Transcript 11.coevolution

d. Nematodes in UK hares (Townsend et al., 2009)
4. Conclusions
• just because they ‘can’, doesn’t mean they ‘do’
• problem of managed or artificial model systems
• status of Anderson vs. Holmes controversy
• single factor vs. multiple factors
• indirect effects and population regulation
• interactions bw immunity, nutrition, parasitism
Evolution and coevolution in host/ps interactions
1. Key questions:
• Can parasites mediate natural selection in their hosts ?
• How does virulence evolve over time?
• Is directional selection for resistance common?
• How does the host compete in this asymmetrical relationship ?
• New vs. old interactions ?
2. Application:
• Virulence of Syphilis over 400 years ?
• Plasmodium falciparum vs. climate change ?
• Dicrocoelium in cattle vs elk, etc ?
• Emerging diseases?
3. Historical Perspective
• Classical views from medical and veterinary literature
– ‘pathogenic parasites are poorly adapted’
– ‘A fully evolved ps would not harm the host it needs for
survival, reproduction and transmission’
– ‘Strong virulence is primitive’
• Sharp criticism in 1980’s (Anderson and May)
– link between reproduction and transmission
• Empirical studies in 1990’s confirm that virulence is one of
many adaptive characteristics
• What factors lead toward intense exploitation of hosts in some
interactions, and mild coexistence in others?
Common cold
Smallpox
What is virulence ?
• Generally = ’harm’ as measured in increased
mortality, lowered fecundity
• Specifically = loss of host fitness due to infection
• virulence vs. contagiousness
4. Factors leading to increased exploitation
a. Transmission via dead (or dying) hosts
Glugea (microsporidian) in sticklebacks
‘Whitespot’ (ciliate) in fish
– Glugea in sticklebacks, ‘whitespot’ in fish, Trichinella ?,
brainworm in minnows ?
– predator - prey pathways (all intermediate hosts?) (common,
but high costs to parasite transmission)
b. Interparasite (or interclone) competition
– multiple parasites or multiple clones within one individual
host - who wins?
– e.g. pathogenic outcome of HIV?
– malaria in rodents
5. Factors leading to decreased exploitation:
a. Host resistance and other host traits
– host epidermis, enzymes, blood flow, antibodies etc.
– in the face of strong host resistance, selection should
decrease parasite exploitation
b. Parasite fitness linked to host survival
– e.g. Trypanosomes in newts
– e.g. Monogenean in desert toads
– e.g. Brainworm in minnows?
c. Parasite fitness linked to host activity
– e.g. patterns with vectored vs non-vectored microparasites
• Vectors can infect alternative, non-morbid hosts
• Selection may favour reduced host mobility
– e.g. dlc nematodes less pathogenic than vectored ones
6. Cautions
• the problem of multiple final hosts (e.g. Trichinella, Giardia) and
spurious interpretation
• the problem of complex life-cycles
Parasite-mediated natural selection
• previous examples ?
• do parasites mediate NS in long-standing (natural) systems?
• how do we find out?
– are requirements for PMNS met ?
• variation in parasite intensity
• variation in intensity correlated with variation in fitness
• intensity covaries with another trait
• Heritability (of what?)
• Anecdotal Evidence
– evolution of avirulence in ‘new’ interactions
– structure of MHC complex
• Empirical Evidence
a. Monitoring change in host response in ‘new’ systems
• e.g. avian malaria
• avian malaria in Hawaii
Abundance of native birds vs Plasmodium
• e.g. myxoma virus in rabbits
b. Empirical Evidence
• evidence from heritability studies
• evidence from artificial selection expts
– e.g. resistance/susc in snails exposed to S. mansoni
– e.g. nematodes in mice
Constraints on PMNS
– Environmental heterogeneity (space and time)
• grouse on different moors, climate effects, stochasticity
– Costs of resistance
• reduced productivity (e.g. fever)
• reproductive costs
– Immunopathology (selection for genes that ‘down-regulate’
immunity?)
– Susceptibility to other species
Ps/hs coevolution
• recall framework from plant/insect interactions
• e.g. 5-step process from Erlich and Raven
• e.g. snake/newt interaction
Models of hs/ps coevolution
• Allopatric speciation model
– leads to cospeciation and phylogenetic tracking
• Arms-Race model
– involves 5-step ER process
– mutual aggression (maybe gene for gene?)
– can lead also to cospeciation
Empirical tests of Arms Race Model of coevolution
• Tracking hs and ps responses over long term
– Myxoma virus in rabbits (part B)
Evolution of avirulence
• Horizontal vs vertical transmission
– lice (v) vs mites (h) in gerbils
– fig wasps and their nematodes (Herre)
• Parasites and host sexual reproduction
Conclusions
• Host:
– directional selection to start; balancing selection to end
– selection is for diversity of response
– (at the cost of high intensity, sometimes pathogenic
infections)
– sexual repro can produce rare genotypes
• Parasite:
– link between reproduction, transmission, and virulence
(untested)
• coevolution occurs on local scales
• many paths and outcomes of arms races
• continuum of ‘exploitation’ to ‘commensalism’