Bacteria interact with one another in many ways, through helpful behaviours like producing fitness-enhancing secretions and signals as well as harmful ones like the release of anti-competitor toxins. These interactions are essential for bacterial growth and survival and can have substantial impacts on the virulence of bacterial pathogens. This thesis explores the theory of social interactions among bacteria, focusing on both the mechanisms that underlie them as well the consequences for pathogens coinfecting a host. I first propose a hypothesis for the regulation of competitive traits in bacteria. By analysing published literature on anti-competitor toxin regulation I suggest that one of the principal mediators of antagonistic behaviour in bacteria is sensing harm from competitors. In particular, I argue that certain types of stress responses, known to protect bacteria from environmental assault, are fundamental in allowing bacteria to sense competitive threats. Next I focus on another mechanism of sensing social partners, quorum sensing, which has been argued alternatively to either sense bacterial cell density or the mass transfer properties of an environment. I propose a hypothesis on how the use of multiple quorum sensing signals molecules, a common feature across many bacteria, can potentially help resolve ambiguity between social and physical aspects of a cell’s environment. The rest of the thesis focuses on the epidemiology of coinfection, bacterial and otherwise. In some parasites, high coinfection rates lead to an increased level of evolved virulence due to competition between lineages inside the host. In contrast, when cooperative secretions contribute to virulence, the opposite can occur because high producing virulent strains are out-competed by parasites that do not produce public goods. I develop a mathematical model to show that the structure of parasites inside the host largely determines the fate of virulence when there is social interaction at a local level within the host. This analysis shows that multiplicity of infection can have either a positive or negative effect on virulence depending on structuring within the host. Lastly I explore how host contact structure influences coinfection rates and show that when hosts have very heterogeneous numbers of contacts, a small fraction of individuals in the population has a disproportionate effect on coinfection, which in turn shapes pathogen evolution.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:699928 |
| Date | January 2014 |
| Creators | Cornforth, Daniel Michael |
| Contributors | Brown, Sam ; Rambaut, Andrew |
| Publisher | University of Edinburgh |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://hdl.handle.net/1842/17609 |
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