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disease because the behavior of the infectious animal becomes erratic and combat-
ive, and the disease is then spread during contact with healthy foxes through biting.
The incubation period for fox rabies varies from 14 to 90 days, ending in clinical
illness. An animal may be infectious for up to a week before the onset of symptoms
and remains infectious until death. Model parameters such as the effective biting
rate and the actual length of the infected and infectious periods are difficult to deter-
mine in the field. We have used the best available data and determined an effective
biting coefficient by trial and error comparisons of fox densities gained from the
literature cited below.
A complete model of the fox and fox behavior might include a set of sex dif-
ferentiated age cohorts. We found however, that the history of the disease and of
fox behavior could be adequately represented by a simple four stock model of both
healthy and sick juveniles and adults. The model includes both deterministic and
stochastic components and can be adapted to any disease that possesses spatial dy-
namics by simply adjusting the input data. The results of our epidemic model indi-
cate that the incidence of fox rabies can be decreased with an intervention strategy
such as hunting. However, the results also indicate that the current fox hunting pres-
sures, coupled with the introduction of the rabies disease, would lead to elimination
of the fox in Illinois. Our results suggest that a reduced hunting pressure can leave a
sustainable fox population in spite of the occasional introduction of the disease from
surrounding areas. The disease can also be controlled by aerial deposition of baited
vaccines over a large area. The model indicates the spatial dynamics of diseased
foxes, and thus allows the most judicious and least expensive aerial deployment of
the vaccine.
15.2.3 Previous Fox Rabies Models
Dynamic models of rabies in wildlife populations have been proposed by others
5
.
These models have focused on the spatial spread of disease and potential impact
of various control measures. But the addition of a spatial component to the disease
dynamic is, in our opinion, a critical component. Spatial components can more eas-
ily explain variation in the rate of disease spread through a population
6
,aswell
as provide a more holistic view of the dynamic interaction of animal, disease, and
landscape. Since wildlife populations are not indolent and are typically in a perpet-
ual state of flux, contact rates between diseased and healthy animals depend to some
5
David, J.M., L. Andral, and M. Artois. 1982. Ecological Modeling 15 107-125.
Bacon, P.J. 1985. Population Dynamics of Rabies in Wildlife, Academic Press, New York, NY.
White, P.C.L., S. Harris, and G.C. Smith. 1995. Journal of Applied Ecology 32 693-706.
Murray, J.D., E.A. Stanley, and D.L. Brown. 1986. Proceedings of the Royal Society of London
B229 111-150.
Gardner, G., A. Leslie, R.T. Gardner, and J. Cunningham 1990. Verlag der Zeitschrift fur Natur-
forschung 45c 1230-1240.
6
Bacon, P.J. and D. MacDonald,. 1980. Nature 289 634-635.
