Climate change is (appropriately) a big topic in the ecological literature. We have a pressing need to understand how climate change is going to affect individuals, populations, communities, and ecosystems. And of course, we need to know how climate change is going to alter disease dynamics, so that we can be ready to control/manage important parasites and pathogens if we need to.
As I’ve discussed before, at one point, there was a lot of concern that the geographic ranges of diseases (like malaria) were going to increase dramatically with climate change. In 2009, Lafferty published a paper where he pointed out that warmer isn’t always better for parasites. He argued that we’re probably more likely to see range shifts than range expansions. Similarly, a few months ago, I posted about a paper by Pickles et al. (2013) that supported Lafferty’s hypothesis. Pickles et al. (2013) used models to show that in some parts of its range, the adult meningeal worm is likely to go extinct because its hosts will not be there, and in other places, the adult meningeal worm will be able to invade new areas along with its hosts. In total, the parasite’s range is expected to shift, but not to increase.
The Pickles et al. (2013) paper was about how hosts and parasites might end up having a mismatch in space, so that parasites suddenly can’t find their hosts in areas that used to have hosts. There has also been a lot of interest in how climate change might cause temporal mismatches among interacting species (e.g., predators and prey, plants and pollinators). These mismatches result from climate-induced changes in the phenology of species. And now we ask: will climate change cause temporal mismatches between hosts and parasites?
Paull and Johnson (2014) performed a mesocosm experiment to consider how one aspect of climate change – increased temperature – might affect disease dynamics in a trematode system. They studied a particularly important trematode (Ribeiroia ondatrae) that causes mortality and severe limb malformations in some amphibian species. The internet is rather devoid of good diagrams of the life cycle of R. ondatrae, but here’s a link to one such copyrighted diagram. (If asked very nicely, I might cartoon one myself.) Briefly, the adult trematode uses a heron as the definitive host. The adult trematode releases eggs in the aquatic environment (e.g., pond), and those eggs hatch into free-living miracidia that swim around looking for a snail to infect. After the parasite has sufficient time to develop and asexually reproduce in the snail, the snails release another free-living parasite stage called a cercaria. (You guys should be familiar with cercariae at this point because they’re my go-to cartoon parasite.) Cercariae swim around until they find a tadpole to infect, and then they encyst in the tadpole’s tissues. If the tadpole lives long enough, it metamorphoses into an adult frog – possibility with limb malformations – and gets eaten by a heron. Etc.
Paull and Johnson (2014) put snails in 36 mesocosms (miniature ponds) in August. Half of the mesocosms had greenhouse lids that caused them to be heated to 3˚C warmer than the other mesocosms. Then they added R. ondatrae eggs to the mesocosms so that the eggs could hatch into miracidia and infect the snails. For the next year, they checked every few weeks to quantify 1) snail mortality, 2) what percentage of snails were infected, and 3) how many cercariae the infected snails were releasing per night. Also, starting in April, they added one bullfrog tadpole to each mesocosm each month, let the tadpoles hang out for two days getting infected, and then dissected them to quantify infection. Then in May, they added 20 chorus frog tadpoles to each mesocosm and left them until they started metamorphosing. Then they quantified survival, limb malformations, and infection of the chorus frog tadpoles. They also quantified a bunch of other stuff, but all that is less important to the story.
When the mesocosms weren’t heated, infected snails started releasing cercariae in late spring. In the heated mesocosms, infected snails started releasing cercariae nine months earlier, in the fall! The warmer temperatures vastly increased the developmental rates of the parasites. Furthermore, more second-generation snails got infected in the heated treatment. So, did this increase in parasite development rates and the percentage of infected second-generation snails result in more tadpole infection? Actually, no! First of all, more adult snails died in the heated treatment and there were fewer total second-generation snails in that treatment, too. So, the total number of shedding snails was actually lower in the heated treatment. Second, in the unheated treatment, snail infection peaked just when the tadpoles were available in the spring, whereas snail infection in the heated treatment rapidly declined in the spring. The total number of cercariae was the same in both treatment groups, but due to the temporal mismatch and increased snail mortality, tadpole infection actually declined under the warmer temperature scenario.
So, this was a very cool study. Climate change experiments are really difficult to tackle because running long-term experiments with frequent sampling events is hard work! And trying to manipulate multiple species in biologically relevant ways can be tricky. In this case, the results of this experiment would likely be very sensitive to the timing of the input of R. ondatrae eggs. Paull and Johnson (2014) did just one pulse of eggs in the fall. If eggs also enter the system in the early spring, infection dynamics might be quite different under the +3˚C warming scenario.
Ok! I’m ready to see more work like this.
Paull, S.H., and P.T.J. Johnson. 2014. Experimental warming drives a seasonal shift in the timing of host-parasite dynamics with consequences for disease risk. Ecology Letters.