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Resource availability is one of the main factors determining the ecological dynamics of populations or species. Fluctuations in resource availability can increase or decrease the intensity of resource competition. Resource availability and competition can also cause evolutionary changes in life-history traits. We studied how community structure and resource fluctuations affect the evolution of fitness related traits using a two-species bacterial model system. Replicated populations of Serratia marcescens (copiotroph) and Novosphingobium capsulatum (oligotroph) were reared alone or together in environments with intergenerational, pulsed resource renewal. The comparison of ancestral and evolved bacterial clones with 1 or 13 weeks history in pulsed resource environment revealed species-specific changes in life-history traits. Co-evolution with S. marcescens caused N. capsulatum clones to grow faster. The evolved S. marcescens clones had higher survival and slower growth rate then their ancestor. The survival increased in all treatments after one week, and thereafter continued to increase only in the S. marcescens monocultures that experienced large resource pulses. Though adaptive radiation is often reported in evolution studies with bacteria, clonal variation increased only in N. capsulatum growth rate. Our results suggest that S. marcescens adapted to the resource renewal cycle whereas N. capsulatum was more affected by the interspecific competition. Our results exemplify species-specific evolutionary response to both competition and environmental variation.

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.

Most theories of the evolution of virulence concentrate on obligatory host-pathogen relationship. Yet, many pathogens replicate in the environment outside-host where they compete with non-pathogenic forms. Thus, replication and competition in the outside-host environment may have profound influence on the evolution of virulence and disease dynamics. These environmentally growing opportunistic pathogens are also a logical step towards obligatory pathogenicity. Efficient treatment methods against these diseases, such as columnaris disease in fishes, are lacking because of their opportunist nature. We present a novel epidemiological model in which replication and competition in the outside-host environment influences the invasion ability of a novel pathogen. We also analyze the long-term host-pathogen dynamics. Model parameterization is based on the columnaris disease, a bacterial fresh water fish disease that causes major losses in fish farms worldwide. Our model demonstrates that strong competition in the outside-host environment can prevent the invasion of a new environmentally growing opportunist pathogen and long-term disease outbreaks.

Background Environmentally growing pathogens present an increasing threat for human health, wildlife and food production. Treating the hosts with antibiotics or parasitic bacteriophages fail to eliminate diseases that grow also in the outside-host environment. However, bacteriophages could be utilized to suppress the pathogen population sizes in the outside-host environment in order to prevent disease outbreaks. Here, we introduce a novel epidemiological model to assess how the phage infections of the bacterial pathogens affect epidemiological dynamics of the environmentally growing pathogens. We assess whether the phage therapy in the outside-host environment could be utilized as a biological control method against these diseases. We also consider how phage-resistant competitors affect the outcome, a common problem in phage therapy. The models give predictions for the scenarios where the outside-host phage therapy will work and where it will fail to control the disease. Parameterization of the model is based on the fish columnaris disease that causes significant economic losses to aquaculture worldwide. However, the model is also suitable for other environmentally growing bacterial diseases. Results Transmission rates of the phage determine the success of infectious disease control, with high-transmission phage enabling the recovery of the host population that would in the absence of the phage go asymptotically extinct due to the disease. In the presence of outside-host bacterial competition between the pathogen and phage-resistant strain, the trade-off between the pathogen infectivity and the phage resistance determines phage therapy outcome from stable coexistence to local host extinction. Conclusions We propose that the success of phage therapy strongly depends on the underlying biology, such as the strength of trade-off between the pathogen infectivity and the phage-resistance, as well as on the rate that the phages infect the bacteria. Our results indicate that phage therapy can fail if there are phage-resistant bacteria and the trade-off between pathogen infectivity and phage resistance does not completely inhibit the pathogen infectivity. Also, the rate that the phages infect the bacteria should be sufficiently high for phage-therapy to succeed.

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.

Pathogen virulence is usually thought to evolve in reciprocal selection with the host. While this might be true for obligate pathogens, the life histories of opportunistic pathogens typically alternate between within-host and outside-host environments during the infection-transmission cycle. As a result, opportunistic pathogens are likely to experience conflicting selection pressures across different environments, and this could affect their virulence through life-history trait correlations. We studied these correlations experimentally by exposing an opportunistic bacterial pathogen Serratia marcescens to its natural protist predator Tetrahymena thermophila for 13 weeks, after which we measured changes in bacterial traits related to both anti-predator defence and virulence. We found that anti-predator adaptation (producing predator-resistant biofilm) caused a correlative attenuation in virulence. Even though the direct mechanism was not found, reduction in virulence was most clearly connected to a predator-driven loss of a red bacterial pigment, prodigiosin. Moreover, life-history trait evolution was more divergent among replicate populations in the absence of predation, leading also to lowered virulence in some of the 'predator absent' selection lines. Together these findings suggest that the virulence of non-obligatory, opportunistic bacterial pathogens can decrease in environmental reservoirs through life history trade-offs, or random accumulation of mutations that impair virulence traits under relaxed selection.

Phenotypic variation is suggested to facilitate the persistence of environmentally growing pathogens under environmental change. Here, we hypothesized that the intensive farming environment induces higher phenotypic variation in microbial pathogens than natural environment, because of high stochasticity for growth and stronger survival selection compared to the natural environment. We tested the hypothesis with an opportunistic fish pathogen Flavobacterium columnare isolated either from fish farms or from natural waters. We measured growth parameters of two morphotypes from all isolates in different resource concentrations and two temperatures relevant for the occurrence of disease epidemics at farms and tested their virulence using a zebrafish (Danio rerio) infection model. According to our hypothesis, isolates originating from the fish farms had higher phenotypic variation in growth between the morphotypes than the isolates from natural waters. The difference was more pronounced in higher resource concentrations and the higher temperature, suggesting that phenotypic variation is driven by the exploitation of increased outside‐host resources at farms. Phenotypic variation of virulence was not observed based on isolate origin but only based on morphotype. However, when in contact with the larger fish, the less virulent morphotype of some of the isolates also had high virulence. As the less virulent morphotype also had higher growth rate in outside‐host resources, the results suggest that both morphotypes can contribute to F. columnare epidemics at fish farms, especially with current prospects of warming temperatures. Our results suggest that higher phenotypic variation per se does not lead to higher virulence, but that environmental conditions at fish farms could select isolates with high phenotypic variation in bacterial population and hence affect evolution in F. columnare at fish farms. Our results highlight the multifaceted effects of human‐induced environmental alterations in shaping epidemiology and evolution in microbial pathogens.

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.