Journal of Animal Science, Vol 79, Issue 8 2057-2065, Copyright © 2001 by American Society of Animal Science

JOURNAL ARTICLE

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

K. MacKenzie and S. C. Bishop
Roslin Institute (Edinburgh), Roslin, Midlothian, United Kingdom. Katrin.MacKenzie@bbsrc.ac.uk

This paper demonstrates the use of stochastic genetic epidemiological models 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 breeding for resistance to specific diseases. The model is parameterized for transmissible gastroenteritis, a viral disease affecting pigs, and selection for resistance to this disease on a structured pig farm is simulated. Two genetic models are used, both of which involve selection of sires. The first involves selection with the assumption of continuous genetic variation (the continuous selection model). The second involves selection with the assumption of introgression of a major recessive gene that confers resistance (the gene introgression model). In the base population, the basic reproductive ratio, R0 (i.e., the expected number of secondary cases after the introduction of a single infected animal) was 2.24, in agreement with previous studies. The probabilities of no epidemic, a minor epidemic (one that dies out without intervention), and a major epidemic were 0.55, 0.20, and 0.25, respectively. Selection for resistance, under both genetic models, resulted in a nonlinear decline in the probability of a major epidemic and a decrease in the severity of the epidemic, should it occur, until R0 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 R0 reached 1.0, at which point the probabilities also fell to zero. The epidemic probabilities were critically dependent on the location on the farm where infected animals were situated, and the relative risks of different groups of animals changed with selection. The main difference between the two genetic models was in the time scale; the introgression results simply depended on how quickly the resistance allele could be introgressed into the population. 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.