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Spillover of viruses into novel host species occurs frequently. Often, spillover results in dead-end infections in novel hosts, sometimes, in stuttering transmission chains that die out, and rarely, in large epidemics with sustained transmission. If we could identify early which outcome will occur following a spillover event, we could more appropriately invest in efforts to surveil, respond to, or prevent disease emergence. Our goal was to identify early epidemiological characteristics that correlate with these outcomes, including those predictive of population-level virus persistence in novel hosts. To identify these characteristics, we experimentally induced spillover in the Caenorhabditis nematode-Orsay virus system and measured infection prevalence in exposed populations and virus shedding and infection intensity from infected hosts in replicate populations of eight strains belonging to seven non-native host species. We then passaged 20 adult nematodes from exposed populations to virus-free plates where they reproduced, initiating new populations to which they had the potential to transmit virus. We used quantitative PCR to track virus presence in passaged host populations for 10 passages or until virus was undetectable, indicating its loss. We then used a correlative modeling and a mechanistic modeling approach to understand which epidemiological characteristics were associated with population-level viral persistence. In our correlative models, we found that the number of passages until virus loss was associated with early epidemiological characteristics in the spillover host populations, including infection prevalence in the initially exposed population, the ability of hosts to detectably shed the virus, and the relative susceptibility of the host species, but not infection intensity. When all these characteristics were included simultaneously in a correlative model, only infection prevalence and shedding were significantly associated with virus maintenance, and the model explained over half of the variation in the data. We then developed a mechanistic model that attempts to explain virus passage success by using our epidemiological characteristics data to calculate the probability that at least one worm infectious enough to infect a conspecific is transferred during passage. This mechanistic model explained 38% of the variation in the data on its own. With the goal of understanding how our mechanistic model falls short, we used model selection to test a suite of larger models that included or excluded each epidemiological characteristic and included random effects of strain, experimental line, passage number, and block while the mechanistic prediction was included as an offset. We found that 66% of the variation in our data could be explained by a model that included our mechanistic prediction in addition to infection prevalence, infection intensity, and random effects. Altogether, our study demonstrates that early epidemiological characteristics can play a substantial role in explaining the ultimate outcome of a spillover event.

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.

Many organisms can reproduce both asexually and sexually. For cyclical parthenogens, periods of asexual reproduction are punctuated by bouts of sexual reproduction, and the shift from asexual to sexual reproduction has large impacts on fitness and population dynamics. We studied populations of Daphnia dentifera to determine the amount of investment in sexual reproduction as well as the factors associated with variation in investment in sex. To do so, we tracked host density, infections by nine different parasites, and sexual reproduction in 15 lake populations of D. dentifera for 3 years. Sexual reproduction was seasonal, with male and ephippial female production beginning as early as late September and generally increasing through November. However, there was substantial variation in the prevalence of sexual individuals across populations, with some populations remaining entirely asexual throughout the study period and others shifting almost entirely to sexual females and males. We found strong relationships between density, prevalence of infection, parasite species richness, and sexual reproduction in these populations. However, strong collinearity between density, parasitism, and sexual reproduction means that further work will be required to disentangle the causal mechanisms underlying these relationships. Lake populations of Daphnia varied substantially in investment in sex, with some populations reproducing entirely asexually throughout the study period and others shifting almost entirely to sexual reproduction by late autumn. We found that higher Daphnia density and parasitism were associated with greater investment in sex.

Humans have contributed to the increased frequency and severity of emerging infectious diseases, which pose a significant threat to wild and domestic species, as well as human health. This review examines major pathways by which humans influence parasitism by altering (co)evolutionary interactions between hosts and parasites on ecological timescales. There is still much to learn about these interactions, but a few well-studied cases show that humans influence disease emergence every step of the way. Human actions significantly increase dispersal of host, parasite and vector species, enabling greater frequency of infection in naive host populations and host switches. Very dense host populations resulting from urbanization and agriculture can drive the evolution of more virulent parasites and, in some cases, more resistant host populations. Human activities that reduce host genetic diversity or impose abiotic stress can impair the ability of hosts to adapt to disease threats. Further, evolutionary responses of hosts and parasites can thwart disease management and biocontrol efforts. Finally, in rare cases, humans influence evolution by eradicating an infectious disease. If we hope to fully understand the factors driving disease emergence and potentially control these epidemics we must consider the widespread influence of humans on host and parasite evolutionary trajectories. This article is part of the themed issue ‘Human influences on evolution, and the ecological and societal consequences’.

Parasite fitness depends on a successful journey from one host to another. For parasites that are transmitted environmentally, abiotic conditions might modulate the success of this journey. Here we evaluate how light, a key abiotic factor, influences spatiotemporal patterns of zooplankton disease where light varies seasonally, across lakes, and with depth in a lake. In an in situ experiment using those three sources of variation, we tested sensitivity of spores of two parasites to ambient light. Infectivity of both parasites was lower when exposed to ambient light in comparison to parasites exposed to otherwise similar conditions in the dark. The more sensitive parasite (the fungus, Metschnikowia) was damaged even under lower ambient light during late fall (November). With this differential sensitivity established, we evaluated links between light environment and natural outbreaks in lakes. Consistent with the incubations, epidemics of the less sensitive parasite (the bacterium, Pasteuria) started earlier in the fall (under higher ambient light), and both parasites had smaller outbreaks in more transparent lakes. Overall, light environment may impact the timing and size of disease outbreaks. Outbreaks could thus become exacerbated by human activities that darken waters, including lake browning associated with climate change and eutrophication.

Myriad ecological and evolutionary factors can influence whether a particular parasite successfully transmits to a new host during a disease outbreak, with consequences for the structure and diversity of parasite populations. However, even though the diversity and evolution of parasite populations are of clear fundamental and applied importance, we have surprisingly few studies that track how genetic structure of parasites changes during naturally occurring outbreaks in non‐human populations. Here, we used population genetic approaches to reveal how genotypes of a bacterial parasite, Pasteuria ramosa, change over time, focusing on how infecting P. ramosa genotypes change during the course of epidemics in Daphnia populations in two lakes. We found evidence for genetic change – and, therefore, evolution – of the parasite during outbreaks. In one lake, P. ramosa genotypes were structured by sampling date; in both lakes, genetic distance between groups of P. ramosa isolates increased with time between sampling. Diversity in parasite populations remained constant over epidemics, although one epidemic (which was large) had low genetic diversity while the other epidemic (which was small) had high genetic diversity. Our findings demonstrate that patterns of parasite evolution differ between outbreaks; future studies exploring the feedbacks among epidemic size, host diversity, and parasite genetic diversity would improve our understanding of parasite dynamics and evolution. We examined the genetic structure and diversity of the parasite Pasteuria ramosa in two natural outbreaks using variable number tandem repeats to genotype the parasite in infected Daphnia dentifera hosts. We found evidence for parasite evolution within these outbreaks: the genetic distance between sampled parasite genotypes infecting hosts increased with time between sampling, but with notable differences between the two lakes. Although genotype diversity remained flat over time in both outbreaks, it was significantly higher in the lake with the smaller outbreak. This work is valuable for understanding evolution and patterns of parasite genetic diversity within outbreaks.

Genetic variation in parasites has important consequences for host–parasite interactions. Prior studies of the ecologically important parasite Metschnikowia bicuspidata have suggested low genetic variation in the species. Here, we collected M. bicuspidata from two host species (Daphnia dentifera and Ceriodaphnia dubia) and two regions (Michigan and Indiana, USA). Within a lake, outbreaks tended to occur in one host species but not the other. Using microsatellite markers, we identified six parasite genotypes grouped within three distinct clades, one of which was rare. Of the two main clades, one was generally associated with D. dentifera, with lakes in both regions containing a single genotype. The other M. bicuspidata clade was mainly associated with C. dubia, with a different genotype dominating in each region. Despite these associations, both D. dentifera- and C. dubia-associated genotypes were found infecting both hosts in lakes. However, in lab experiments, the D. dentifera-associated genotype infected both D. dentifera and C. dubia, but the C. dubia-associated genotype, which had spores that were approximately 30% smaller, did not infect D. dentifera. We hypothesize that variation in spore size might help explain patterns of cross-species transmission. Future studies exploring the causes and consequences of variation in spore size may help explain patterns of infection and the maintenance of genotypic diversity in this ecologically important system.

Virulence, the degree to which a pathogen harms its host, is an important but poorly understood aspect of host-pathogen interactions. Virulence is not static, instead depending on ecological context and potentially evolving rapidly. For instance, at the start of an epidemic, when susceptible hosts are plentiful, pathogens may evolve increased virulence if this maximizes their intrinsic growth rate. However, if host density declines during an epidemic, theory predicts evolution of reduced virulence. Although well-studied theoretically, there is still little empirical evidence for virulence evolution in epidemics, especially in natural settings with native host and pathogen species. Here, we used a combination of field observations and lab assays in the Daphnia-Pasteuria model system to look for evidence of virulence evolution in nature. We monitored a large, naturally occurring outbreak of Pasteuria ramosa in Daphnia dentifera, where infection prevalence peaked at ~ 40% of the population infected and host density declined precipitously during the outbreak. In controlled infections in the lab, lifespan and reproduction of infected hosts was lower than that of unexposed control hosts and of hosts that were exposed but not infected. We did not detect any significant changes in host resistance or parasite infectivity, nor did we find evidence for shifts in parasite virulence (quantified by host lifespan and number of clutches produced by hosts). However, over the epidemic, the parasite evolved to produce significantly fewer spores in infected hosts. While this finding was unexpected, it might reflect previously quantified tradeoffs: parasites in high mortality (e.g., high predation) environments shift from vegetative growth to spore production sooner in infections, reducing spore yield. Future studies that track evolution of parasite spore yield in more populations, and that link those changes with genetic changes and with predation rates, will yield better insight into the drivers of parasite evolution in the wild.

Salinization of freshwater systems is a global concern. In the northern United States, a large driver of freshwater salinization is the application of road salt which runs into freshwater systems. We tested the effects of salinization on traits and population densities of the freshwater crustacean, Daphnia dentifera, a common species in the Midwestern United States. We first measured the effects of salinity on resource acquisition (feeding rates), birth rates, and death rates of individual D. dentifera. Then we performed an experiment to quantify the population-level effects of salinity. There was little effect of salinity on individual characteristics; birth and death rates were unaffected by salinity treatment and only one D. dentifera genotype showed lower feeding rates with increased salinity. However, D. dentifera population densities were lower with increased salinity. Our results suggest that studies conducted on individuals may underestimate the population-level effects of salinization. Moreover, since Daphnia are often dominant grazers in freshwater systems, reduced population densities from salinization could have dramatic effects on communities and ecosystems.

Generalist parasites can strongly influence interactions between native and invasive species. Host competence can be used to predict how an invasive species will affect community disease dynamics; the addition of a highly competent, invasive host is predicted to increase disease. However, densities of invasive and native species can also influence the impacts of invasive species on community disease dynamics. We examined whether information on host competence alone could be used to accurately predict the effects of an invasive host on disease in native hosts. We first characterized the relative competence of an invasive species and a native host species to a native parasite. Next, we manipulated species composition in mesocosms and found that host competence results did not accurately predict community dynamics. While the invasive host was more competent than the native, the presence of the native (lower competence) host increased disease in the invasive (higher competence) host. To identify potential mechanisms driving these patterns, we analyzed a two-host, one-parasite model parameterized for our system. Our results demonstrate that patterns of disease were primarily driven by relative population densities, mediated by asymmetry in intra- and interspecific competition. Thus, information on host competence alone may not accurately predict how an invasive species will influence disease in native species.