While there are many mechanisms by which disease can influence invasions (Prenter et al. 2004), relatively little is known regarding how epidemics in native species can influence invasions. In our laboratory microcosm experiment we found few effects of our treatments on the invasive species; our treatments did not affect invasive species densities, but there were more ephippia in the absence of the parasite compared to when the parasite was present. Integrated densities of the native species were reduced by the presence of the parasite, and the late invasion treatments had lower native densities than the early invasion treatment when the parasite was present. Additionally, native species infection prevalence and number of infected individuals were impacted by the timing of the introduction of the invasive species. Together, these results imply that parasitism and the timing of a species invasion can interact to affect the success and impact of an invasion.
The parasite reduced the native species densities (Figs. 2a, c & 3b), but this reduction did not allow the invasive species to increase in density. When native densities are low and resources are held constant (as in our experiment) higher invasive densities are predicted because there are more resources for the invaders (Prenter et al. 2004; Searle et al. 2018). However, in our study, the density of the invasive species did not differ across treatments and the number of ephippia at the end of the experiment was higher in the parasite-free treatments, where native densities were also high. These results indicate that the invasive species was unable to increase their population size to utilize the space and resources left when the native species declined in density. This result is likely due to the invasive species becoming infected by the parasite. Throughout the course of the experiment, 10% of all the native species were infected, and 19% of all the invasive species were infected. Because the invasive species were becoming infected at relatively high prevalence, they may have been unable to benefit from the reduction in native densities caused by the parasite, resulting in both species suffering the effects of the epidemic together.
Measuring both ephippia and the invasive species density is useful for measuring the success of an invasion. Typically, with a higher invasive density it can be assumed that the invasive species is establishing well in the new environment. Density represents immediate reproduction, as more individuals are created that utilize more resources, take up space, and diminish native densities. Because ephippia are dormant and can remain viable for years, they can be long-lived and extend the generation time of the invasive species (Panov et al. 2004), which can induce population perseverance in volatile environments, and demonstrates investment in future populations (Cáceres 1998). In this experiment, we found more ephippia from the invasive species in the uninfected treatments (Fig. 5), even though there was no detectable difference in invasive species density across parasite treatments. This pattern of higher ephippia densities in the absence of the parasite may be caused by the higher densities of the native species in these treatments, which led to crowding and triggered production of resting eggs (Smith et al. 2009). Using both invasive species density and ephippia as estimates of invasion success in water crustacean studies can be useful tools for predicting immediate and future invasion success.
There was an interactive effect of the parasite and the timing of invasion on native densities (Figs. 2a, c, & 3b). In particular, the integrated native densities were lower in the late invasion treatments compared to the early invasion treatments, but only when the parasite was present (Fig. 3b). Therefore, while the parasite alone reduced native densities, the parasite plus late invasion combination was particularly detrimental to native populations. This interactive effect may be caused by the negative effects of both the parasite and the invasion occurring simultaneously. Native populations may have been able to mitigate the negative effects of the invasive species before the epidemic occurred but were unable to cope with the invasion when also experiencing the epidemic. Therefore, the timing of an invasion during an epidemic in the native species can affect how it is influenced by the invasion, even when there is no immediate detectable difference in the success of the invader.
Resources are often a key driver of invasion success (Prenter et al. 2004; Guo et al. 2015). In particular, resources are typically considered a crucial component to an invasive species prosperity in a novel environment because they help the species establish, reproduce quickly, and compete with the native species (Byers 2002; Guo et al. 2015). It is predicted that invasive species should establish and proliferate more readily in communities with more resources (McKenzie and Townsend 2007; Guo et al. 2015). In our study, we did not find a detectable difference in chlorophyll levels (a measure of algal food resources) across our treatments on the day of invasion (Online Resource Figs. S2 & S3). This lack of changes to chlorophyll across treatments may have prevented our treatments from influencing invasive density (Fig. 3a).
Disease is known to influence invasion success (Prenter et al. 2004); however, the ways in which parasites in native species and the timing of the invasion affects invasion success are relatively unknown. Our study found that native epidemics and the timing of an invasion may interact to affect the native species (e.g., Fig. 3b), even when there are minimal effects of these variables on the invasive species (e.g., Fig. 3a). Understanding how disease and invasive species interact to influence invasions will be helpful with determining whether certain populations will be at risk of invasion and how disease will impact invasions in aquatic communities.