Call number: LD2668 .T4 1962 J65

Call number: LD2668 .T4 1979 A431 / Master of Science

Call number: LD2668 .T4 1966 R923 / Master of Science

Forty-two Blarina brevicauda and 50 Sorex cinereus from various locations in Delaware County, Indiana, were examined for helminth parasites. From zero to eight parasites were found in 98 percent of the B. brevicauda. From zero to five parasites were found in 92 percent of the S. cinereus. Longistriata depressa, Porrocaecum americanum, P. encapsulatum, Capillaria blarinae, Protogynella sp., Hymenolepis anthocephalus, Panopistus pricei, Entosiphonus thompsoni, Brachylaima rhomboideus, Trichuris sp., Parastrongyloides winchesi, and a larval spirurid nematode, probably Physaloptera limbata, parasitized B. brevicauda. Larval nematodes, which may be Angiostrongylus michiganensis were abundant in the digestive and respiratory tracts. B. brevicauda also contained a minute, unidentifiable nematode from the small intestine. Tapeworms from four different B. brevicauda were in such poor condition as to make positive identification difficult. These were probably H. blarinae. H. parva; H. serrula; H. faculata; H, longi; two different unidentifiable hymenolepids; P. americanum; P. encapsulatum; A. michiganensis; Pseudophysaloptera formosana soricina; L. depressa; P, pricei; C. rauschi; P. winchesi; larval capillarid nematodes from the liver, probably C. hepatica; and three small unidentifiable nematodes parasitized S. cinereus.First reports include: P. winchesi in an American Sorex sp., Trichuris sp. from the intestine of B. brevicauda, P, pricei in S. cinereus, and larval capillarids, possibly C. hepatica, from the liver of S. cinereus.Possible relationships between the parasites' life cycles and the hosts' habitats were discussed.

Almost 2 billion people world-wide are infected with parasitic helminths. These complex multicellular eukaryotic organisms are capable of establishing long-term infections even in the face of an intact immune response. Typically, in these settings regulatory components of the immune response, such as Foxp3+ T regulatory cells (Tregs), become dominant, limiting protective effector responses towards the parasite. Helminths are thought to have evolved mechanisms, including release of immunomodulatory molecules termed excretory-secretory products (ES), to sway the balance between the regulatory and effector arms of the immune response to favour their persistence. In this thesis both the development of a protective immune response toward, and the potential manipulation of the immune response by, the rodent gastrointestinal nematode Heligmosomoides polygyrus have been studied. Firstly, the effects of H. polygyrus ES (HES) on bone-marrow derived dendritic cells (DCs) were analysed. Although HES did not alter the phenotype of the DC it was found to be able to suppress the ability of the DC to respond to inflammatory stimuli. This activity was lost when HES was heat-inactivated (hiHES). After adoptive transfer, HES-pulsed DCs were able to induce a HESspecific T helper (Th)2-type response even if co-treated with an inflammatory stimulus. Th2-type responses are protective against H. polygyrus infection. Surprisingly, the ability of HES to generate a Th2-response in a co-treatment situation was not related to its anti-inflammatory properties; DCs co-treated with hiHES and an inflammatory stimulus were able to drive an equivalent Th2-response to HES in this situation. Next, making use of mouse strains with different susceptibility phenotypes to primary H. polygyrus infection, potential mechanisms of resistance were characterised. Development of granulomas in the gut wall were found to be associated with reduced worm burdens. Furthermore, in highly susceptible C57BL/6 mice, production of IL-23 was shown to be counter-regulatory to this process, as mice on the same background but deficient in this cytokine have increased numbers of granulomas and dramatically enhanced resistance. Susceptibility to H. polygyrus was also considered at the level of epigenetic regulation. A protein that binds specifically to methylated DNA, methyl-CpG binding domain protein (MBD)2, was found to affect the proportion of Foxp3+ Tregs within the CD4+ T cell population in vivo. Additionally, in vitro induction of Foxp3 in response to TGF-β was enhanced in MBD2-/- CD4+ T cells. MBD2-/- mice had a trend towards increased worm burdens when infected with H. polygyrus, suggesting that the difference in proportion of Tregs may limit generation of an effector response. Finally, the ability of HES to directly affect the regulatory arm of the immune response was focussed upon. It was found that HES was able to induce Foxp3 expression in naïve peripheral T cells, and that this was mediated by stimulation of the TGF-β pathway. The TGF-β mimic was of parasite origin as a pan-vertebrate TGF-β antibody was unable to block its effects but sera from H. polygyrus infected animals was competent to do this. Activity of this type was not limited to HES as ES from the ovine helminth Haemonchus contortus was found to have the same property. These data imply that some helminth parasites have evolved mechanisms to support generation of Foxp3+ Tregs, thus favouring the regulatory arm of the immune response and hence their own persistence.

There is a growing interest in the nature of parasite-host interactions, the role these relationships play in ecological communities, and how human activities alter these associations. Furthermore, because inference about these interactions is usually gained by methods of statistical hypothesis testing, additional importance should be placed on the analysis and interpretation of parasite-host interactions. In this dissertation I address these ideas in three separate but interrelated studies with the three following questions: 1) How do two parasites with complex life-cycles alter the behavior of a novel amphipod host, and how do host and non-host predators respond to infected amphipod prey? In contrast to other studies, I found that two parasites of an endemic amphipod at Montezuma Well had little affect on their amphipod host, and that these associations had little affect on predation rates by both host and non-host predators. Results from this study underscore the importance of further investigating novel parasite-host interactions and placing them in their phylogenetic and evolutionary context. 2) Does human recreation affect spatial patterns of infection in an otherwise natural ecosystem? This study demonstrates that human visitors to Montezuma Castle National Monument alter patterns of waterfowl space use that in turn affect spatial patterns of disease in invertebrate hosts. This is the first study to document such an effect, and I discuss the important implications of this finding. 3) How is hypothesis testing applied in studies of wildlife disease, what conclusions can we make about the relative usefulness of these methodologies, and how can the analysis and interpretation of wildlife disease studies be improved? In this final study I conducted a literature review, computed statistical power for methodologies used in the literature, and re-analyzed published data to provide an example of the advantages of my suggested approach. I conclude that many studies report findings using methods that could be more informative and some studies may lack statistical power, demonstrating the importance of using prospective power analysis in the design of future studies. Furthermore, using statistical techniques that estimate the observed effect size can aid in increasing information transfer in studies of wildlife disease.

Thesis (MSc (Veterinary Tropical Diseases.))--University of Pretoria, 2008. / Includes bibliographical references. Also available in print format.

Thesis (M.P.H.M. (Primary Health Care Management))--Mahidol University, 2000.

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