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A Spatially Aggregated Disease/Host Model for Bovine Tb in New Zealand Possum Populations

N. D. Barlow
Journal of Applied Ecology
Vol. 28, No. 3 (Dec., 1991), pp. 777-793
DOI: 10.2307/2404207
Stable URL: http://www.jstor.org/stable/2404207
Page Count: 17
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
A Spatially Aggregated Disease/Host Model for Bovine Tb in New Zealand Possum Populations
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Abstract

(1) Deterministic disease/host models based on differential equations, with and without age-structure, are used to aid understanding of the epidemiology of bovine Tb in New Zealand's possum Trichosurus vulpecula populations. (2) The intrinsic rate of increase for possums is calculated to be 0.2-0.3 year-1, density dependence is associated more with mortality than recruitment and affects all age-classes. (3) Bovine Tb in possums is characterized by low prevalence, around 5%, little effect on host density but moderately rapid dynamics. Its behaviour cannot be accounted for by the classic models which assume homogenous mixing. In these models low prevalence is invariably associated either with a significant reduction in host density or extremely slow rates of change of the disease. (4) The classic models are therefore modified to include spatial aggregation of disease, which is quantified using field data. (5) Three scenarios for the disease are considered which agree with observations: chronic disease with a short latent period relative to the infectious period (e.g. 6 months and 1.5 years respectively) and most animals with gross lesions infectious; acute disease with a relatively long latent period (e.g. 1 year latent period and 3 months infectious period) and few animals with gross lesions infectious; and an acute disease with short latent and infectious periods (e.g. 2-3 months) and most animals with gross lesions infectious. The latter appears the most likely. (6) For both the chronic and acute scenarios and likely combinations of disease parameters, the basic reproductive rate for the disease, R0, is approximately 1.8-2.0. (7) It is suggested that the transmission coefficient for the disease (β) varies inversely with the possum carrying capacity (K), explaining why prevalence and disease dynamics vary little with K or the habitat. In simpler Australian habitats, low β values due to more intense spacing behaviour, as well as very much lower K values, may explain why Tb is absent from possums.

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