The host-parasite interface between the branchiobdellid Cambarincola vitrea Ellis and its crayfish host is investigated along ecological, ultrastructural, serological, and endocrinological lines of evidence. Monthly analysis of a natural branchiobdellid from a vernal habitat demonstrates the annelid to be particularly sensitive to changes involving both the physical habitat as well as the host crayfish.

No description available.

Biological rhythms are thought to have evolved to enable organisms to organise their activities according to the Earth’s predictable cycles, but quantifying the fitness advantages of rhythms is challenging and data revealing their costs and benefits are scarce. More difficult still is explaining why parasites that exclusively live within the bodies of other organisms have biological rhythms. Rhythms exist in the development and traits of parasites, in host immune responses, and in disease susceptibility. This raises the possibility that timing matters for how hosts and parasites interact and, consequently, for the severity and transmission of diseases. Despite their obvious importance in other fields, circadian rhythms are a neglected aspect of ecology and evolutionary biology. The ambitions of this thesis are to integrate chronobiology, parasitology and evolutionary theory with mathematical models to obtain a greater understanding about how and suggest why malaria parasites have rhythms as well as the effect of infection on host rhythms. First, I identify how malaria parasites lose their developmental rhythms in culture, when they lack any potential time cues from the host. Next, I characterise parasite rhythms inside the mammalian host in terms of synchrony and timing and demonstrate there is genotype by environment interactions for characteristics of parasite rhythms. Then, I investigate the effect that parasite infection has on host rhythms and show there is variation between parasite genotypes in their effect on host locomotor activity and body temperature rhythms during infections. Finally, I explore which host rhythms may be driving parasite synchrony and timing and demonstrate the importance of peripheral host rhythms for the timing of malaria parasite developmental rhythms. The data presented here provides novel and important information on the role of rhythms during disease and opens up a new arena for studying host-parasite coevolution.

<p>  </p> <p>Predators and parasites are critical, interconnected members of the community and have the potential to influence host populations. Predators, in particular, can have direct and indirect impacts on disease dynamics. By removing hosts and their parasites, predators alter both host and parasite populations and ultimately shape disease transmission. Our ability to accurately predict disease dynamics requires understanding the ecological effects of predation on prey and host densities and its role in the coevolution of host resistance and parasite virulence. While the impact of predators on disease dynamics has received considerable attention, research has focused on selective predation on infected prey. There is, however, substantial evidence that some predators avoid infected prey, preferentially attacking uninfected individuals. Such different strategies of prey selectivity by predators modulate host-parasite interactions, changing the fitness payoffs both for hosts and their parasites. I use empirical results and theoretical predictions as a framework to discuss the mechanisms by which predation for infected versus uninfected individuals can affect disease dynamics. First, by integrating hypotheses from behavioral ecology and disease ecology, I outlined novel perspectives that complement the prevailing view of selective predation of infected individuals (Chapter 1). Then, exploring short-term ecological outcomes and long-term host-parasite coevolution, I investigated patterns of <em>Daphnia dentifera</em> host population densities and host susceptibility over several generations under different types of predation pressure, including selective predation on infected and uninfected individuals (Chapter 2). Finally, building on the results of this research, I developed a high school project-based lesson plan that facilitates the instruction of the nature of science, implementing on-going ecological research in activities to improve student learning based on a constructivist approach to learning (Chapter 3). Together this research highlights the differential ecological and evolutionary outcomes of host-parasite interactions under varying community contexts.</p>

Call number: LD2668 .T4 1979 S73 / Master of Science

Call number: LD2668 .T4 1986 C374 / Master of Science / Plant Pathology

No description available.

In this thesis, I study a radiation of brood-parasitic finch species, the indigobirds and whydahs (genus Vidua), that occur across Africa. Host colonisation is tightly linked to speciation in Vidua because of their remarkable capacity to imprint on their hosts, with mating traits and host preferences being influenced by the parasite's early environment. The challenge of explaining why the radiation has diversified to the extent it has therefore simplifies to understanding why only certain potential host species have been successfully colonised. Following on from the introduction (Chapter 1), I begin by critically examining the logic with which mimicry in the natural world can be conceptually organized (Chapter 2). This creates a “mimicry landscape” in which to situate the mimetic adaptations of hosts exhibited by Vidua. The framework can be used to contrast and draw parallels between these and other mimetic adaptations present in the natural world. In Chapter 3, I review the literature on begging call mimicry and development across all avian brood parasite species. I outline the conditions under which we expect begging call mimicry to evolve, and when we expect it to develop primarily through genetic or environmental cues. This provides clear predictions for what we expect to occur in Vidua finches, which are tested in Chapters 4 and 5. In Chapter 4, I quantify the mimicry of host nestlings by Vidua in detail. I provide the first quantitative evidence that Vidua nestlings mimic the begging calls and show for the first time that Vidua are imperfect mimics of their hosts. In Chapter 5, I simulate the colonisation of a new host by transferring Vidua eggs into the nest of a new host species. I monitor Vidua survival in the foreign host environment and test several hypotheses about what explains differences in chick survival. I find that Vidua survive poorly in the new nest environment and that they do not show adaptive plasticity in begging calls or head movements. This poor survival occurs despite there being minimal differences in the diets each host species feeds their young. Finally, in Chapter 6, I carry out a comparative analysis on the evolution of estrildid mouth markings. Estrildid finches are the hosts of Vidua and so provide the landscape of potential ecological niches that Vidua may colonise and adapt to. I demonstrate that the host family shows strong phylogenetic signal in mouth marking traits, and find no evidence that ecological factors such as light environment or predation pressure has shaped estrildid mouth marking evolution. The work in this thesis highlights how difficult successfully colonising new hosts is for Vidua finches. Vidua must mimic hosts in multiple traits (mouth markings, begging calls, head movements) to obtain sufficient amounts of food from host parents. Overall, habitat filters, the complex and diverse begging displays of estrildid nestlings, the discriminatory behaviour of estrildid parents against mismatching chicks and the lack of adaptive plasticity in begging displays by Vidua together help explain why the Vidua radiation consists of only 19 species rather than many more or fewer.

No description available.

Includes bibliography.