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Thesis (Ph. D.)--University of Queensland, 2002. / Includes bibliographical references.

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At the author’s request, the abstract has been removed due to the confidential nature of the thesis. It will be added once the embargo period has passed.

A model for experimental cecal and hepatic amebiasis was developed and characterized in the gerbil (Meriones unguiculatus). Pathogenic and non-pathogenic Entamoeba histolytica strains were shown to cause damage in the cecum, proportional to their previous behavior in humans. Secretion of intestinal mucus, crypt hyperplasia and cytolysis of interglandular epithelium were prerequisites for amebic invasion. Ulcerative lesions with destruction of mucosal and submucosal tissues led to amebic dissemination to the liver. Formation of amebic liver abscesses followed subacute changes in the liver. Liver lesions resulted from the cytolytic effects of the enzymes of destroyed neutrophils. Growth of liver abscesses followed cytolysis of the fibrogranuloma walls. Immunodepression in amebiasis was confirmed by serologic findings and histologic alterations in the lymph nodes and spleen, and by a lowered antiamebic effect of lymphoid cells in vitro. A neutrophil stimulating and chemotactic factor from pathogenic amebic membranes was isolated and characterized. It was shown that both host and parasite factors are involved in the pathogenesis and pathology of amebiasis.

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This thesis looks at developing an immunotherapy strategy for prostate cancer patients.

The scientific method requires the creation of a unifying hypothesis that reconciles an observed health outcome of infection with experimental data gathered about the disease process following infection. In this era of unprecedented amounts of data and information for various disease models, the creation and articulation of such hypothesis are often beyond human capacity. Modeling offers a means to generate hypothesis that provide complex mechanisms that reconcile seemingly contradictory data as well as quantitatively assess the relative plausibility of different mechanisms proposed to explain the same data/health outcome association. Here I explain the modeling approach to hypothesis generation and offer several examples of its implementation to address the role of the natural host immune response in determining outcomes of infection by a specific microbe including pathogenesis and microbial clearance. Such knowledge is key to devising sophisticated disease intervention strategies. The systems studied are i) Inflammatory Bowel Disease, where I explore mechanisms of inflammation regulation and how they break down to give rise to a chronic inflammatory disease, ii)H. pylori infection, in which I explore potential bacterial strategies for persistence as a commensal of the microflora or as a pathogen, and iii) HIV infection, where I explore the role of inflammatory and anti-inflammatory mechanisms in establishing viral infection. I present both mathematical, equation based models as well as agent-based, computational models offering a comparison of each method. / Ph. D.