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Under conditions of global warming, organisms are expected to track their thermal preferences, invading new habitats at higher latitudes and altitudes and altering the structure of local communities. To fend off potential invaders, indigenous communities/populations will have to rapidly adapt to the increase in temperature. In this study, we tested if decades of artificial water heating changed the structure of communities and populations of the Daphnia longispina species complex. We compared the species composition of contemporary Daphnia communities inhabiting five lakes heated by power plants and four non-heated control lakes. The heated lakes are ca. 3–4 °C warmer, as all lakes are expected to be by 2100 according to climate change forecasts. We also genotyped subfossil resting eggs to describe past shifts in Daphnia community structure that were induced by lake heating. Both approaches revealed a rapid replacement of indigenous D. longispina and D. cucullata by invader D. galeata immediately after the onset of heating, followed by a gradual recovery of the D. cucullata population. Our findings clearly indicate that, in response to global warming, community restructuring may occur faster than evolutionary adaptation. The eventual recolonisation by D. cucullata indicates that adaptation to novel conditions can be time-lagged, and suggests that the long-term consequences of ecosystem disturbance may differ from short-term observations.

Understanding the factors that modify infection probability and virulence is crucial for identifying the drivers of infection outbreaks and modeling disease epidemic progression, and increases our ability to control diseases and reduce the harm they cause. One factor that can strongly influence infection probability and virulence is the presence of other pathogens. However, while coexposures and coinfections are incredibly common, we still have only a limited understanding of how pathogen interactions alter infection outcomes or whether their impacts are scale dependent. We used a system of one host and two pathogens to show that sequential coinfection can have a tremendous impact on the host and the infecting pathogens and that the outcome of (co-)infection can be negative or positive depending on the focal organization level.

Organisms are increasingly facing multiple stressors, which can simultaneously interact to cause unpredictable impacts compared with a single stressor alone. Recent evidence suggests that phenotypic plasticity can allow for rapid responses to altered environments, including biotic and abiotic stressors, both within a generation and across generations (transgenerational plasticity). Parents can potentially “prime” their offspring to better cope with similar stressors or, alternatively, might produce offspring that are less fit because of energetic constraints. At present, it remains unclear exactly how biotic and abiotic stressors jointly mediate the responses of transgenerational plasticity and whether this plasticity is adaptive. Here, we test the effects of biotic and abiotic environmental changes on within‐ and transgenerational plasticity using a Daphnia–Metschnikowia zooplankton‐fungal parasite system. By exposing parents and their offspring consecutively to the single and combined effects of elevated temperature and parasite infection, we showed that transgenerational plasticity induced by temperature and parasite stress influenced host fecundity and lifespan; offsprings of mothers who were exposed to one of the stressors were better able to tolerate elevated temperature, compared with the offspring of mothers who were exposed to neither or both stressors. Yet, the negative effects caused by parasite infection were much stronger, and this greater reduction in host fitness was not mitigated by transgenerational plasticity. We also showed that elevated temperature led to a lower average immune response, and that the relationship between immune response and lifetime fecundity reversed under elevated temperature: the daughters of exposed mothers showed decreased fecundity with increased hemocyte production at ambient temperature but the opposite relationship at elevated temperature. Together, our results highlight the need to address questions at the interface of multiple stressors and transgenerational plasticity and the importance of considering multiple fitness‐associated traits when evaluating the adaptive value of transgenerational plasticity under changing environments. Different environmental stressors, including biotic and abiotic, can interact and cause unpredictable impacts. Yet, it is unclear when transgenerational effects might help or hinder the fitness of the next generation. Our study shows the evidence of stressor‐induced transgenerational plasticity, but its adaptive significance depends on the identity and combinations of environmental stressors.

The net outcome of symbiosis depends on the costs and benefits to each partner. Those can be context dependent, driving the potential for an interaction to change between parasitism and mutualism. Understanding the baseline fitness impact in an interaction can help us understand those shifts; for an organism that is generally parasitic, it should be easier for it to become a mutualist if its baseline virulence is relatively low. Recently, a microsporidian was found to become beneficial to its Daphnia hosts in certain ecological contexts, but little was known about the symbiont (including its species identity). Here, we identify it as the microsporidium Ordospora pajunii . Despite the parasitic nature of microsporidia, we found O. pajunii to be, at most, mildly virulent; this helps explain why it can shift toward mutualism in certain ecological contexts and helps establish O. pajunii is a valuable model for investigating shifts along the mutualism-parasitism continuum.

Recent studies have shown that the filamentous cyanobacterium Aphanizomenon gracile Lemmermann, strain SAG 31.79, consists of two types of filaments that differ in thickness. These two types are known to vary in resistance to Daphnia magna grazing: thin filaments (<2.5 µm) are more vulnerable to grazing than the thick ones (>2.5 µm). In this study, we investigated whether the difference in the vulnerability to grazing of thin and thick filaments is a result of different thickness of their cell walls, a filament stiffness determinant. We expected thick filaments to have thicker cell walls than the thin ones. Additionally, we analysed whether cell wall thickness correlates with filament thickness regardless of the filament type. A morphometric analysis of cell walls was performed using transmission electron micrographs of ultra-thin sections of the batch-cultured cyanobacterial material.  Our study revealed that the thin type of filaments had thinner cell walls than the thick filaments. Moreover, cell wall thickness was positively correlated with filament thickness. TEM (transmission electron microscopy) observations also revealed that the thin type of filaments was often at different stages of autocatalytic cell destruction, which was mainly manifested in the increase in cell vacuolization and degradation of the cytoplasm content. Based on our findings, we assume that previously reported higher resistance of thick filaments to Daphnia grazing results from greater stiffness and excellent physiological conditions of thick filaments. 

Transgenerational plasticity can help organisms respond rapidly to changing environments. Most prior studies of transgenerational plasticity in host–parasite interactions have focused on the host, leaving us with a limited understanding of transgenerational plasticity of parasites. We tested whether exposure to elevated temperatures while spores are developing can modify the ability of those spores to infect new hosts, as well as the growth and virulence of the next generation of parasites in the new host. We exposed Daphnia dentifera to its naturally co-occurring fungal parasite Metschnikowia bicuspidata, rearing the parasite at cooler (20°C) or warmer (24°C) temperatures and then, factorially, using those spores to infect at 20 and 24°C. Infections by parasites reared at warmer past temperatures produced more mature spores, but only when the current infections were at cooler temperatures. Moreover, the percentage of mature spores was impacted by both rearing and current temperatures, and was highest for infections with spores reared in a warmer environment that infected hosts in a cooler environment. In contrast, virulence was influenced only by current temperatures. These results demonstrate transgenerational plasticity of parasites in response to temperature changes, with fitness impacts that are dependent on both past and current environments.

Infectious disease can threaten host populations. Hosts can rapidly evolve resistance during epidemics, with this evolution often modulated by fitness trade-offs (e.g., between resistance and fecundity). However, many organisms switch between asexual and sexual reproduction, and this shift in reproductive strategy can also alter how resistance in host populations persists through time. Recombination can shuffle alleles selected for during an asexual phase, uncoupling the combinations of alleles that facilitated resistance to parasites and altering the distribution of resistance phenotypes in populations. Furthermore, in host species that produce diapausing propagules (e.g., seeds, spores, or resting eggs) after sex, accumulation of propagules into and gene flow out of a germ bank introduce allele combinations from past populations. Thus, recombination and gene flow might shift populations away from the trait distribution reached after selection by parasites. To understand how recombination and gene flow alter host population resistance, we tracked the genotypic diversity and resistance distributions of two wild populations of cyclical parthenogens. In one population, resistance and genetic diversity increased after recombination whereas, in the other, recombination did not shift already high resistance and genetic diversity. In both lakes, resistance remained high after temporal gene flow. This observation surprised us: due to costs to resistance imposed by a fecundity-resistance trade-off, we expected that high population resistance would be a transient state that would be eroded through time by recombination and gene flow. Instead, low resistance was the transient state, while recombination and gene flow re-established or maintained high resistance to this virulent parasite. We propose this outcome may have been driven by the joint influence of fitness trade-offs, genetic slippage after recombination, and temporal gene flow via the egg bank.

Pathogens can alter the phenotype not only of exposed hosts, but also of future generations. Transgenerational immune priming, where parental infection drives reduced susceptibility of offspring, has been particularly well explored, but pathogens can also alter life history traits of offspring. Here, we examined the potential for transgenerational impacts of a microsporidian pathogen, Ordospora pajunii, by experimentally measuring the impact of maternal exposure on offspring fitness in the presence and absence of parasites, and then developing mathematical models that explored the population-level impacts of these transgenerational effects. We did not find evidence of transgenerational immune priming: offspring of exposed mothers became infected at high rates, similar to offspring of unexposed mothers, and the infection burden did not differ between these two groups. We also did not find any evidence of transgenerational tolerance, where daughters of exposed mothers have higher fitness after infection. Instead, we found evidence for negative transgenerational impacts of infection: uninfected offspring of exposed mothers had substantially greater early life mortality than uninfected offspring of unexposed mothers. Offspring of exposed mothers also had reduced growth rate, fewer clutches, and fewer offspring. We propose that these observations should be considered transgenerational virulence, where a pathogen reduces the fitness of the offspring of infected hosts. Our parameterized mathematical model allowed us to explore the impacts of transgenerational virulence at the population level. If transgenerational virulence manifests as decreased reproduction or increased mortality in offspring, as we saw in the empirical portion of our study, this reduces total host density, infection prevalence, and infected host density, which could have implications for both host conservation and spillover risk. We propose that transgenerational virulence might be common and is a concept worthy of further empirical and theoretical exploration.

Spirobacillus cienkowskii (Spirobacillus, hereafter) is a widely distributed bacterial pathogen that has significant impacts on the population dynamics of zooplankton (Daphnia spp.), particularly in months when Daphnia are asexually reproducing. Yet little is known about Spirobacillus’ virulence, transmission mode and dynamics. As a result, we cannot explain the dynamics of Spirobacillus epidemics in nature or use Spirobacillus as a model pathogen, despite Daphnia’s tractability as a model-host. Here, we work to fill these knowledge gaps experimentally. We found that Spirobacillus is among the most virulent of Daphnia pathogens, killing its host within a week and reducing host fecundity. We further found that Spirobacillus did not transmit horizontally among hosts unless the host died or was destroyed (i.e., it is an “obligate killer”). In experiments aimed at quantifying the dynamics of horizontal transmission among asexually reproducing Daphnia, we demonstrated that Spirobacillus transmits poorly in the laboratory. In mesocosms, Spirobacillus failed to generate epidemics; in experiments wherein individual Daphnia were exposed, Spirobacillus’ transmission success was low. In the (limited) set of conditions we considered, Spirobacillus’ transmission success did not change with host density or pathogen dose and declined following environmental incubation. Lastly, we conducted a field survey of Spirobacillus’ prevalence within egg-cases (ephippia) made by sexually reproducing Daphnia. We found Spirobacillus DNA in ∼40% of ephippia, suggesting that, in addition to transmitting horizontally among asexually reproducing Daphnia, Spirobacillus may transmit vertically from sexually reproducing Daphnia. Our work fills critical gaps in the biology of Spirobacillus and illuminates new hypotheses vis-à-vis its life-history. Spirobacillus cienkowskii is a bacterial pathogen of zooplankton, first described in the 19th Century and recently placed in a new family of bacteria, the Silvanigrellaceae. Spirobacillus causes epidemics in lake zooplankton populations and increases the probability that zooplankton will be eaten by predators. However, little is known about how Spirobacillus transmits among hosts, its impact on host survival and reproduction (i.e., how virulent it is) in laboratory conditions and what role virulence plays in Spirobacillus’ life cycle. Here, we experimentally quantified Spirobacillus’ virulence and showed that Spirobacillus must kill its host to transmit horizontally. We also found evidence that Spirobacillus may transmit vertically via Daphnia’s seed-like egg cases. Our work will help scientists to (i) understand Spirobacillus epidemics, (ii) use Spirobacillus as a model pathogen for the study of host-parasite interactions and (iii) better understand the unusual group of bacteria to which Spirobacillus belongs.