The influence of energy restriction on the transmission dynamics of a direct life cycle nematode, Heligmosomoides polygyrus, within free-running arena Systems has to date remained unexplored. Indoor populations of CD-1 outbred mice were established for 12 weeks in arenas and fed either energy-suffi ci ent (ES) or energy-restricted (ER-20% réduction in metabolizable energy) diets. Infection was introduced to ail arenas following 3 weeks of diet treatment. Contrary to previous findings, the mice fed the ER diets compensated for the deficiency by increasing food consumption and thus, while early in the experiment energy restriction was evident, dietary effects were no longer observed after 6 weeks. Worm burdens, measured at 4 time points over the course of the experiment, were higher in mice fed the ES diets. Although mice fed the ER diets had greater contact with infected areas, the mice fed the ES diets increased the duration of behaviours that heighten ingestion of the parasite - self and allogrooming. Dietary effects on behaviour were observed only after infection was introduced and were more pronounced in the durations of individual bouts rather than in overall durations or time budgets. Nesting bouts were prolonged in mice in the ER arenas perhaps as a means of thermoregulation to counteract the combined effects of infection and energy restriction. The duration of exploratory bouts was also higher in the ER mice possibly due to an inability to receive or process information in their environment. Social interactions, predominantly involving sniffing, increased after infection was introduced, supporting the rôle of odour in communicating infection status in same-sex conspecifics. Together these results provide a more comprehensive ethogram of mice in a semi-natural setting and highlight those behaviours where adaptive plasticity allows response to dietary and infection stresses.

In mice infected with 10$ sp4$ Giardia muris cysts, a peak lymphocyte proliferation in the spleen and Peyer's patches in response to Giardia extract occurred during the elimination and latent phases, respectively. This shows that the Peyer's patch cells are more responsive than the spleen to Giardia infection. Th2-type cytokines produced by Peyer's patch cells may play a protective role during the latent and acute phases. Th1-type cytokines may contribute to this production during the elimination phase. Cytokine production in response to Giardia extract in vitro was observed in mice immunized with this extract, but not in control mice. Therefore, Giardia antigen can induce cytokine production in vitro in a specific manner.

Interactions among zinc deficiency, energy restriction, immunity and Heligmosomoides polygyrus (Nematoda) infection in mice were investigated. Mice were fed zinc-sufficient (Zn+: 60mg zinc/kg diet), zinc-deficient (Zn$-$: 0.75 mg/kg) or pair-fed (PF) diets. Liver and serum zinc concentrations were reduced in Zn$-$ mice, but zinc content of worms was unaffected by host diet. Both zinc deficiency and energy restriction accelerated worm maturation during a primary infection, but zinc deficiency caused stunting of female worms. Energy restriction led to a anteriorad distribution of worms along the intestine whereas zinc deficiency led to a posteriorad distribution. Enhanced parasite survival in Zn$-$ and PF mice was associated with a decreased immune response in both primary and challenge infections. In the primary infection, spleen cell production of interleukin-4 (IL-4) and interferon-gamma (IFN-$ gamma$), peripheral eosinophilia and serum levels of IgE and IgG1 were reduced by zinc deficiency, whereas the reduced delayed type hypersensitivity (DTH) response and impaired interleukin-5 (IL-5) production were attributed to energy restriction. In the challenge infection, reduced antibody levels (total IgE and IgG1, parasite-specific IgG1 and IgG3) and eosinophilia were attributed to zinc deficiency whereas the higher worm numbers were attributed to a combined effect of zinc deficiency and energy restriction. Although the absolute number of spleen cells was reduced in both Zn$-$ and PF mice, neither deficiency altered the proportion of the cell subpopulations. In vitro functional assays in response to parasite antigen (Ag) revealed that T cell proliferation was reduced by a direct effect of zinc deficiency on T cells, and by the effects of energy restriction on antigen presenting cells (APC). Impaired cytokine production in Zn$-$ mice was more complex. Zinc deficiency reduced T cell function (IL-4 production), energy restriction decreased T cell (IFN-$ gamma$ productio

Both major histocompatibility genes (MHC) and infection have been shown to influence urinary odours in mice, and mice may use MHC-associated odours to detect kin for the purpose of choosing communal nesting partners, or to avoid mating with close relatives. Additionally, mice may use infection-related odours to avoid mating with sick individuals or those genetically susceptible to infection. I tested the above theories using urine as the source of odour. In a series of odour preference experiments, employing two MHC-congenic strains of mice (B10 and B10.Q), I tested the proposition that females prefer MHC-similar female odours when choosing female relatives as nesting partners, and that females prefer MHC-disparate male odours for the purpose of disassoratative mating. I found that females did not display a preference for MHC-similar female odours or MHC-disparate male odours. However, when B10.Q male urine donors were infected with 100 L3 larvae of Heligmosomoides polygyrus (Nematoda), both strains of female displayed a significant preference for the odours of uninfected B10 males. To determine whether female odour preference for uninfected males extended to actual mate choice, I subsequently examined female mate choice in a controlled setting. Using CD-1 outbred mice, I found that females preferred to mate with uninfected males over males subclinically infected with 200 L3 of H. polygyrus , as evidenced by first ejaculation preferences. In this experiment, males were tethered, and as such, male dominance interactions were prevented. Thus, in the final experiment, to assess whether male dominance interactions influenced female mate choice, in addition to infection, I tested female mate choice in a seminatural setting, which allowed for social interactions to occur. In this study, paternity was ascertained through DNA analysis and the resulting data indicated that neither male dominance status nor infection had a substantial impact on fema / Overall, the data do not support the theory that MHC-based preferences occur through urinary odours. However, the results do substantiate previous findings regarding female preferences for the odours of uninfected males. Furthermore, data from the controlled mate choice assay indicate that female odour preference for uninfected males extends to actual mate choice. Conversely, in the seminatural setting neither dominance nor infection prevailed as factors driving female mate choice. I suggest that this may be a consequence of the structural complexity of my arenas.

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