Effects of infective stage density, host density and surface area available for transmission on the rate of transmission of the nematode Heligmosomoides polygyrus were investigated in a controlled environment where naive CD1 outbred mice were naturally infected. Within a range of densities of infective larvae (500-6000/cage), randomly spread on damp peat moss, a linear increase was observed in the mean number of fourth stage larvae embedded in the intestinal mucosa per host. As host density increased (1-6 mice/cage), but exposure dose held constant (8000L$ sb3$), the mean number of L$ sb4$ recovered per mouse decreased at a faster rate than expected assuming a constant per capita rate of transmission. In an attempt to interpret the experimental data, mathematical models were generated. Although the inclusion of a death rate of infective larvae dependent on mouse density did improve the fit of the mathematical model based on a constant per capita rate of transmission, the best fit was provided by a model assuming a per capita rate of transmission dependent on mouse density. An independent experiment exploring the impact of surface area available for transmission on the relationship between host density and the rate of infection confirmed the adequacy of the mouse density-dependent per capita rate of transmission hypothesis.

The importance of host heterogeneity in generating aggregation was investigated using Heligmosomoides polygyrus (Nematoda) in laboratory mice. The protocol compared parameters of infection between inbred and outbred mice, primary and challenge infections, and gavage and natural exposure, to investigate the relative effects of innate resistance, acquired resistance and behaviour, respectively. The results show that heterogeneity in acquired resistance is the most consistent factor contributing to the variability and aggregation of H. polygyrus. When groups of mice did not acquire resistance, either in certain inbred strains or when mice were immunosuppressed, variability after the challenge was comparable with that after a primary infection. Heterogeneity in host behaviour, particularly in behaviours enhancing skin contact with larvae, frequently increased aggregation above that detected in both primary and challenge infections. Surprisingly, inconsistent results were obtained when inbred and outbred groups of mice were compared. The results suggest that the relative contribution of these three factors is likely to vary spatially and temporally.

The digenean parasite, Plagiorchis elegans can establish infections in the incompatible snail, Biomphalaria glabrata , a vector of human schistosomiasis. Although embryonic development is arrested at the sporocyst stage, infection with a single parasite egg reduced reproductive success of this incompatible host to 64%. Heavier doses reduced this to 45%. Biomphalaria glabrata quickly acquired large numbers of parasites by ad libitum browsing on egg-contaminated substrates. Age of the host at exposure affected subsequent reproductive success and survival. Snails exposed as young (3mm), produced 54% fewer eggs, and suffered relatively high mortality. Adults (9mm) were affected only marginally. Plagiorchis elegans shares its ability to establish truncated infections in incompatible hosts with at least one other plagiorchiid. Haematoloechus medioplexus castrated the snail Stagnicola elodes, but not B. glabrata. Findings are discussed in the context of using incompatible digenean parasites as agents in the biological control of snails and snail-borne diseases, and ecological consequences of these infections.

Thesis (M.Sc.1981) from the Department of Zoology, University of Adelaide.

Thesis (Ph.D.)--Murdoch University, 2002. / Thesis submitted to the Division of Veterinary and Biomedical Sciences. Bibliography: p. 129-141.

Diss.

Proefschrift--Utrecht. / Summary in English. "Stellingen": [2] p. laid in. "Lijst van geraadpleedge literatuur": p. [82]-84.

Proefschrift--Utrecht. / Summary in English. "Stellingen": [2] p. laid in. "Lijst van geraadpleedge literatuur": p. [82]-84.

Thesis (Ph. D.)--Brigham Young University. Dept. of Microbiology and Molecular Biology, 2007. / Includes bibliographical references (p. 75-82).

Thèse de doctorat--Sciences naturelles--Faculté des sciences de Paris, 1907. N°: 1263. / Notes bibliogr.