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D Mollison

Publications and source records attributed to D Mollison.

4 recordsLinked to original sources

Dependence of epidemic and population velocities on basic parameters.

This paper describes the use of linear deterministic models for examining the spread of population processes, discussing their advantages and limitations. Their main advantages are that their assumptions are relatively transparent and that they are easy to analyze, yet they generally give the same velocity as more complex linear stochastic and nonlinear deterministic models. Their simplicity, especially if we use the elegant reproduction and dispersal kernel formulation of Diekmann and van den Bosch et al., allows us greater freedom to choose a biologically realistic model and greatly facilitates examination of the dependence of conclusions on model components and of how these are incorporated into the model and fitted from data. This is illustrated by consideration of a range of examples, including both diffusion and dispersal models and by discussion of their application to both epidemic and population dynamic problems. A general limitation on fitting models results from the poor accuracy of most ecological data, especially on dispersal distances. Confirmation of a model is thus rarely as convincing as those cases where we can clearly reject one. We also need to be aware that linear models provide only an upper bound for the velocity of more realistic nonlinear stochastic models and are almost wholly inadequate when it comes to modeling more complex aspects such as the transition to endemicity and endemic patterns. These limitations are, however, to a great extent shared by linear stochastic and nonlinear deterministic models.

Animals

Simplifying simple epidemic models.

Interest has recently revived in the use of simple models for epidemic diseases. In particular, Anderson et al. have introduced an improved simple differential equation model for diseases such as fox rabies which regulate the population density of their host. Here I describe how such apparently simple models can be dissected into their basic components. This dissection facilitates a structural sensitivity analysis in which we explore the dependence of features of a model's behaviour on the assumptions regarding each component. I report that particular features can be related to particular components, for example, oscillations depend mainly on population growth and the generation gap of the disease, while estimates of the effect of potential control strategies such as vaccination or culling can be related directly to assumptions concerning the infection term and the way it changes with population density. Some features, for example, the level of prevalence of the disease and the period of any oscillations, turn out to be robust, depending mainly on basic ecological parameters. Others, including the crucial estimates regarding control, prove very sensitive to the details of the model. This is unfortunate, as the detailed form of the components is to a large extent chosen, not for ecological reasons, but to keep models simple, for example, the infectious period of a disease is often assumed to have an exponential distribution because this implies a constant death or recovery rate for infectious individuals which is mathematically very convenient for a continuous-time model. Because our dissection is in terms of components with straightforward ecological interpretations, any required improvements in modelling can be related to observational evidence which either exists or for which experiments can be suggested.

Animal Diseases