Methods for human disease are therefore able to be much more demanding of data, and may correspondingly be more complex than methods that can usefully be applied to animal populations. The data available in human disease epidemiology are typically of much better quality than those available for wildlife disease (for example, records of measles infection are available covering 70 years, on a monthly basis, in most developed countries nothing approaching this quality is available for any freeranging animal). Covering the problems of parameterizing models of disease in humans is beyond the scope of this book. The key processes that must be understood and parameterized are transmission and the effect that the parasite or pathogen has upon the host.įor obvious reasons, models of host–parasite and host–pathogen interactions are most highly developed for organisms that cause disease in humans (see, for example, Anderson & May, 1991). The extremely close association between exploiter and victim, which is characteristic of host–pathogen and host–parasite interactions, means that the structure of models of these interactions is rather different from those of predator–prey interactions. Host–parasite and host–pathogen interactions are similar to predator–prey or host–parasitoid interactions, because they are interactions where one species uses the other as a resource.
C H A P T E R 1 0 Host–pathogen and host–parasite models
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