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Parasite/pathogen
Host pathogen co-evolution
| Question | Answer |
|---|---|
| Co-evolution | - the joint evolution of two (or more) ecologically interacting species, each of which evolves in response to selection imposed by the other - the evolution of one species caused by its interaction with another |
| Each party exerts selective pressure on the other, thereby affecting each others' evolution | |
| Pathogens and hosts in conflict | Pathogens: attempt to consume host resources convert it into more pathogens Hosts: limit damage by slowing or killing the pathogen Strong selection pressure – and responses? |
| Co-evolutionary concepts | A) specific host/pathogen co-evolve B) several species involved, effects not independent ie. one may evolve more C) host evolves new defence - escapes pathogen and can diversify - new pathogens later adapt |
| Assessing host/pathogen co-evolution | • Phylogenetic analysis • Mainly congruent phylogeny – but with some mismatches • Host switching |
| Example | Two types of lice on pigeons – wing and body lice Body lice competitively superior to wing lice But much more host switching in wing lice Both normally transmit vertically – parent-offspring But wing lice also have phoretic horizontal transmission |
| Example | Form of transmission – vertical vs. horizontal = key factor |
| Process of co-evolution: attack | Some parasites have very specific, easy to see, coadaptations Parasitic trematode larvae (Leucochloridium) - migrates to the eye stalk of its intermediate host (land snail) |
| Process of co-evolution: defence | Toxic compounds in host tissues Wild parsnip (Pastinaca Sativa) – webworms Defence = furanocoumarins The acquired immune system (vertebrates) • Major Histocompatability Complex |
| Example | Wild parsnip – webworms • high energetic cost to producing furanocoumarins • Up to 10% energy costs in some plants • Parsnip with high furanocoumarins produce less seeds (Berenbaum & Zangerl 1988) |
| Outcomes | Co-evolution of pathogen and host • Unending arms race • Extinction of one of the species • Stable genetic equilibrium |
| Models of co-evolution | Complex models: • Attack and defence • Cost and benefits • Mechanisms of pathogen mediated selection – Frequency dependence – Heterozygote advantage – Fluctuating selection |
| Evolution of virulence | Impact of a pathogen on its host can differ considerably; Virulence: – the relative ability of a pathogen to cause disease. – the host's loss of fitness due to the pathogen Virulence depends on host-pathogen co-evolution |
| Coincidental evolution | Virulence – accidental by-product of selection for other traits E.g. tetanus in humans, bacteria (Claustridium tetanae) • chemical secretions - selected for life in soil, • But neurotoxins in humans |
| Short sighted evolution | – Generations of evolution within host before transmission – Traits for within-host fitness of parasite evolve – Even if detrimental to transmission to new host (high virulence) Poliovirus • May evolve to exploit nervous system • Not transmitted |
| Trade-off hypothesis | - Pathogens cannot reproduce inside host without doing it some harm WHY? – Pathogens with higher reproduction – should have higher transmission – But if pathogen harms the host too severely – transmission rate is reduced |
| Selection favours | Selection favours pathogens that strike the optimal balance between the cost and benefits of harming their hosts - to optimise transmission rates What factors affect this trade-off ? |
| Factors that effect trade-off and virulence | Multiple infections Competition between different strains of pathogen within host Speed/effectiveness of the hosts immune system Pathogen transmission Form of transmission – horizontal vs. vertical Means of transmission – vector vs. direct contact |
| A non-lethal virus (bacteriophage F1) living in E.coli – transmits in two ways | - vertical: E.coli divides - virus copies in both daughter cells - horizontal: virus induces cell to produce and secrete new phages – but this slows E.coli cell growth |
| Blocking transmission | 1) Anti-virals to block horizontal 2) To block vertical transmission - move phages to new uninfected E. coli cultures every generation |
| Predictions based on the trade-off hypothesis | 1) Correlation between phage reproduction rate and virulence - virus lines that reproduce most - slow host growth most |
| Predictions based on the trade-off hypothesis | 2) mainly vertical transmission lines – evolve lower phage reproduction rates and lower virulence - (allow their host to reproduce more) |
| Predictions based on the trade-off hypothesis | 3) mainly horizontal transmission lines – favour viral strains that reproduce quicker – more virulent - (health of host doesn’t matter!) |
| Theory of evolution of virulence; form of transmission | - viruses given more opportunities for horizontal transmission, the virus developed higher virulence and reproductive rate over viruses not given much opportunities |
| Means of transmission | - direct vs vector borne transmission 1. Vector borne pathogens – carried away from severely debilitated host 2. Pathogens transmitted by direct contact – cannot afford to be too virulent |
| Conclusions | Evidence from – Form of transmission – Means of transmission - Shows there is a trade-off between virulence and transmission |
| Evolution of myoxma virus | - virus infects european rabbit rabbit - reduced population severely >95% infected rabbits - effectiveness soon dropped off.... |
| Resistance develops | Rabbit populations that had previously been exposed to more myxoma epidemics had lower mortality Genetic variation conferring resistance to myxoma existed before introduction of virus Myxoma epidemics exerted strong selective pressure for resistance |
| Virus reaction | Virus samples taken from wild rabbits in different years (wildtype virus) • Tested for virulence in original, standard (unchanging) lab strain of rabbit • Virus evolves lower virulence |
| Virus reaction | • Virus strains that didn’t kill hosts were more readily dispersed to new hosts • Why? • Stabilises at an intermediate level of virulence - equilibrium state? |
| Endosymbiotic theory | - ultimate co-evolution - Mitochondria organelles within eukaryote cells |
Created by:
rose.coo
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