1,721,167 research outputs found
Spite and virulence in the bacterium Pseudomonas aeruginosa.
Full text linkSocial interactions within populations of pathogenic microbes may play an important role in determining disease virulence. One such ubiquitous interaction is the production of anticompetitor toxins; an example of a spiteful behavior, because it results in direct fitness costs to both the actor and recipient. Following from predictions made by mathematical models, we carried out experiments using the bacterium Pseudomonas aeruginosa to test under what social conditions toxin (bacteriocin) production is favored and how this in turn affects virulence in the larvae of the wax moth Galleria mellonella. Consistent with theory, we found that the growth of bacteriocin producers relative to sensitive non-producers is maximized when toxin producers are at intermediate frequencies in the population. Furthermore, growth rate and virulence in caterpillars was minimized when bacteriocin producers have the greatest relative growth advantage. These results suggest that spiteful interactions may play an important role in the population dynamics and virulence of natural bacterial infections
Understanding the evolutionary ecology of dispersal: An experimental approach using the bacterium Pseudomonas aeruginosa
Full text linkUnderstanding dispersal is a central aim of evolutionary ecology. Theoretical analyses of dispersal have been crucial in identifying key variables which contribute to its evolution and maintenance, but the supporting empirical data remains elusive. Microbes offer a powerful model system on which ecological and evolutionary theory can be experimentally tested with controlled and replicated experiments, and with the convenient malleability of selective pressures and bacterial genomics. Pseudomonas aeruginosa is an ubiquitous, opportunistic pathogen that is able to induce acute or chronic infections in a broad array of hosts. As well as in vivo environments, P. aeruginosa can be found in a range of ecological habitats, from solid to aqueous, and as such requires a variety of dispersal mechanisms (including swimming, gliding on a surfactant and ‘crawling’) for effective colonisation and infectivity. In this thesis, I present a collection of papers which outline empirical ecological and evolutionary experiments to identify the abiotic and biotic forces that shape the evolution of these different dispersal mechanisms, with particular focus on the theoretically important role of kin competition and the structure of the abiotic environment
An investigation into the effects of phage diversity on the evolution of bacterial resistance mechanisms
Full text linkBacteria possess multiple resistance mechanisms, but little is known why one mechanism can be favoured over others. With a focus on two resistance mechanisms of the pathogenic bacteria Pseudomonas aeruginosa, I expand on present knowledge by looking at ecological and genetic selection pressures that drive the adaptive resistance mechanism of the CRISPR-Cas (Clustered Regular Interspaced Short Palindromic Repeats – CRISPR associated) system compared with general resistance through cell surface modification. Specifically, I show that 1) the evolution of CRISPR-Cas immunity is not general across all phage species. 2) I examine how adaptive evolution is affected when a phage species, known to elicit CRISPR-Cas evolution, is mixed with novel phage species and demonstrate that the resistance mechanism is switched in combination with multiple phages, to surface modification. 3) I show how priming is important for continued resistance when phage have escaped the CRISPR-Cas system. However, significant detection of priming may vary between different host-phage interactions. 4) I then show how primed bacterial strains fail to evolve CRISPR-Cas resistance when infected with phage mixtures, even though prior spacer acquisition exists. 5) Finally, the benefit of the CRISPR-Cas system in generating genetic diversity is shown to rapidly clear phage from the environment. Combined, these results show that, even though there are substantial fitness benefits associated with CRISPR-Cas immunity, P. aeruginosa will develop resistance by means of surface modification in the face of phage diversity
The ecology and evolution of diversity and cooperation in bacterial public-goods
Full text linkExplaining why cooperation exists despite the persistent advantage of cheats has been the focus of much theoretical and empirical attention in biology. Using the bacterium Pseudomonas aeruginosa as a model system for the evolution of cooperation, I investigate two distinct phenomena which may develop our understanding of how cooperation is maintained; 1) tag-based cooperation and diversity; and 2) environmental heterogeneity.
The first investigates how diversity in cooperative systems may be a response to the selective pressure exerted by cheating, and how cheats may then regulate communities to maintain diversity: I demonstrate that in competition, tag-based cooperation is able to evade parasitism, provided the public-good is only accessible to producer strains, i.e., the cheat possesses the “wrong” tag. I also demonstrate that cheats can have a marked influence on diversity: In a community of two producer strains with different tags, if a third cheater strain is introduced, it will drive both its own producer and itself extinct. I do not find that the presence of cheats maintains diversity in either structured or unstructured environments, and discuss the possible causes of this.
In the second topic of this thesis, I investigate the effect of environmental heterogeneity in resource availability, through space and time, on the evolution of cooperation. Environmental heterogeneity is a ubiquitous feature of natural landscapes, yet its effect on the evolution of cooperation has not been extensively studied. I demonstrate that resource availability heterogeneity, in both time and space, acts to maintain cooperation at higher levels than homogeneous environments of the same total resource value. This effect is due to the covariance between productivity and the cost of cooperation: high resource availability periods and spaces are highly productive, and also incur a relatively lower cost of cooperation.BBSR
The effects of contact patterns and genetic specificity on host and parasite evolution
Full text linkMany bacteria, viruses and other parasites cause severe morbidity or mortality in their host populations, creating strong selection for physiological or behavioural mechanisms to avoid disease. Likewise, changes in host susceptibility and contact patterns can dramatically influence the spread of infectious diseases, and hence selection for traits such as virulence and infectivity range in parasites. Understanding how ecological and evolutionary changes in one population affect selection in another represents a key challenge for theoreticians and empiricists alike, and is essential for gaining further insights into host-parasite relationships. This thesis contains theoretical models that explore how genetic and environmental factors shape the evolutionary and coevolutionary dynamics of hosts and parasites. In particular, the roles of genetic specificity (i.e. genotype-by-genotype interactions) and population mixing patterns are investigated, using both mathematical models and computer simulations. A broad range of scenarios are covered, including the coevolution of broad resistance and infectivity ranges (generalism), the persistence of coevolutionary cycling and the maintenance of sex, the effects of mating behaviour on disease prevalence and evolution, and the evolution of sexual and social behaviour. The models presented herein develop our understanding of host-parasite relationships and highlight the importance of genetic interactions and ecological feedbacks
Advances in the Social Evolution and Ecology of Bacterial Public Goods
No full textThe altruistic production of public goods is one of most popular puzzles in evolutionary biology, and is most commonly explained by the indirect fitness benefit accrued by producers. I develop our understanding of the ecology and evolution of public good production by considering how inter- and intraspecific interactions can affect indirect fitness benefits, and ultimately, the evolutionary trajectory of public good cooperation in a bacterial public good system: 1) I demonstrate the ability of public good cooperators to adapt to the presence of cheats by reducing their own cooperative output, constraining cheat fitness as a consequence. 2) I examine the relative contributions of inter- (bacteriophage) and intraspecific (social cheats) parasites on shaping bacterial mutation rates, and demonstrate that social cheats can gain a fitness advantage in the presence compared with the absence of interspecific parasites. 3) I formally show for the first time, that siderophore-mediated detoxification can be an altruistic trait, rapidly selecting for the evolution of de novo cheats, and discuss the implications this process may have for community structure and function. 4) I extend (3) to assess the impact the natural microbial community has on the fitness consequences of siderophore-mediated detoxification in a natural soil environment. 5) I discuss the interplay between rapid microbial evolution and community context, and propose the impacts such interplay may have for biotechnological applications.University of Exete
An investigation into the impacts of an emerging viral pathogen on wild UK populations of European common frog (Rana temporaria).
No full textRanaviruses, the causative viral pathogens behind one of the most widespread and deadly amphibian diseases have been present in the UK since at least the late 1980s. They have been implicated as the cause of mass mortality events and associated populations declines observed in the European common frog (Rana temporaria). Early public engagement in the study of ranaviral emergence in the UK led to the formation of a unique network of mostly privately owned field sites, each housing a population of R. temporaria of known ranaviral disease history. Working within this comparative network of populations, I investigated how a history of ranaviral disease impacts upon various aspects of R. temporaria populations. An experimental infection trial demonstrated that prior population history of ranaviral infection does not influence the ability of metamorphic R. temporaria to control pathogen burdens after primary infection, though individual body weight does. A comparative wild transcriptomics study, implemented using novel methodologies, found no evidence that a positive history of ranavirosis results in significant functional changes in the transcriptome of frog populations. An extensive study of the skin microbiomes of wild R. temporaria revealed for the first time that the commensal bacterial communities present on the skin of wild amphibians might be as intimately linked to ranaviruses as they are to other amphibian pathogens. And finally, skeletochronological analysis of wild adult R. temporaria provided first evidence that infection with a ranavirus reduces the age distribution in positive disease history populations, potentially altering host life history strategies and heightening risk of local extinction.Natural Environment Research Counci
Inapparent and Vertically Transmitted Infections in Two Host-Virus Systems
No full textDespite the advances made since the advent of germ theory, infectious diseases still wreak havoc on human societies, not only affecting us directly but impacting the crops and livestock upon which we rely. Infectious diseases also have dramatic effects on wildlife ecology. Therefore research into infectious diseases could not only directly lead to the improvement and saving of human lives, but aid in food security and the conservation of many wildlife species. Of vital importance in understanding the ecology of infectious diseases are the mechanisms by which they persist in host populations. One possible mechanism is vertical transmission: the transmission of a pathogen from a parent to its offspring as a result of the process of host reproduction. Another possible mechanism is inapparant infections, where an infected host does not display symptoms. Focusing on dengue fever and the Plodia interpunctella granulovirus laboratory system, this PhD thesis looks at the role these two mechanisms play on the persistence of two viral infections and their ecology. Regarding the Plodia interpunctella granulovirus (PiGV) low host food quality led to greater detection of vertically transmitted inapparant PiGV, but did not lead to its activation to an apparent form. Host inbreeding did not lead to vertically transmitted inapparant PiGV’s activation, nor had an effect on its vertical transmission. The vertical infection rate of PiGV was very low. I would therefore suggest that it may be better to use an insect virus system with a higher rate of vertical infection in future research into vertically transmitting inapparent infections. Regarding dengue virus I conclude that vertical transmission is not likely to play a role in the persistence of this virus. However modelling work found that inapparent infections could provide dengue viruses with a means of persistence and should be subject to further research
Multi-scale immune selection and the maintenance of structured antigenic diversity in the malaria parasite Plasmodium falciparum
Full text linkThe most virulent malaria parasite, Plasmodium falciparum, makes use of extensive antigenic diversity to maximise its transmission potential. Parasite genomes contain several highly polymorphic gene families, whose products are the target of protective immune responses. The best studied of these are the PfEMP1 surface proteins, which are encoded by the var multi-gene family and are important virulence factors. During infection, the parasite switches expression between PfEMP1 variants in order to evade adaptive immune responses and prolong infection. On the population level, parasites appear to be structured with respect to their var genes into non-overlapping repertoires, which can lead to high reinfection rates. This non-random structuring of antigenic diversity can also be found at the level of individual var gene repertoires and var genes themselves. However, not much is known about the evolutionary determinants which select for and maintain this structure at different ecological scales. In this thesis I investigate the mechanisms by which multi-scale immune selection and other ecological factors influence the evolution of structured diversity. Using a suite of theoretical frameworks I show that treating diversity as a dynamic property, which emerges from the underlying infection and transmission processes, has a major effect on the relationship between the parasite’s transmis- sion potential and disease prevalence, with important implications for monitoring control efforts. Furthermore, I show that an evolutionary trade-off between within-host and between-host fitness together with functional constraints on diversification can explain the structured diversity found at both the repertoire and parasite population level and might also account for empirically observed exposure-dependent acquisition of immunity. Together, this work highlights the need to consider evolutionary factors acting at different ecological scales to gain a more comprehensive understanding of the complex immune-epidemiology of P. falciparum malaria
Developments in social evolution and virulence in parasites
Full text linkThe study of social evolution and virulence in parasites is concerned with fitness consequences of trade-offs between parasite life history traits and interactions between parasite species and/or genotypes with their hosts. I develop our understanding of social evolution and virulence in parasites in several ways. (1) I review empirical evidence for the fundamental predictions of virulence-transmission trade-off theory and demonstrate that the fit between theory and data is primarily qualitative rather than quantitative; that parasites differ in their degree of host generalism, and this is likely to impact virulence in four ways. (2) I take a comparative approach to examine the underlying causes of an observed statistical variation in the size of parasite infectious doses across taxa, revealing that mechanisms used by parasites to infect hosts are able to explain variation in both infectious dose and virulence. (3) I formally compare data on human pathogens to explain variation in virulence across taxa, revealing that immune subversion and not growth rate, explains variation in virulence. This allows me to predict that immune subverters and not fast growing parasites are likely to cause the most virulent clinical infections. (4) Using bacteria and their naturally infecting viruses (bacteriophage), I take an experimental approach to investigate the consequences of coinfection for parasite life history traits, and find that viruses cultured under a mix of single infections and coinfections evolved plasticity; they killed hosts more rapidly when coinfecting, and this resulted in high fitness under both single infection and coinfection conditions. (5) I experimentally investigate how selection within and between hosts and patches of hosts affects the fitness and virulence of populations of these viruses. I find that limited host availability favours virulent, faster killing parasites with reduced transmission; suggesting high, rather than low, virulence may be common in spatially structured host-parasite communities
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