Evaluation of a nematode (Capillaria hepatica Bancroft, 1893) as a control agent for populations of house mice (Mus musculus domesticus Schwartz and Schwartz, 1943).

Sudden, large-scale infestations of house mice (Mus musculus domesticus) occur irregularly in the cereal-growing regions of Australia, resulting in substantial economic losses. Mathematical modelling has been used to evaluate the use of the liver nematode Capillaria hepatica as a potential agent for the biological control of mouse populations. The models suggest that C. hepatica is unlikely to be successful as a single-release control agent: instead, the parasite would need to be released when it becomes apparent that an outbreak is likely. Stage-structured models, including time delays and seasonal mouse demographic parameters, suggest that the parasite may be successful as a control agent, provided it can be introduced into the mouse population at least one year before an outbreak occurs. The optimum time for introduction is in summer or autumn. Some generalisations of this work are discussed. A parasite which affects fecundity alone is unlikely to be a good control agent, because it will destabilize the host population. Macroparasites may be unable to spread sufficiently rapidly to control sudden rises in vertebrate populations.

The potential of Capillaria hepatica to control mouse plagues.

The potential of helminths as bio-control agents of mammalian pests has been largely ignored. However, the nematode Capillaria hepatica is currently being examined for its potential to control population outbreaks of house mice in Australia. Grant Singleton and Hamish McCallum discuss laboratory and ecological studies of the parasite and host, and describe the results of two models that explore the interaction between C. hepatica and mouse populations.

Covariance in parasite burdens: the effect of predisposition to infection.

Recently the phenomenon of predisposition to helminth infection has been reported in a number of studies: those individuals which are heavily infected before treatment with an anthelmintic tend also to acquire heavy parasite burdens following a period of reinfection. This correlation between parasite burdens in initial and reinfections is generated by differences between hosts in their exposure to infective stages and in their susceptibility to infection. Inter-host differences in these factors also generate the aggregated or over-dispersed parasite distributions that are usually observed. This paper uses probability theory to predict the correlation between initial and reinfection parasite burdens assuming that those inter-host differences which generate over-dispersion remain constant for a given individual between initial and reinfection periods. The predicted correlation is considerably greater than is observed in most published data sets. Over-dispersion is thus generated by variability between hosts which has components that remain constant between initial and reinfection and also components which vary between infection periods. The model is modified to account for those two sources of variability, and the result applied to published data to determine the contributions made by short and long-term factors to the observed distributions.

Models to assess the potential of Capillaria hepatica to control population outbreaks of house mice.

Population outbreaks of house mice (Mus domesticus) occur periodically in the wheatlands of southeastern Australia. This paper uses mathematical models to assist in the evaluation of the potential of a nematode, Capillaria hepatica, as a biological control agent to reduce the severity of these 'plagues'. C. hepatica is unique amongst helminths of mammals in that its eggs are released only upon the death of an infected host. The major goal of the modelling in this paper is to determine the impact of this feature on the population dynamics of the host-parasite interaction. Simple differential equation models are used to examine the general properties of the system and determine which population parameters are most crucial to the outcome of the interaction. These models are supplemented by age-structured models which investigate the initial behaviour of the system after introduction of the parasite. The necessity of host death for transmission is a strongly destabilizing factor, suggesting that C. hepatica cannot regulate most populations stably in the absence of strong resource limitation, although it has the potential to depress mouse populations below infection-free levels. Although C. hepatica influences mouse fecundity at lower burdens than it affects mortality, the age-structured models show that parasite-induced host death cannot be neglected. Because transmission requires host death, the parasite life-cycle operates on a time-scale similar to that of the hosts, and introduction of the parasite as early as possible in the development period of an outbreak will therefore be necessary to achieve substantial reductions in plague intensity.

Acquired resistance of black mollies Poecilia latipinna to infection by Ichthyophthirius multifiliis.

Changes in the response of black mollies Poecilia latipinna to infection with Ichthyophthirius multifiliis subsequent to single I. multifiliis infections were examined experimentally. Incomplete resistance to infection was established, the degree of which did not depend on the intensity of the initial infection. Resistance was maintained for longer periods, however, by those fish with higher initial levels of infection. Previous experience of infection by their hosts had a significant, though small, effect on the time for which trophozoites remained on the fish. The influence of these results on the population dynamics of the Ichthyophthirius-fish interaction is examined with the aid of simple mathematical models.

Systematic temporal changes in host susceptibility to infection: demographic mechanisms.

Simple mathematical models are developed to examine the influence of variability in host susceptibility to infection, on the dynamics of host-parasite population interactions. When hosts differ in their innate susceptibility (at birth), to infection by a specific parasite, the average susceptibility of the host population as a whole may show systematic changes through time. Such patterns may arise as a result of demographic factors associated with the interaction between host and parasite populations, in the absence of inheritance mechanisms (a genetic component) or acquired resistance (an immunological component). The general significance of this observation is discussed in terms of the coevolution of host-parasite associations.