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The theory of species coexistence is a key concept in ecology that has received much attention. The role of rapid evolution for determining species coexistence is still poorly understood although evolutionary change on ecological time-scales has the potential to change almost any ecological process. The influence of evolution on coexistence can be especially pronounced in microbial communities where organisms often have large population sizes and short generation times. Previous work on coexistence has assumed that traits involved in resource use and species interactions are constant or change very slowly in terms of ecological time-scales. However, recent work suggests that these traits can evolve rapidly. Nevertheless, the importance of rapid evolution to coexistence has not been tested experimentally. Here, we show how rapid evolution alters the frequency of two bacterial competitors over time when grown together with specialist consumers (bacteriophages), a generalist consumer (protozoan) and all in combination. We find that consumers facilitate coexistence in a manner consistent with classic ecological theory. However, through disentangling the relative contributions of ecology (changes in consumer abundance) and evolution (changes in traits mediating species interactions) on the frequency of the two competitors over time, we find differences between the consumer types and combinations. Overall, our results indicate that the influence of evolution on species coexistence strongly depends on the traits and species interactions considered.

An infective prey has the potential to infect, kill and consume its predator. Such a prey-predator relationship fundamentally differs from the predator-prey interaction because the prey can directly profit from the predator as a growth resource. Here we present a population dynamics model of partial role reversal in the predator-prey interaction of two species, the bottom dwelling marine deposit feeder sea cucumber Apostichopus japonicus and an important food source for the sea cucumber but potentially infective bacterium Vibrio splendidus . We analyse the effects of different parameters, e.g. infectivity and grazing rate, on the population sizes. We show that relative population sizes of the sea cucumber and V . Splendidus may switch with increasing infectivity. We also show that in the partial role reversal interaction the infective prey may benefit from the presence of the predator such that the population size may exceed the value of the carrying capacity of the prey in the absence of the predator. We also analysed the conditions for species extinction. The extinction of the prey, V . splendidus , may occur when its growth rate is low, or in the absence of infectivity. The extinction of the predator, A . japonicus , may follow if either the infectivity of the prey is high or a moderately infective prey is abundant. We conclude that partial role reversal is an undervalued subject in predator-prey studies.

Changing environmental conditions can infer structural modifications of predator‐prey communities. New conditions often increase mortality which reduces population sizes. Following this, predation pressure may decrease until populations are dense again. Dilution may thus have substantial impact not only on ecological but also on evolutionary dynamics because it amends population densities. Experimental studies, in which microbial populations are maintained by a repeated dilution into fresh conditions after a certain period, are extensively used approaches allowing us to obtain mechanistic insights into fundamental processes. By design, dilution, which depends on transfer volume (modifying mortality) and transfer interval (determining the time of interaction), is an inherent feature of these experiments, but often receives little attention. We further explore previously published data from a live predator‐prey (bacteria and ciliates) system which investigated eco‐evolutionary principles and apply a mathematical model to predict how various transfer volumes and transfer intervals would affect such an experiment. We find not only the ecological dynamics to be modified by both factors but also the evolutionary rates to be affected. Our work predicts that the evolution of the anti‐predator defense in the bacteria, and the evolution of the predation efficiency in the ciliates, both slow down with lower transfer volume, but speed up with longer transfer intervals. Our results provide testable hypotheses for future studies of predator‐prey systems, and we hope this work will help improve our understanding of how ecological and evolutionary processes together shape composition of microbial communities. Experiments using microbes contribute to our understanding of ecological and evolutionary principles how communities function. Often in experiments those communities are maintained by regular transfers, but details of how that is done often receive little attention. Here, we model experimental data and allow different designs and our findings suggest that this may have substantial impact on the results.

Understanding the role of variation in host resistance and the multitude of transmission modes of parasites infecting hosts with complex behavioral interactions is essential for the control of emerging diseases. We used a discrete stage model to study the invasion dynamics of crayfish plague—an example of a detrimental disease—into a naïve host population that displays within‐population variation in resistance of environmental infections and juvenile classes that are safe from contacts with adults. In the model, infection sources include four age classes of crayfish, contaminated carcasses, and free‐dwelling zoospores. Disease transmission occurs via environment with a threshold infection density and through contacts, cannibalism, and scavenging of disease‐killed conspecifics. Even if the infection is fatal, coexistence of the host and the parasite can be facilitated by variance of resistance and survival of the hiding juveniles. The model can be applied in the control of emerging diseases especially in crayfish‐like organisms. To control emerging diseases, we need to understand the effects of variation in host resistance and the multitude of transmission modes of parasites combined with hosts' complex behavioral interactions. Based on a discrete stage model, we propose that even if the infection is fatal, coexistence of the host and the parasite can be facilitated by variance in resistance and the partial separation of juveniles from adults.

Many socio-economically important pathogens persist and grow in the outside host environment and opportunistically invade host individuals. The environmental growth and opportunistic nature of these pathogens has received only little attention in epidemiology. Environmental reservoirs are, however, an important source of novel diseases. Thus, attempts to control these diseases require different approaches than in traditional epidemiology focusing on obligatory parasites. Conditions in the outside-host environment are prone to fluctuate over time. This variation is a potentially important driver of epidemiological dynamics and affect the evolution of novel diseases. Using a modelling approach combining the traditional SIRS models to environmental opportunist pathogens and environmental variability, we show that epidemiological dynamics of opportunist diseases are profoundly driven by the quality of environmental variability, such as the long-term predictability and magnitude of fluctuations. When comparing periodic and stochastic environmental factors, for a given variance, stochastic variation is more likely to cause outbreaks than periodic variation. This is due to the extreme values being further away from the mean. Moreover, the effects of variability depend on the underlying biology of the epidemiological system, and which part of the system is being affected. Variation in host susceptibility leads to more severe pathogen outbreaks than variation in pathogen growth rate in the environment. Positive correlation in variation on both targets can cancel the effect of variation altogether. Moreover, the severity of outbreaks is significantly reduced by increase in the duration of immunity. Uncovering these issues helps in understanding and controlling diseases caused by environmental pathogens.

Emerging infectious diseases are a persistent threat to humans and food production but the mechanisms promoting the emergence of novel pathogens are not fully understood. The widely discussed explanations for pathogen emergence include range shifts, coincidental evolution of virulence, and host immunity variation. Here we propose a novel mechanism of virulence evolution that relies on environmental variability. Our model combines an environmental community experiencing random or periodic variability, to a classical SIR epidemiological model. We assume that environmentally growing, potentially infective variants arise at low frequency from a resident, non-infective (benign microbial) strain through random variation on genetic material. We found that environmental perturbations commonly promote establishment of sporadic infections or persistent epidemics, by creating transient periods of low competition, which can in turn be exploited by an infective strain. Given the ubiquitous nature of potentially pathogenic environmental micro-organisms and environmental variability, this mechanism provides a plausible explanation for emerging diseases.

Theoretical models of environmentally transmitted diseases often assume that transmission is a constant process, which scales linearly with pathogen dose. Here we question the applicability of such an assumption and propose a sigmoidal form for the pathogens infectivity response. In our formulation, this response arises under two assumptions: 1) multiple invasion events are required for a successful pathogen infection and 2) the host invasion state is reversible. The first assumption reduces pathogen infection rates at low pathogen doses, while the second assumption, due to host immune function, leads to a saturating infection rate at high doses. The derived pathogen dose:infection rate relationship was tested against an experimental data on host mortality rates across different pathogen doses. Compared to two simpler alternatives, the sigmoidal function gave a better fit to patterns in host mortality rate (process), as well as host mortality (endpoint). Combining these alternative approaches made us more confident to conclude that the proposed model for disease transmission is theoretically sound, provides a good description of the data at hand, and is likely to be useful in developing more reliable models for infectious diseases.

Environmentally transmitted pathogens face ecological interactions (e.g., competition, predation, parasitism) in the outside-host environment and host immune system during infection. Despite the ubiquitousness of environmental opportunist pathogens, traditional epidemiology focuses on obligatory pathogens incapable of environmental growth. Here we ask how competitive interactions in the outside-host environment affect the dynamics of an opportunist pathogen. We present a model coupling the classical SI and Lotka-Volterra competition models. In this model we compare a linear infectivity response and a sigmoidal infectivity response. An important assumption is that pathogen virulence is traded off with competitive ability in the environment. Removing this trade-off easily results in host extinction. The sigmoidal response is associated with catastrophic appearances of disease outbreaks when outside-host species richness, or overall competition pressure, decreases. This indicates that alleviating outside-host competition with antibacterial substances that also target the competitors can have unexpected outcomes by providing benefits for opportunist pathogens. These findings may help in developing alternative ways of controlling environmental opportunist pathogens.

Understanding the ultimate causes of population declines and extinction is vital in our quest to stop the currently rampant biodiversity loss. Comparison of ecological characteristics between threatened and nonthreatened species may reveal these ultimate causes. Here, we report an analysis of ecological characteristics of 23 threatened and 72 nonthreatened butterfly species. Our analysis reveals that threatened butterflies are characterized by narrow niche breadth, restricted resource distribution, poor dispersal ability, and short flight period. Based on the characteristics, we constructed an ecological extinction risk rank and predicted which of the currently nonthreatened species are at the highest risk of extinction. Our analysis reveals that two species currently classified as nonthreatened are, in fact, at high risk of extinction, and that the status of a further five species should be reconsidered.

Opportunist saprotrophic pathogens differ from obligatory pathogens due to their capability in host-independent growth in environmental reservoirs. Thus, the outside-host environment potentially influences host-pathogen dynamics. Despite the socio-economical importance of these pathogens, theory on their dynamics is practically missing. We analyzed a novel epidemiological model that couples outside-host density-dependent growth to host-pathogen dynamics. Parameterization was based on columnaris disease, a major hazard in fresh water fish farms caused by saprotrophic Flavobacterium columnare. Stability analysis and numerical simulations revealed that the outside-host growth maintains high proportion of infected individuals, and under some conditions can drive host extinct. The model can show stable or cyclic dynamics, and the outside-host growth regulates the frequency and intensity of outbreaks. This result emerges because the density-dependence stabilizes dynamics. Our analysis demonstrates that coupling of outside-host growth and traditional host-pathogen dynamics has profound influence on disease prevalence and dynamics. This also has implications on the control of these diseases.