treeless

Question 43

Recovery of wildebeests and woodlands:

Answer 43

-increased grazing pressure and reduced grass
-fewer wildfires and trees returned
*allowed woodlands to return to Serengeti

Question 44

Summary of rinderpest story:

Answer 44

-novel pathogen decimated wildebeest populations
-reduction in grazing=increased buildup of kindling and frequency of wildfires (killed young trees)
-eradication of rinderpest -> population recovery of wildebeests -> predators (lions and hyenas) and trees returned to Serengeti
*wildebeest is a keystone species

Question 45

Wildebeest is a keystone species:

Answer 45

-has effects on plants and predators
-infectious diseases on them can have LONG-TERM repercussions on entire ecosystems