Epidemiology strongly parallels the study of ecology, primarily being concernedwith the incidence, distribution, reproduction and persistence of species. Thespread of disease, or its transmission, is arguably the most important incidentstudied in epidemiology, underpinning a pathogen’s ability to reproduce andpersist within a host population. However, observations of individualtransmission events are often impossible to observe directly, making variation inthis process difficult to study. This has resulted in a great deal ofepidemiological theory being based on homogenous transmission of diseasethrough host populations. Understanding disease transmission as aheterogeneous process requires an appreciation of the ecological dynamicsdetermining a pathogens ability to transmit. In this thesis a cross-disciplinaryapproach is taken to examine the ecological dynamics that may affect diseasetransmission at different ecological scales.In Chapter 2 I review empirical evidence in support of density dependenttransmission. Transmission rates of density dependent transmitted diseases areoften assumed to scale linearly with host population density. This assumption ispertinent to the calculation of the basic reproductive number R0. As R0 isimportant in determining optimal vaccination strategies, population thresholdsand epidemic sizes, incorrect assumptions used in its calculation have thepotential to misinform disease control strategies. Alarmingly, there is very littleevidence to suggest that the prior assumption of a linear relationship betweendisease transmission rates and host population density exists. Where evidence ofdensity dependent transmission has been found this has been best explained bynon-linear relationships. Furthermore, density may have much stronger effectson disease transmission at small, local, scales (for example within one socialgrouping of hosts). Disease transmission between groups of hosts, at globalscales, is more likely to follow frequency dependent dynamics. Diseasetransmission rates should thus be thought of as variable across populations thatare not homogenously distributed in space, or across social structures.In Chapter 3 a community of pathogens infecting a population of rural red foxes,Vulpes vulpes, is described. Foxes cadavers were collected from a private estate2in Canterbury, Kent and a combination of direct and indirect testing for diseaseis used to maximise the scope of disease considered as part of this community.Specifically, I examine if any of the diseases included in this study occurtogether, or apart, more frequently than expected by chance alone. Within thesamples collected it is found that the intracellular protozoan Toxoplasma gondiico-occurs with the virus canine adenovirus type-I (CAV-I) more frequently thanexpected by chance. Foxes concomitantly infected with these pathogens havelower condition scores than foxes who were not positive for both pathogens.From the data collected it is not clear whether hosts of lower condition aremore susceptible to co-infection or if the co-infection is more harmful to hoststhan being singly infected. T. gondii is not transmitted by foxes, but if infectionwith this parasite increases susceptibility to CAV-I then this virus may benefitfrom the presence of T. gondii within its host population. If it is the case thatfoxes of lower condition are simply more prone to co-infection then it should beexpected that individual differences between hosts would cause heterogeneityin disease transmission. The need for cross-disciplinary approaches whenstudying pathogen communities is well demonstrated by this study, as is theneed for more consideration to be paid to the community ecology of pathogensin epidemiological studies.In Chapter 4 a model is formulated to explore the effects of an interactionbetween a micro and a macro parasite. This is performed in the context of theincreased prevalence and geographical range of the highly zoonotic small foxtapeworm Echinococcus multilocularis following successful rabies elimination inWestern Europe. I explore the hypothesis that foxes with extremely high burdensmay be at a higher risk of contracting rabies than foxes with low worm burdens,and thus rabies may have a regulatory effect on E. multilocularis populations bypreferentially removing “super spreading” hosts. It is demonstrated that rabieslimits E. multilocularis populations by limiting the density of available hosts. Aninteraction between rabies transmission rate and worm burden only caused aweak additional suppression on E. multilocularis populations, regardless ofwhether this relationship was linear or exponential. The elimination of rabiesacross Western Europe is certainly to be applauded. However, it should be notedfrom this work that surveillance of pathogen communities following successfuleradication of one pathogen is of the upmost importance.3Finally, in Chapter 5 I examine how parasites adapt their investment intransmission in response to environmental changes experienced within a host.This is done by fitting models to data collected from mice infected with themalaria parasite Plasmodium chabaudi during the acute stage of inaction.Parasites are predicted to alter their behaviour in response to host stress,immunity and the availability of resources. However, theoretical andexperimental studies reach conflicting conclusions regarding the “optimalresponse” to degradation of their habitat. Models were fitted to time series datafrom infection with one of six distinct genotypes. It is found that proportionalallocation of resources into transmission, rather than replication, is highlysensitive to red blood cell (RBC) densities, with investment in transmissionincreasing as RBC resources become scarce. Investment in transmission alsoincreases, albeit more weakly, in response to low parasite densities. Theseanalyses highlight the fact that the complexity of interactions between parasitesand their host hinder the identification of causal relationships, but supportsrecent work that questions the role of terminal investment in transmission inresponse to changes in the within-host environment.The broad scope of work presented here investigates a wide range of ecologicalfactors (including community dynamics, habitat variability and reproductivesuccess) at different ecological scales, responsible for heterogeneity in diseasetransmission. Transmission is a dynamic, and heterogeneous process. To betterunderstand the ecology of disease it is logical to investigate the mechanismsbehind this variation.
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