Genetic and environmental drivers

Why do we see so much infection in some places, some hosts, some species, and much less in others? What are the ecological and genetic drivers of this variation?

Fine-scale spatial variation in infection prevalence

My study lake, Lake Alexandrina, is not big, only 6.4 square kilometers (shown below). Some of our study sites are within 150 meters of one another. Nonetheless, decades of field sampling show dramatic spatial and temporal variation in the proportion of snails infected with Microphallus along the shoreline of Lake Alexandrina (Jokela et al. 2009, Gibson et al 2016 Am Nat). For example, nearly 70% of snails may be castrated by Microphallus at one site, while, at a nearby site, practically 0% are infected. What explains such variation between nearby sites?

Do hosts from different sites vary in how susceptible they are, genetically, to local Microphallus? Given the high rates of gene flow between snails from different sites at Lake Alexandrina (shown by analysis of neutral markers – Fox et al. 1996, Paczesniak et al. 2014), we might expect that migration and gene flow between nearby sites would erode genetic variation for susceptibility. Hence environmental variables should be a bigger factor in explaining variation in Microphallus prevalence at this spatial scale.

Not so! (see Gibson et al. 2016 Am Nat)There is up to 6.5-fold variation in susceptibility of snails from different sites to local Microphallus. Moreover, mean susceptibility explains one-third of the variation in infection prevalence between sites: sites with a greater proportion of snails susceptible to Microphallus also had higher prevalence of Microphallus, on average. Because susceptibility has a strong genetic basis, we take this as evidence for a substantial contribution of host genetic variation to variation in infection prevalence.

We have preliminary data suggesting that the remaining ~2/3 of the variation in infection prevalence between sites may arise from spatial variation in exposure, with snails at some sites getting exposed to more parasites than others. Snails acquire Microphallus from duck feces – we currently know relatively little about how duck distribution and behavior contributes to the distribution of Microphallus eggs in the water.

*Potamopyrgus antipodarum* (left) and its trematode parasite *Microphallus*. In the center, you can see a healthy snail (shell removed) vs. an infected snail, which is packed full of larval trematodes or metacercariae. They have replaced the snails gonads, castrating it! *Microphallus* is a complex life cycle parasite – it travels trophically from snails to duck guts to duck poop back to snails. Image on the left courtesy of Bart Zjilstra. Central image courtesy of Gape Harp, used under Creative Commons BY-SA 4.0. Modified from originals: images combined, line and text elements added.

References

Fox, J., M. F. Dybdahl, J. Jokela, and C. M. Lively. 1996. Genetic structure of coexisting sexual and clonal subpopulations in a freshwater snail (Potamopyrgus antipodarum). Evolution 50:1541-1548.
Jokela, J., M. F. Dybdahl, and C. M. Lively. 2009. The maintenance of sex, clonal dynamics, and host-parasite coevolution in a mixed population of sexual and asexual snails. Am Nat 174:S43-S53.
Paczesniak, D., S. Adolfsson, K. Liljeroos, K. Klappert, C. M. Lively, and J. Jokela. 2014. Faster clonal turnover in high-infection habitats provides evidence for parasite-mediated selection. J Evol Biol 27:417-428.