The effect of climate change across multiple epidemics

Climate change is causing shifts in the timing and severity of epidemics, and this will alter the way hosts and parasites (co)evolve. My lab examines how environmental variation affects epidemiological and coevolutionary dynamics across multiple epidemics. This is being done using  controlled lab experiments, a long-term outdoor mesocosm experiment (Stirling Outdoor Disease Experiment), field surveys, and simulation modelling.












In collaboration with Andrew Dobson.

Host sex and host-parasite coevolution

The fact that sex is the dominant reproductive mode and asex is rare is one of the big puzzles in evolutionary biology. An asexual female produces only daughters (to whom she passes on her full genome), whereas, a sexual female produces both daughters and sons (to whom she passes only half of her genome). Asexual females should therefore come to dominate host populations, but in reality they do not. Why? One hypothesis explaining the benefits of sex is that sex leads to genetic recombination which forges unique offspring genotypes. Sex facilitates adaptation in an ever-changing environment, and sexual lineages are thought to evolve faster than asexual ones. Parasites are constantly evolving and are thus an example of such a changing environment. The ubiquity of parasites therefore makes them prime candidates for explaining the advantages of sex.DSCF5147

Using the facultatively sexual crustacean Daphnia magna and its virulent sterilizing parasite Pasteuria ramosa, we are investigating how host sex drives evolution in the host and parasite population. Does host sex generate variation in host resistance to the parasite, and does it drive evolution in the parasite population? This work involves field study, laboratory experiments and theory.


Evolution in multihost-multiparasite systems

*Featured on the Daily Parasite*

Most studies of host-parasite interactions focus on a single host and a single parasite species. However in nature, most host species encounter multiple parasites, and most parasite species are able to infect multiple hosts (often to differing degrees). How do different host species vary in their ability to transmit a particular parasite? How does between-host variation in resistance influence the evolution of parasite virulence? Are the genetic mechanisms that maintain host and parasite polymorphism similar for different parasite species in a host-multiparasite system?

We are currently asking these questions using naturally occurring aquatic host-parasite systems. This work uses a two North American Cladoceran species: Daphnia dentifera, and Ceriodaphnia dubia, and two parasite species: Pasteuria ramosa (a sterilizing bacterium) and Metschnikowia bicuspidata (a fecundity-reducing and longevity-reducing yeast). This work involves field study of natural populations, controlled laboratory experiments and theory.

Our early findings  (Auld et al., 2012 PLoS ONE) show that D. dentifera infection with Pasteuria depends on genetic specificity, and that host resistance to Pasteuria does not correlate with host resistance to Metschnikowia. Further, Metschnikowia kills its hosts much earlier than Pasteuria, yet Pasteuria has a much stronger impact on host fitness because of its capacity to sterilize.

Top figure shows genetic specificity for infection in tthe Daphnia dentifera-Pasteuria ramosa system; bottom fitgure shots the fitness impacts of Pasteuria and Metschnikowia infection on D. dentifera.

In collaboration with Meghan Duffy and Spencer Hall.

How predators affect the evolution of Daphnia microparasites

In nature, many organisms are exposed to both parasites and predators. Using the host Daphnia dentifera, its fish predator, Lepomis macrochirus and its two microparasites Metschnikowia bicuspidata and Pasteuria ramosa, we are asking how predation can influence the evolution of parasite traits.

Theory often assumes hosts are either uninfected or infected and contain the maximum number of parasite transmission stages. However in reality, hosts that have been infected for a long time have many more parasite spores than hosts that are recently infected. If predation results in the death of the parasites, does it select for more rapid parasite within-host growth and for higher virulence? We found that predation of infected hosts shapes the ecology of the infecting parasites: predation allows the fungus, Metschnikowia bicuspidata, to dominate over the sterilising bacterium, Pasteuria ramosa, in natural populations. However, simulated predation on the bacterium (but not the fungus) selects for more rapid production of mature spores, thus reducing the fungus’s advantage (Auld et al., in press Am. Nat.).

In collaboration with Meghan Duffy and Spencer Hall.

The fitness consequences of immune responses

*Recommended by Faculty of 1000*

Linking measures of host immune function with infection, and ultimately, host and parasite fitness is a major goal in ecological immunology. And yet, it is still frequently assumed that higher immune activity means greater host resistance against parasites (Graham et al., 2011 Funct. Ecol.). Also, invertebrate immune systems are thought to only be able to distinguish between broad classes of infectious agent (e.g. Gram positive and Gram negative bacteria). However, infection is often dependent on the specific combination of host and parasite genotypes (termed genetic specificity). How can genetic specificity be so widespread when immune responses are so general?

Using the European Cladoceran, Daphnia magna and its sterilizing parasite Pasteuria ramosa, we have linked measures of the host cellular response with the likelihood of infection (and thus sterilization) from P. ramosa. The cellular response in Daphnia was first documented in 1884 by one of the fathers of modern immunology, Illya Metchnikoff. However, apart from this (very) early work, little is known about this immune response and its possible role in mediating host parasite interactions. After finding genetic variation for D. magna cellular response against P. ramosa (Auld et al., 2010 Proc. Roy. Soc. Ser-B), we have gone on to demonstrate that haemocyte number related to infection in natural field populations (Auld et al., 2012 Funct. Ecol.) and show how it relates to the phenomenon of genetic specificity (Auld et al., 2012 Evol.).

Top figure shows genetic specificity for Daphnia magna cellular response and infection outcome; bottom figure shows haemocyte number in Pasteuria-infected and healthy Daphnia in the wild.

In collaboration with Tom Little and Andrea Graham.

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