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Title: Disease transmission and the ecological context
Author: Cameron, Angus
ISNI:       0000 0004 2723 4341
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 2012
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Epidemiology strongly parallels the study of ecology, primarily being concerned with the incidence, distribution, reproduction and persistence of species. The spread of disease, or its transmission, is arguably the most important incident studied in epidemiology, underpinning a pathogen’s ability to reproduce and persist within a host population. However, observations of individual transmission events are often impossible to observe directly, making variation in this process difficult to study. This has resulted in a great deal of epidemiological theory being based on homogenous transmission of disease through host populations. Understanding disease transmission as a heterogeneous process requires an appreciation of the ecological dynamics determining a pathogens ability to transmit. In this thesis a cross-disciplinary approach is taken to examine the ecological dynamics that may affect disease transmission at different ecological scales. In Chapter 2 I review empirical evidence in support of density dependent transmission. Transmission rates of density dependent transmitted diseases are often assumed to scale linearly with host population density. This assumption is pertinent to the calculation of the basic reproductive number R0. As R0 is important in determining optimal vaccination strategies, population thresholds and epidemic sizes, incorrect assumptions used in its calculation have the potential to misinform disease control strategies. Alarmingly, there is very little evidence to suggest that the prior assumption of a linear relationship between disease transmission rates and host population density exists. Where evidence of density dependent transmission has been found this has been best explained by non-linear relationships. Furthermore, density may have much stronger effects on disease transmission at small, local, scales (for example within one social grouping of hosts). Disease transmission between groups of hosts, at global scales, is more likely to follow frequency dependent dynamics. Disease transmission rates should thus be thought of as variable across populations that are 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 estate 2 in Canterbury, Kent and a combination of direct and indirect testing for disease is 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 occur together, or apart, more frequently than expected by chance alone. Within the samples collected it is found that the intracellular protozoan Toxoplasma gondii co-occurs with the virus canine adenovirus type-I (CAV-I) more frequently than expected by chance. Foxes concomitantly infected with these pathogens have lower condition scores than foxes who were not positive for both pathogens. From the data collected it is not clear whether hosts of lower condition are more susceptible to co-infection or if the co-infection is more harmful to hosts than being singly infected. T. gondii is not transmitted by foxes, but if infection with this parasite increases susceptibility to CAV-I then this virus may benefit from the presence of T. gondii within its host population. If it is the case that foxes of lower condition are simply more prone to co-infection then it should be expected that individual differences between hosts would cause heterogeneity in disease transmission. The need for cross-disciplinary approaches when studying pathogen communities is well demonstrated by this study, as is the need for more consideration to be paid to the community ecology of pathogens in epidemiological studies. In Chapter 4 a model is formulated to explore the effects of an interaction between a micro and a macro parasite. This is performed in the context of the increased prevalence and geographical range of the highly zoonotic small fox tapeworm Echinococcus multilocularis following successful rabies elimination in Western Europe. I explore the hypothesis that foxes with extremely high burdens may 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 by preferentially removing “super spreading” hosts. It is demonstrated that rabies limits E. multilocularis populations by limiting the density of available hosts. An interaction between rabies transmission rate and worm burden only caused a weak additional suppression on E. multilocularis populations, regardless of whether this relationship was linear or exponential. The elimination of rabies across Western Europe is certainly to be applauded. However, it should be noted from this work that surveillance of pathogen communities following successful eradication of one pathogen is of the upmost importance. 3 Finally, in Chapter 5 I examine how parasites adapt their investment in transmission in response to environmental changes experienced within a host. This is done by fitting models to data collected from mice infected with the malaria 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 and experimental studies reach conflicting conclusions regarding the “optimal response” to degradation of their habitat. Models were fitted to time series data from infection with one of six distinct genotypes. It is found that proportional allocation of resources into transmission, rather than replication, is highly sensitive to red blood cell (RBC) densities, with investment in transmission increasing as RBC resources become scarce. Investment in transmission also increases, albeit more weakly, in response to low parasite densities. These analyses highlight the fact that the complexity of interactions between parasites and their host hinder the identification of causal relationships, but supports recent work that questions the role of terminal investment in transmission in response to changes in the within-host environment. The broad scope of work presented here investigates a wide range of ecological factors (including community dynamics, habitat variability and reproductive success) at different ecological scales, responsible for heterogeneity in disease transmission. Transmission is a dynamic, and heterogeneous process. To better understand the ecology of disease it is logical to investigate the mechanisms behind this variation.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available
Keywords: QL Zoology