Blog written by Victoria L. Pike. Read the full paper here.
Virtually all organisms are being constantly attacked by parasites. Hosts can deal with it in a variety of ways, but they ideally want to limit the damage caused by the parasite. One strategy that can limit damage to host reproductive success is ‘fecundity compensation’ (Minchella, 1985; Vale and Little, 2012), a response to infection exhibited by species across the animal kingdom including fish, snails, planktonic crustaceans and mice. Fecundity compensation involves an increase in the number of offspring produced when hosts are exposed to parasites, allowing the host to counteract any reduction in lifespan caused by infection.
Despite the widespread occurrence of fecundity compensation, understanding how hosts can manipulate their reproduction in response to the threat of parasites remains largely unknown. Previous work has shown that potential links between other damage limiting responses (e.g., physically evading pathogens), stress responses, and the immune response (Gleichsner et al., 2016; Schulenburg and Ewbank, 2007).
In our study, we investigated whether fecundity compensation was linked with the stress hosts experience when faced with parasite infection. We used a microscopic worm, Caenorhabditis elegans, as the host in our experiment and a parasitic bacterium, Staphylococcus aureus, that produces toxins that destroy gut cells when inside the worm. This animalwas a good choice of host for this experiment as it has a rapid life cycle which it completes in around 3.5 days (Hope, 1999), meaning that experiments can be replicated quickly. Additionally, the worm’s diet is made up of microbes, so it can be easily infected by eating the parasite. Moreover, mutants of this animal have been made which allow us to knock down or ramp up the host stress response relative to a wild-type worm.
In our study, we used three different mutants of the wormwith either a normal, suppressed or heightened stress response to explore links between stress response and fecundity compensation upon parasite attack. We also maintained control groups of each worm mutants only given food to eat, not parasites. We then counted the number of offspring mutant and wild-type worms produced once exposed to parasites or only fed food.
Our results showed that fecundity compensation is linked to host stress in C. elegans worms. Once they survived parasite exposure, both wild-type worms and those with the heightened stress response, increased their reproductive output in the presence of the parasite. Worms with a suppressed stress and dampened immune response, however, did not produce more offspring relative to the control after parasite exposure.
These results have helped to reveal a valuable system for future research on fecundity compensation. The worm’s rapid lifecycle makes it suitable for experimental evolution approaches, as experiments can take place in large populations and over multiple generations quickly. Using this model, one could thus investigate the conditions under which fecundity compensation might evolve and be maintained. Biologists can also further investigate the mechanism of fecundity compensation in the worms. We have uncovered a potential mechanism linking fecundity compensation to stress, but more experiments with a greater diversity of mutants, targeting different pathways of the stress response, could help to clarify this mechanism. Furthermore, we only conducted our experiment with one type of parasite – it would be interesting to see whether fecundity compensation varies with different parasites that vary in the harm they cause.
Parasites are everywhere. With global change increasing the contact organisms have with infections (Altizer et al., 2013; Harvell, 2002) and ramping up the environmental stress hosts can experience (Gleichsner et al., 2016), it is crucial we understand the ways parasites can alter host reproduction. In our study, we have uncovered a link between enhanced offspring production and the host’s stress response. This research provides a springboard for further investigation into how fecundity compensation works.
Altizer, S., Ostfeld, R.S., Johnson, P.T.J., Kutz, S., Harvell, C.D., 2013. Climate Change and Infectious Diseases: From Evidence to a Predictive Framework. Science 341, 514. https://doi.org/10.1126/science.1239401
Gleichsner, A.M., Cleveland, J.A., Minchella, D.J., 2016. One stimulus—Two responses: Host and parasite life-history variation in response to environmental stress. Evolution 70, 2640–2646. https://doi.org/10.1111/evo.13061
Harvell, C.D., 2002. Climate Warming and Disease Risks for Terrestrial and Marine Biota. Science 296, 2158–2162. https://doi.org/10.1126/science.1063699
Hope, I.A., 1999. C. elegans : a practical approach. Oxford University Press.
Minchella, D.J., 1985. Host life-history variation in response to parasitism. Parasitology 90, 205. https://doi.org/10.1017/S0031182000049143
Schulenburg, H., Ewbank, J.J., 2007. The genetics of pathogen avoidance in Caenorhabditis elegans. Molecular Microbiology 66, 563–570. https://doi.org/10.1111/j.1365-2958.2007.05946.x
Vale, P.F., Little, T.J., 2012. Fecundity compensation and tolerance to a sterilizing pathogen in Daphnia. Journal of Evolutionary Biology 25, 1888–1896. https://doi.org/10.1111/j.1420-9101.2012.02579.x