Utilizing stochastic genetic epidemiological models to quantify the impactof selection for resistance to infectious diseases in domestic livestock

Citation
K. Mackenzie et Sc. Bishop, Utilizing stochastic genetic epidemiological models to quantify the impactof selection for resistance to infectious diseases in domestic livestock, J ANIM SCI, 79(8), 2001, pp. 2057-2065
Citations number
16
Categorie Soggetti
Animal Sciences
Journal title
JOURNAL OF ANIMAL SCIENCE
ISSN journal
00218812 → ACNP
Volume
79
Issue
8
Year of publication
2001
Pages
2057 - 2065
Database
ISI
SICI code
0021-8812(200108)79:8<2057:USGEMT>2.0.ZU;2-5
Abstract
This paper demonstrates the use of stochastic genetic epidemiological model s for quantifying the consequences of selecting animals for resistance to a microparasitic infectious disease. The model is relevant for many classes of infectious diseases where sporadic epidemics occur, and it is a powerful tool for investigating the costs, benefits, and risks associated with bree ding for resistance to specific diseases. The model is parameterized for tr ansmissible gastroenteritis, a viral disease affecting pigs, and selection for resistance to this disease on a structured pig farm is simulated. Two g enetic models are used, both of which involve selection of sires. The first involves selection with the assumption of continuous genetic variation (th e continuous selection model). The second involves selection with the assum ption of introgression of a major recessive gene that confers resistance (t he gene introgression model). In the base population, the basic reproductiv e ratio, R-0 (i.e., the expected number of secondary cases after the introd uction of a single infected animal) was 2.24, in agreement with previous st udies. The probabilities of no epidemic, a minor epidemic (one that dies ou t without intervention), and a major epidemic were 0.55, 0.20, and 0.25, re spectively. Selection for resistance, under both genetic models, resulted i n a nonlinear decline in the probability of a major epidemic and a decrease in the severity of the epidemic, should it occur, until R-0 was less than 1.0, at which point the probability of a major epidemic was zero. For minor epidemics, the probability and severity of the epidemic increased until R- 0 reached 1.0, at which point the probabilities also fell to zero. The epid emic probabilities were critically dependent on the location on the farm wh ere infected animals were situated, and the relative risks of different gro ups of animals changed with selection. The main difference between the two genetic models was in the time scale; the introgression results simply depe nded on how quickly the resistance allele could be introgressed into the po pulation. For the introgression model, the probability of a major epidemic declined to zero when 0.6 of the animals were homozygous for the resistance allele.