Host-Parasite Interactions PDF

8 Host_parasite 22 (1) Tuesday, 19 December 2023 8 Host_para… 13:09 Complex life cycles - go through multiple hosts Here this parasite cause changes in stickleback behaviour for i parasite lays its eggs, which go back into water to be eaten by again. A single worm weighs the same as the host...

8 Host_parasite 22 (1) Tuesday, 19 December 2023 8 Host_para… 13:09 Complex life cycles - go through multiple hosts Here this parasite cause changes in stickleback behaviour for i parasite lays its eggs, which go back into water to be eaten by again. A single worm weighs the same as the host This is schistocephalus it to be eaten by birds, which is where the y small marine life then by sticklebacks There is a broad range of host parasite interactions Viruses Ectoparasites - ticks Intracellular - malaria Extracellular There are other examples that fit the budget; Butterflies parasitise any colonies, or cuckoos etc Parasites don’t kill their hosts or reproduce before killing it. Parasitioids do intent to kill their host, but only after a long assoc ciations, and kill when they emerge. Parasites don’t kill their hosts or reproduce before killing it. Parasitioids do intent to kill their host, but only after a long assoc Difference between predator-prey and parasite- host is to do w More likely to get specialist and co evolution interactions with Optimal virulence - what is optimal way to behave and And host perspective how to resist parasite ciations, and kill when they emerge. with time period. h parasites. exploit host Optimal virulence ( important ) - Damage a parasite will do to host - Additional mortality the parasite adds to host ( parasitism n - Quite hard to measure in populations Hard to measure to empirical biologist use other measures of dam reduced ( reproductive success ) In a novel interaction with parasite virulence is high then it drops - this is an idea that H-P become mutualism But modern idea is that virulence is shaped by natural selection it tries to extract from the host but still not trying to kill the hos host its pointless ) normally ends in higher mortality ) mage, how other measure of fitness is t will decay to a mutualism as virulence n which parasites have to balance, where st, before it reproduces ( as if it kills the host its pointless ) Myxomatosis Host - rabbit ( O.cuniculus ) Parasite - In lots of places where rabbits get introduced, in many areas th have damaged grazing etc - turn grassland into desert as they h Many rabbit proof fences built to stop rabbits from spreading. In a famous example of control - they developed a disease, my It was originated in south America, but was bred in Britain to b After making It as virulent as possible, it was released in places whe On left shows changes of virulence of virus, - by showing rabbits teste wild and reinoculates lab rabbits X axis is the virulence grade, 1 kills 99% of organisms and 5 kills 50%, hey lead to big outbreaks e.g., where they have no natural predators in Australia. yxomatosis. be very nasty to kill rabbits. ere rabbits were a problem. ed with virus, so take virus from Std = lab virus or rabbit On left shows changes of virulence of virus, - by showing rabbits teste wild and reinoculates lab rabbits X axis is the virulence grade, 1 kills 99% of organisms and 5 kills 50%, Over time virulence drops stabilises around middle virulence On the right - inoculated back into wild rabbits in Australian and Brit There is change going on in both parties Its hard to tell without looking at both the effect in co evolution bu lack of confounding variables and easy to do with these organisms Here we are looking at both side changes, because there may not s queen effects but there are changes. Patterns of change of virulence in different countries - UK France The virulence number ends up in different places in different coun E.g., British rabbits it stays between 2-3 but France and Australia Thought this is due to difference of what transmits the virus. The main vector back in 1953 was rabbit flea but in France and ed with virus, so take virus from tish rabbits ut here you can due to nice design and s. seem no change sometimes due to red Australia. nties it went to 3-4 Australia it was mosquitos Std = lab virus or rabbit Thought this is due to difference of what transmits the virus. The main vector back in 1953 was rabbit flea but in France and Fleas can feed on rabbits after death, can select for higher virul The way in which virulence evolves R nought - parasite intrinsic reproductive rate. ( mean number of individual ) needs to be above 1 for an infection to spread. Each c infection to spread otherwise it is dying ( how infectious is it ) Top half = rate of which new cases are created B = transmission rate = how easily they get from one to anothe N = population density Bottom = how they are being taken away from population A = die from disease ( virulence ) B = die also just in general V = individuals recover Makes you think high virulence - Virulence is not independ - Co variances - normally vi down Australia it was mosquitos lence. f new cases made from one infected case needs to make 1 new case for er host is a bad thing, but forget that dent of recovery or transmission rate irulence and transmission rate go up together and recovery rate goes V = individuals recover Makes you think high virulence - Virulence is not independ - Co variances - normally vi down Myxmatosis Rabbits recover slower from worse version of virus Recovery rate ( V ) decreases with increased virulence ( a ) Transmission rate ( B ) increases with virulence ( a ) There is a hump in R0 - it first increases then Means its unlikely the a new disease will kill Commonly things that kill us a lot have to be meaning But the faster they kill us the less likely they There is a trade off between virulence and transmission Examples of this trade off Figs and fig wasps Fig wasps lay eggs in figs is a bad thing, but forget that dent of recovery or transmission rate irulence and transmission rate go up together and recovery rate goes n declines with virulence us all e able to spread, y can jump to next person Examples of this trade off Figs and fig wasps Fig wasps lay eggs in figs Parasitic nematodes infect wasps and get carried around betw Different wasps have different habits, some lay lots of eggs in Where there are lots of females laying eggs in a fig there is a b wasps which correlates with virulence. Difference in virulence in vector borne and directly transmitted dis Direct - common cold etc Vector - use a vector e.g., malaria Virulence varies between 0.1-10% Shifted upwards for vector borne diseases ween figs, a fig some don’t big opportunity for transmission between seases, Virulence varies between 0.1-10% Shifted upwards for vector borne diseases Directly transmitted diseases are much less dangerous Idea as they need us to be in contract with each other, but Virulence of disease associated with ability to infect others Outbreaks that are water borne are much more virulent t not in vectors its better if we are alone, s Vector borne diseases being more virulent due to size of inoculum Vector gives you more particles of a virus compared to picking up Another idea affect virulence is vertical and horizontal tranmission m, the cold from a door n differneces Another idea affect virulence is vertical and horizontal tranmission Horizontal - transmission between people directly, Favours increased virulence As host doesn’t have to live Vertical - is parent to offspring Favours decreased virulence Because it needs to keep its host alive to get anything out of it E.g., Wolbachia vertically transmission normally Here horizontal transmission was forced Over generations virulence increases n differneces Over generations virulence increases Why don’t host evolve to become completely resistant to all forms to everything from evolving There are different trade offs As resistance goes up, the fecundity breeding value goes down Trade off of resistance and fecundity Fecundity - ability to produce new offspring Similar study in salmon and trout and parasite D.pseudospathaceuem s of disease; what prevents resistnace m Similar study in salmon and trout and parasite D.pseudospathaceuem Trade off between resistance ( killing parasite ) and tolerance ( pu infection, not necessarily to put selection on parasite ) Parasite - microphallus - with complex life cycle Organism - new Zealand snail p.antipodarum m ut in place mechanisms to cope with Different clones within a lake. Trade off between susceptibility and fecundity Continuous frequency dependent selection As host becomes common, it gets more exploited by parasite, a Predictions; - Common genotypes are more heavily infected - Increases in frequency ( commonness ) leads to increase Infection rate in common and uncommon clones of snails in lak - Infection rate in common clone is high - Infection rate in rare clones is low and vice versa in infection kes Daphnia infected by Pasteuria ramosa, Stops daphnia from reproducing Daphnia and pasteruria both produce resting stages like spores lakes Deep to core = past Up to surface = forward in time Daphnia get infected by parasites by both past and future soil a s, and produce these into mud cores in areas Daphnia get infected by parasites by both past and future soil a Parasite is best at exploiting daphnia that are here now, not pa Suggests cycling interaction. areas ast or future daphnia, Geographic mosaic co evolution of host and parasite Lots of different lochs in this island shown, Lot of variation of water chemistry In lochs E.g., eastern is very acidic and west they are alkaline They all have three spine sticklebacks in lochs which are very diffe Infected by g.aracatus, they reproduce asexually but are bo Doing artificial infections of parasite. Isolates of parasite in different locations you have obse reiv and scad parasites with obse reiv and scad ho erent orn pregnant so they can expand very quickly osts coloured in on x ais