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Although individual parasite species commonly infect many populations across physical space as well as multiple host species, the extent to which parasites traverse physical and phylogenetic distances is unclear. Population genetic analyses of parasite populations can reveal how parasites move across space or between host species, including helping assess whether a parasite is more likely to infect a different host species in the same location or the same host species in a different location. Identifying these transmission barriers could be exploited for effective disease control. Here, we analysed population genetic structuring of the parasite Pasteuria ramosa in daphniid host species from different lakes. Outbreaks occurred most often in the common host species Daphnia dentifera and Daphnia retrocurva. The genetic distance between parasite samples tended to be smaller when samples were collected from the same lake, the same host species and closer in time. Within lakes, the parasite showed structure by host species and sampling date; within a host species, the parasite showed structure by lake and sampling date. However, despite this structuring, we found the same parasite genotype infecting closely related host species, and we sometimes found the same genotype in nearby lakes. Thus, P. ramosa experiences challenges infecting different host species and moving between populations, but doing so is possible. In addition, the structuring by sampling date indicates potential adaptation to or coevolution with host populations and supports prior findings that parasite population structure is dynamic during outbreaks.

Despite substantial progress for women in science, women remain underrepresented in many aspects of the scholarly publication process. We examined how the gender diversity of editors and reviewers changed over time for six journals in ecology and evolution (2003–2015 for four journals, 2007–2015 or 2009–2015 for the other two), and how several aspects of the peer review process differed between female and male editors and reviewers. We found that for five of the six journals, women were either absent or very poorly represented as handling editors at the beginning of our dataset. The representation of women increased gradually and consistently, with women making up 29% of the handling editors (averaged across journals) in 2015, similar to the representation of women as last authors on ecology papers (23% in 2015) but lower than the proportion of women among all authors (31%) and among members of the societies that own the journals (37%–40%). The proportion of women among reviewers has also gradually but consistently increased over time, reaching 27% by 2015. Female editors invited more female reviewers than did male editors, and this difference increased with age of the editor. Men and women who were invited to review did not differ in whether they responded to the review invitation, but, of those that responded, women were slightly more likely to agree to review. In contrast, women were less likely than men to accept invitations to serve on journal editorial boards. Our analyses indicate that there has been progress in the representation of women as reviewers and editors in ecology and evolutionary biology, but women are still underrepresented among the gatekeepers of scholarly publishing relative to their representation among researchers. We examined how the gender diversity of editors and reviewers changed over time for six journals in ecology and evolution, and how several aspects of the peer review process differed between female and male editors and reviewers. Our analyses indicate that there has been progress in the representation of women as reviewers and editors in ecology and evolutionary biology, but women are still underrepresented among the gatekeepers of scholarly publishing relative to their representation among researchers.

Disease ecologists now recognize the limitation behind examining host–parasite interactions in isolation: community members—especially predators—dramatically affect host–parasite dynamics. Although the initial paradigm was that predation should reduce disease in prey populations (“healthy herds hypothesis”), researchers have realized that predators sometimes increase disease in their prey. These “predator–spreaders” are now recognized as critical to disease dynamics, but empirical research on the topic remains fragmented. In a narrow sense, a “predator–spreader” would be defined as a predator that mechanically spreads parasites via feeding. However, predators affect their prey and, subsequently, disease transmission in many other ways such as altering prey population structure, behavior, and physiology. We review the existing evidence for these mechanisms and provide heuristics that incorporate features of the host, predator, parasite, and environment to understand whether or not a predator is likely to be a predator–spreader. We also provide guidance for targeted study of each mechanism and quantifying the effects of predators on parasitism in a way that yields more general insights into the factors that promote predator spreading. We aim to offer a better understanding of this important and underappreciated interaction and a path toward being able to predict how changes in predation will influence parasite dynamics. Although the initial paradigm was that predation should reduce disease in prey populations (“healthy herds hypothesis”), researchers have realized that predators sometimes increase disease in their prey. These “predator‐spreaders” are now recognized as critical to disease dynamics, but empirical research on the topic remains fragmented. We review the existing evidence for these mechanisms and provide heuristics that incorporate features of the host, predator, parasite, and environment to understand whether or not a predator is likely to be a predator‐spreader.

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.

Predators can strongly influence disease transmission and evolution, particularly when they prey selectively on infected hosts. Although selective predation has been observed in numerous systems, why predators select infected prey remains poorly understood. Here, we use a mathematical model of predator vision to test a long‐standing hypothesis about the mechanistic basis of selective predation in a Daphnia–microparasite system, which serves as a model for the ecology and evolution of infectious diseases. Bluegill sunfish feed selectively on Daphnia infected by a variety of parasites, particularly in water uncolored by dissolved organic carbon. The leading hypothesis for selective predation in this system is that infection‐induced changes in the transparency of Daphnia render them more visible to bluegill. Rigorously evaluating this hypothesis requires that we quantify the effect of infection on the visibility of prey from the predator's perspective, rather than our own. Using a model of the bluegill visual system, we show that three common parasites, Metschnikowia bicuspidata, Pasteuria ramosa, and Spirobacillus cienkowskii, decrease the transparency of Daphnia, rendering infected Daphnia darker against a background of bright downwelling light. As a result of this increased brightness contrast, bluegill can see infected Daphnia at greater distances than uninfected Daphnia—between 19% and 33% further, depending on the parasite. Pasteuria and Spirobacillus also increase the chromatic contrast of Daphnia. These findings lend support to the hypothesis that selective predation by fish on infected Daphnia could result from the effects of infection on Daphnia's visibility. However, contrary to expectations, the visibility of Daphnia was not strongly impacted by water color in our model. Our work demonstrates that models of animal visual systems can be useful in understanding ecological interactions that impact disease transmission. The authors use a model of predator vision to assess why parasitized zooplankton more often fall prey to bluegill predators that uninfected prey.

The Red Queen hypothesis can explain the maintenance of host and parasite diversity. However, the Red Queen requires genetic specificity for infection risk (i.e., that infection depends on the exact combination of host and parasite genotypes) and strongly virulent effects of infection on host fitness. A European crustacean (Daphnia magna)--bacterium (Pasteuria ramosa) system typifies such specificity and high virulence. We studied the North American host Daphnia dentifera and its natural parasite Pasteuria ramosa, and also found strong genetic specificity for infection success and high virulence. These results suggest that Pasteuria could promote Red Queen dynamics with D. dentifera populations as well. However, the Red Queen might be undermined in this system by selection from a more common yeast parasite (Metschnikowia bicuspidata). Resistance to the yeast did not correlate with resistance to Pasteuria among host genotypes, suggesting that selection by Metschnikowia should proceed relatively independently of selection by Pasteuria.

Resource quality can have conflicting effects on host–parasite interactions; for example, higher resource quality might increase host investment in immune function, or conversely, might permit greater parasite reproduction. Thus, anticipating the impact of changing resource quality on host–parasite interactions is challenging, especially because we often lack a mechanistic understanding of how resource quality influences host physiology and fitness to alter infection outcomes. We investigated whether there are generalizations in how resource quality affects multiple host clones' interactions with different parasites. We used the Daphnia freshwater zooplankton model system to experimentally investigate how a resource quality gradient from high‐quality green algae to poor‐quality cyanobacteria diets influences host fitness, physiology, and infection by two parasites: a bacterium, Pasteuria ramosa, and a fungus, Metschnikowia bicuspidata. We ran a separate experiment for each parasite using a factorial design with four diets, two Daphnia dentifera host clones, and parasite‐inoculated and ‐uninoculated treatments (16 treatments per experiment). Diet strongly influenced infection by the fungus but not the bacterium. These relationships between diet and infection cannot be explained by changes in feeding rate (and, therefore, parasite exposure). Instead, the impact of diet on fungal infection was associated with impacts of diet on the earliest stage of infection: hosts that fed on poor quality diets had very few attacking spores in their guts. Diet did not significantly influence host immune responses. Diet influenced spore production differently for the two parasites, with reduced resource quality limiting the number of fungal spores and the size (but not number) of bacterial spores. Diet, host clone, and infection all affected host fitness. Interestingly, diet influenced the impact of the bacterium, a parasitic castrator that induces gigantism; for one clone, infected hosts fed high‐quality diets still produced a substantial number of offspring, whereas resource limitation hindered gigantism. Finally, there were often costs of resisting infection, though these generally were not affected by diet. Overall, we show that resource quality differentially impacts the exposure, infection, and proliferation processes for different parasites and host clones, which highlights the need to use multi‐genotype and multi‐parasite studies to better understand these complex interactions.

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.

Secondary metabolites produced by primary producers have a wide range of functions as well as indirect effects outside the scope of their direct target. Research suggests that protease inhibitors produced by cyanobacteria influence grazing by herbivores and may also protect against parasites of cyanobacteria. In this study, we asked whether those same protease inhibitors produced by cyanobacteria could also influence the interactions of herbivores with their parasites. We used the Daphnia‐Metschnikowia zooplankton host‐fungal parasite system to address this question because it is well documented that cyanobacteria protease inhibitors suppress trypsin and chymotrypsin in the gut of Daphnia, and because it is known that Metschnikowia infects via the gut. We tested the hypothesis that Daphnia gut proteases are necessary for Metschnikowia spores to be released from their asci. We then also tested whether diets that decrease trypsin and chymotrypsin activity in the guts of Daphnia lead to lower levels of infection. Our results show that chymotrypsin promotes the release of the fungal spores from their asci. Moreover, a diet that strongly inhibited chymotrypsin activity in Daphnia decreased infection levels, particularly in the most susceptible Daphnia clones. Our results support the growing literature that cyanobacterial diets can be beneficial to zooplankton hosts when challenged by parasites and uncover a mechanism that contributes to the protective effect of cyanobacterial diets. Specifically, we demonstrate that host chymotrypsin enzymes promote the dehiscence of Metschnikowia spores; when cyanobacteria inhibit the activity of chymotrypsin in hosts, this most likely traps the spore inside the ascus, preventing the parasite from puncturing the gut and beginning the infection process. This study illustrates how secondary metabolites of phytoplankton can protect herbivores against their own enemies. Cyanobacteria peptides can inhibit gut enzymes in zooplankton hosts. Here, we present evidence that inhibition of these enzymes by cyanobacteria leads to lower infection prevalence in hosts that are susceptible to a fungal parasite.