Population age structure is a ubiquitous population characteristic, with individuals of different ages in a population often displaying different physiological capabilities, like rates of reproduction and mortality, or different immune capabilities. These measures of performance are also key parameters in epidemiology, however, how heterogeneities in age-specific performance influence pathogen dynamics has received little attention. Investigating the impact of ageing on pathogen dynamics is hampered by a lack of information on whole organism age-specific performance beyond fecundity and mortality rates, particularly outside mammals. It was therefore the ambition of this thesis to integrate experimental observations of individual ageing patterns with mathematical epidemiological models to understand how individual ageing may influence population level pathogen dynamics. This thesis is comprised of a series of experiments using the invertebrate Daphnia magna and bacterial pathogen Pasteuria ramosa, and a series of models informed by the observed biological results. My experimental results reveal that ageing is asynchronous across traits within a single organism, and that ageing should be considered across generations: fitness measured only as offspring quantity may not be synonymous with fitness measured as a product of offspring quality. I go on to show that there is considerable genetic variation in age-specific performance and longevity in D. magna, but there was no evidence to suggest that this is maintained through genetic trade-offs. Furthermore, despite this genetic variation in age specific performance, young hosts always carry higher pathogen loads, and as such, age should be considered as more than just contact rates in the quest to determine what makes a host a super-spreader. The epidemiological models developed in this thesis, show that ageing effects on host susceptibility within and between generations have a direct effect on transmission events, whilst ageing effects on fecundity and mortality rates indirectly drive pathogen dynamics via effects on demography and population density. These drivers of pathogen dynamics also may cause an increase in pathogen transmission if a successful intervention to human ageing is applied. The changes to these vital parameters of epidemiology associated with ageing populations can also result in changes to the optimal level of pathogen virulence. The data presented in this thesis provides novel insight into the many ways in which host age, maternal age and population age structure may influence pathogen dynamics. Much of this work challenges longstanding dogma of ageing theory and is highly relevant in light of ageing human populations, thus providing a tool for evolutionary biologists, demographers and epidemiologists alike.