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dc.contributor.authorBartlett, L
dc.date.accessioned2019-01-28T10:06:51Z
dc.date.issued2019-01-28
dc.description.abstractInfectious diseases shape almost every aspect of nature and society; understanding the multitude of factors influencing infectious diseases is a critical goal of modern evolutionary ecology. This thesis explores this broad topic using theoretical and empirical approaches to understand the forces at work in infectious disease ecology and evolution, with application to the specific system of managed honeybees (Apis mellifera L.). I demonstrate that a well-documented evolutionary trade-off governing pathogen resistance is both constitutive and genetic – critical for supporting assumptions made by mathematical theory. I go further to demonstrate that this trade-off breaks down when the action of selection is reversed, in that when the ‘cost of resistance’ phenotype is selective for, we do not incidentally select for higher resistance too. This is important for understanding genetic linkage of traits and downstream evolutionary modelling. I undertake theoretical modelling on the topic of spatial structure and how it affects pathogen evolution. In doing so I interrogate a critical assumption made in much of the prior theoretical body, showing that the effect of spatial structure on virulence is quantitatively changed when a core assumption concerning reproduction is relaxed, but is otherwise qualitatively robust. I continue on the theme of spatial structuring and pathogens by developing novel theoretical models on how changing apicultural management alters honeybee population spatial structure, surprisingly leading to only marginal changes in pathogen burden. I stay on this topic to examine empirical data on honeybee colony viriomes in an observation experiment showing that colonies from very intensively managed, migratory backgrounds show elevated viral titres – critical for management and wild bee conservation. I synthesise that the honeybee system is our most informative natural experiment in showing that vectored pathogens are more virulent than directly transmitted counterparts. I also show that outbreaking human epidemics (Zika virus) can threaten apiculture – and by extension livelihoods and agriculture.en_GB
dc.description.sponsorshipNatural Environment Research Council (NERC)en_GB
dc.identifier.urihttp://hdl.handle.net/10871/35601
dc.publisherUniversity of Exeteren_GB
dc.rights.embargoreasonStandard period of 18 months because I wish to publish papers using material that is substantially drawn from my thesis.en_GB
dc.subjecthoney beeen_GB
dc.subjectApis melliferaen_GB
dc.subjectinfectious diseaseen_GB
dc.subjectpathogen resistanceen_GB
dc.subjectevolutionen_GB
dc.titleUBI MEL, IBI APES: On the evolutionary ecology of infectious diseases and intersections with apiculture.en_GB
dc.typeThesis or dissertationen_GB
dc.contributor.advisorBoots, Men_GB
dc.contributor.advisorBayer-Wilfert, Len_GB
dc.publisher.departmentBiological Sciencesen_GB
dc.rights.urihttp://www.rioxx.net/licenses/all-rights-reserveden_GB
dc.type.degreetitlePhD in Biological Sciencesen_GB
dc.type.qualificationlevelDoctoralen_GB
dc.type.qualificationnameDoctoral Thesisen_GB
dcterms.dateAccepted2019-01-28
exeter.funder::Natural Environment Research Council (NERC)en_GB
rioxxterms.versionNAen_GB
rioxxterms.licenseref.startdate2019-01-28
rioxxterms.typeThesisen_GB


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