d. Nematodes in UK hares (Townsend et al., 2009)

3. d. Nematodes in UK hares (Townsend et al., 2009)

4. 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

5. 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?

6. 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?

7. Smallpox Common cold

8. What is virulence ? • Generally = ’harm’ as measured in increased mortality, lowered fecundity • Specifically = loss of host fitness due to infection • virulence vs. contagiousness

9. 4. Factors leading to increased exploitation a. Transmission via dead (or dying) hosts

10. Glugea (microsporidian) in sticklebacks

11. ‘Whitespot’ (ciliate) in fish

12. 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

13. 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?

14. 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

15. 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?)

16. Anecdotal Evidence • evolution of avirulence in ‘new’ interactions • structure of MHC complex

18. Empirical Evidence a. Monitoring change in host response in ‘new’ systems • e.g. avian malaria

19. avian malaria in Hawaii

20. Abundance of native birds vs Plasmodium

23. e.g. myxoma virus in rabbits

25. 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

28. 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

29. 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

30. Empirical tests of Arms Race Model of coevolution • Tracking hs and ps responses over long term • Myxoma virus in rabbits (part B)

31. Evolution of avirulence

33. Horizontal vs vertical transmission • lice (v) vs mites (h) in gerbils • fig wasps and their nematodes (Herre) • Parasites and host sexual reproduction

34. 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’