PhD Candidate, The University of Sydney
How do parasites and disease influence population dynamics of overabundant kangaroos
Understanding how parasites and disease influence population dynamics is becoming increasingly important given the overabundance of kangaroos in urban spaces. This project aims to conduct a large field based investigation to shed light on the impact of ectoparasites and gastrointestinal nematodes on host fitness in peri urban eastern grey kangaroos at four populations along the NSW coast. Host fitness will be assessed by measuring individual reproductive success, survival, body condition and blood parameters. The experiment will manipulate parasitism and reproductive hormones in wild kangaroos to estimate the effect hormones play in parasitism and in kangaroo mate selection. Research aims to examine the potential for kangaroos as reservoirs of disease focussing on Q fever, a re-emerging disease that affects humans. A laboratory based disease investigation will be carried out to determine seroprevalence of Q fever in kangaroos in NSW and attempt to ascertain transmission dynamics and subclinical effects Q fever.
Abstract: Provisioning of abundant food resources in human-altered landscapes can have profound effects on wildlife ecology, with important implications for pathogen transmission. While empirical studies have quantified the effects of provisioning on host behaviour and immunology, the net interactive effect of these components on host-pathogen dynamics is unknown. We use simple compartmental models to investigate how provisioning-induced changes to host demography, contact behaviour and immune defence influence pathogen invasion and persistence. We show that pathogen invasion success and equilibrium prevalence depend critically on how provisioning affects host immune defence and that moderate levels of provisioning can lead to drastically different outcomes of pathogen extinction or maximizing prevalence. These results highlight the need for further empirical studies to fully understand how provisioning affects pathogen transmission in urbanized environments.
Pub.: 25 Jul '14, Pinned: 25 Aug '17
Abstract: Tropical savannas cover 20-30% of the world's land surface and exhibit high levels of regional endemism, but the evolutionary histories of their biota remain poorly studied. The most extensive and unmodified tropical savannas occur in Northern Australia, and recent studies suggest this region supports high levels of previously undetected genetic diversity. To examine the importance of barriers to gene flow and the environmental history of Northern Australia in influencing patterns of diversity, we investigated the phylogeography of two closely related, large, vagile macropodid marsupials, the antilopine wallaroo (Macropus antilopinus; n = 78), and the common wallaroo (Macropus robustus; n = 21). Both species are widespread across the tropical savannas of Australia except across the Carpentarian Barrier (CB) where there is a break in the distribution of M. antilopinus. We determined sequence variation in the hypervariable Domain I of the mitochondrial DNA control region and genotyped individuals at 12 polymorphic microsatellite loci to assess the historical and contemporary influence of the CB on these species. Surprisingly, we detected only limited differentiation between the disjunct Northern Territory and QueenslandM. antilopinus populations. In contrast, the continuously distributedM. robustus was highly divergent across the CB. Although unexpected, these contrasting responses appear related to minor differences in species biology. Our results suggest that vicariance may not explain well the phylogeographic patterns in Australia's dynamic monsoonal environments. This is because Quaternary environmental changes in this region have been complex, and diverse individual species' biologies have resulted in less predictable and idiosyncratic responses.
Pub.: 19 Jul '14, Pinned: 25 Aug '17
Abstract: Current understanding of the immune system comes primarily from laboratory‐based studies. There has been substantial interest in examining how it functions in the wild, but studies have been limited by a lack of appropriate assays and study species. The three‐spined stickleback (Gasterosteus aculeatus L.) provides an ideal system in which to advance the study of wild immunology, but requires the development of suitable immune assays. We demonstrate that meaningful variation in the immune response of stickleback can be measured using real‐time PCR to quantify the expression of eight genes, representing the innate response and Th1‐, Th2‐ and Treg‐type adaptive responses. Assays are validated by comparing the immune expression profiles of wild and laboratory‐raised stickleback, and by examining variation across populations on North Uist, Scotland. We also compare the immune response potential of laboratory‐raised individuals from two Icelandic populations by stimulating cells in culture. Immune profiles of wild fish differed from laboratory‐raised fish from the same parental population, with immune expression patterns in the wild converging relative to those in the laboratory. Innate measures differed between wild populations, whilst the adaptive response was associated with variation in age, relative size of fish, reproductive status and S. solidus infection levels. Laboratory‐raised individuals from different populations showed markedly different innate immune response potential. The ability to combine studies in the laboratory and in the wild underlines the potential of this toolkit to advance our understanding of the ecological and evolutionary relevance of immune system variation in a natural setting.
Pub.: 21 Dec '15, Pinned: 25 Aug '17
Abstract: Autoimmune diseases (ADs) represent a heterogeneous group of disorders that affect specific target organs or multiple organ systems. These conditions share common immunopathogenic mechanisms (i.e., the autoimmune tautology), which explain the clinical similarities they have among them as well as their familial clustering (i.e., coaggregation). As part of the autoimmune tautology, the influence of environmental exposure on the risk of developing ADs is paramount (i.e., the autoimmune ecology). In fact, environment, more than genetics, shapes immune system. Autoimmune ecology is akin to exposome, that is all the exposures - internal and external - across the lifespan, interacting with hereditary factors (both genetics and epigenetics) to favor or protect against autoimmunity and its outcomes. Herein, we provide an overview of the autoimmune ecology, focusing on the immune response to environmental agents in general, and microbiota, cigarette smoking, alcohol and coffee consumption, socioeconomic status (SES), gender and sex hormones, vitamin D, organic solvents, and vaccines in particular. Inclusion of the autoimmune ecology in disease etiology and health will improve the way personalized medicine is currently conceived and applied.
Pub.: 21 May '16, Pinned: 25 Aug '17
Abstract: The new fields of ecological immunology and disease ecology have begun to merge, and the classic fields of immunology and epidemiology are beginning to blend with them. This merger is occurring because the integrative study of host-parasite interactions is providing insights into disease in ways that traditional methods have not. With the advent of new tools, mathematical and technological, we could be on the verge of developing a unified theory of infectious disease, one that supersedes the barriers of jargon and tradition. Here we argue that a cornerstone of any such synthesis will be host competence, the propensity of an individual host to generate new infections in other susceptible hosts. In the last few years, the emergence of systems immunology has led to novel insight into how hosts control or eliminate pathogens. Most such efforts have stopped short of considering transmission and the requisite behaviors of infected individuals that mediate it, and few have explicitly incorporated ecological and evolutionary principles. Ultimately though, we expect that the use of a systems immunology perspective will help link suborganismal processes (i.e., health of hosts and selection on genes) to superorganismal outcomes (i.e., community-level disease dynamics and host-parasite coevolution). Recently, physiological regulatory networks (PRNs) were cast as whole-organism regulatory systems that mediate homeostasis and hence link suborganismal processes with the fitness of individuals. Here, we use the PRN construct to develop a roadmap for studying host competence, taking guidance from systems immunology and evolutionary ecology research. We argue that PRN variation underlies heterogeneity in individual host competence and hence host-parasite dynamics.
Pub.: 13 Dec '16, Pinned: 25 Aug '17