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
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.