Growth and reproduction of an estuarine population of the colonial hydroidCordylophora caspia (Pallas) in the northern Baltic Sea

Growth and reproduction of the colonial hydroidCordylophora caspia were monitored during the breeding season in natural conditions. In 1987, a life history study was carried out on the upright stems of the main stolon. Mean size of uprights varied cyclically. The first peak coincided with the peak number of sexual hydranths, after which the mean upright length decreased, possibly indicating somatic costs of sexual reproduction. Extrinsic factors like flooding may also have contributed to cyclical changes in upright size. In 1988 and 1989, colonies were reared on experimental plates in the estuary. In 1988, colonies grew until mid July, after which they regressed to a dormant condition and then started growing again in mid August. Predation and space competition are discussed as possible causes for this dormancy in the middle of the growing season. In 1989, colonies grew continually, with the exception of a decline in colony biomass and number of feeding hydranths at the end of July, just following the peak of sexual reproduction. Sexual reproduction started in the early stages of colonial development for all years. During early summer,C. caspia allocated resources simultaneously in colonial growth and sexual reproduction. However, sexual reproduction had a clear peak in mid summer, and thereafter sexual reproduction ceased while colonial growth continued.     

Fighting costs stabilize aggressive behavior in intersexual conflicts

We analyze the evolution of aggressive behavior in intersexual conflicts, with a special reference to mate guarding behavior in crustaceans. An analysis of a discrete-strategy game shows that an ESS with only one of the sexes being aggressive prevail if fighting costs or fitness values of winning are asymmetric. Non-aggressiveness of both sexes is stable if fighting behavior is very costly for females and if the cost is at least partly paid independent of the strategy of the opponent. Most interestingly, the solutions of both sexes being aggressive prevails only if both sexes have some probability of winning, and if fighting costs are small. Second, we solve for the expected levels of aggressiveness in a game with continuous strategies. The form of the fighting cost function largely determines the stability of the solution. When fighting cost increases linearly with aggressiveness, mutual aggressiveness fluctuates cyclically instead of stabilizing at an ESS. However, if there is an asymmetry in fitness payoffs, a solution with only the sex having most to lose being aggressive alone is possible. With quadratically increasing fighting costs an ES combination of mutual aggressiveness may exist. It is predicted that fights between the sexes should be hardest when payoffs are symmetric, and that an overt behavioral conflict will always take place as long as there is a fitness loss to each of the sexes if losing the conflict and both sexes have a chance to win. We discuss the models in the context of fights preceding precopulatory guarding, but the models offer a general frame for analyzing any intersexual conflict. This revised version was published online in July 2006 with corrections to the Cover Date.     

The effects of functional response and host abundance fluctuations on genetic rescue in parasitoids with single‐locus sex determination

Many parasitoids have single‐locus complementary sex determination (sl‐CSD), which produces sterile or inviable males when homozygous at the sex determining locus. A previous study theoretically showed that small populations have elevated risks of extinction due to the positive feedback between inbreeding and small population size, referred to as the diploid male vortex. A few modeling studies have suggested that the diploid male vortex may not be as common because balancing selection at sex determining loci tends to maintain high allelic diversity in spatially structured populations. However, the generality of the conclusion is yet uncertain, as they were drawn either from models developed for particular systems or from a general‐purpose competition model. To attest the conclusion, we study several well‐studied host–parasitoid models that incorporate functional response specifying the number of attacked hosts given a host density and derive the conditions for a diploid male vortex in a single population. Then, we develop spatially structured individual‐based versions of the models to include female behavior, diploid male fertility, and temporal fluctuations. The results show that producing a handful of successful offspring per female parasitoid could enable parasitoid persistence when a typical number of CSD alleles are present. The effect of functional response depends on the levels of fluctuations in host abundance, and inviable or partially fertile diploid males and a small increase in dispersal can alleviate the risk of a diploid male vortex. Our work supports the generality of effective genetic rescue in spatially connected parasitoid populations with sl‐CSD. However, under more variable climate, the efficacy of the CSD mechanism may substantially decline.     

Environmental Variation Generates Environmental Opportunist Pathogen Outbreaks

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.     

Community stability under different correlation structures of species’ environmental responses

The outcome of species interactions in a variable environment is expected to depend on how similarly different species react to variation in environmental conditions. We study community stability (evenness and species diversity) in competitive communities that are either closed or subjected to random migration, under different regimes of environmental forcing. Community members respond to environmental variation: (i) independently (IR), (ii) in a positively correlated way (CR), or (iii) hierarchically, according to niche differences (HR). Increasing the amplitude of environmental variation and environmental reddening both reduce species evenness in closed communities through a reduction in species richness and increased skew in species abundances, under all three environmental response scenarios, although autocorrelation only has a minor effect with HR. Open communities show important qualitative differences, according to changes in the correlation structure of species’ environmental responses. There is an intermediate minimum in evenness for HR communities with increasing environmental amplitude, explained by the interaction of changes in species richness and changes in the variance of within-species environmental responses across the community. Changes in autocorrelation also lead to qualitative differences between IR, CR and HR communities. Our results highlight the importance of considering mechanistically derived, hierarchical environmental correlations between species when addressing the influence of environmental variation on ecological communities, not only uniform environmental correlation across all species within a community.     

Loss of Competition in the Outside Host Environment Generates Outbreaks of Environmental Opportunist Pathogens

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.     

Bottom-up and cascading top-down control of macroalgae along a depth gradient

On marine rocky shores, macroalgal herbivory is often intense, such that the cascading effects of fish predation may contribute to the control of algal communities. To estimate the magnitudes of top-down and bottom-up control on a macroalgal community, we manipulated the access of carnivorous fish to macroalgal colonization substrates, as well as nutrient availability, at two sub-littoral depths. There were three levels of fish manipulation: natural fish community, no fish and the enclosure of one common species, the perch, Perca fluviatilis. We found a clear cascade effect of fish predation on both the total density and several individual species of macroalgae, which was more pronounced in deep than shallow water. The density of the dominant grazers, i.e. snails, increased in nutrient-enriched conditions; perch were inefficient in controlling herbivores, and had therefore no cascading effect on algal densities under such conditions. Although nutrients enhanced the growth of opportunistic algae, herbivores, in the absence of fish, inhibited this response. While algal diversity was higher in shallow than in deep water, the enrichment effect was opposite at the two depths with lowered diversity in the shallows and increased at depth. Our results indicate that fish predation is an efficient regulator of meso-herbivores and that its effect thereby cascades onto the producer trophic level such that both perennial and opportunistic algae benefit from the presence of fish. This cascade effect is probably stronger at depth where predation efficiency is less disturbed by wave motion.     

Outside-host phage therapy as a biological control against environmental infectious diseases

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.

     

High-performance liquid chromatographic analysis of phlorotannins from the brown alga Fucus vesiculosus

Separating individual compounds by HPLC represents an effective method for the detection and quantification of phenolic compounds and has been widely utilised. However, phlorotannins are commonly quantified using colorimetric methods, as the total amount of the whole compound group. In the present paper the separation of a set of individual soluble phlorotannins from the phenolic crude extract of Fucus vesiculosus was achieved by HPLC with UV photodiode array detection. Different gradient programs for reversed- and normal-phase HPLC methods were developed and tested. Normal-phase (NP) conditions with a silica stationary phase and a mobile phase with a linear gradient of increasing polarity were found to separate 16 individual components of the phenolic extract. The suitability of the NP-HPLC method for mass spectrometric application was preliminarily tested. Sample preparation was found to be a critical step in the analysis owing to the rapid oxidation of phlorotannins; ascorbic acid was used as an antioxidant.     

Fouling mediates grazing: intertwining of resistances to multiple enemies in the brown alga Fucus vesiculosus

Macroalgae have to cope with multiple natural enemies, such as herbivores and epibionts. As these are harmful for the host, the host is expected to show resistance to them. Evolution of resistance is complicated by the interactions among the enemies and the genetic correlations among resistances to different enemies. Here, we explored genetic variation in resistance to epibiosis and herbivory in the brown alga Fucus vesiculosus, both under conditions where the enemies coexisted and where they were isolated. F. vesiculosus showed substantial genetic variation in the resistance to both epibiosis and grazing. Grazing pressure on the alga was generally lower in the presence than in the absence of epibiota. Furthermore, epibiosis modified the susceptibility of different algal genotypes to grazing. Resistances to epibiosis and grazing were independent when measured separately for both enemies but positively correlated when both these enemies coexisted. Thus, when the enemies coexisted, the fate of genotypes with respect to these enemies was intertwined. Genotypic correlation between phlorotannins, brown-algal phenolic secondary metabolites, and the amount of epibiota was negative, indicating that these compounds contribute to resistance to epibiosis. In addition, phlorotannins correlated also with the resistance to grazing, but this correlation disappeared when grazing occurred in the absence of epibiota. This indicates that the patterns of selection for the type of the resistance as well as for the resistance traits vary with the occurrence patterns of the enemies.