Genetic and epidemiological relationships between productivity and diseaseresistance: gastro-intestinal parasite infection in growing lambs

This paper demonstrates how interactions between host genotype for resistan ce to an infectious disease and the epidemiology of that disease can have l arge influences on animal productivity and hence on breeding goals for dome stic livestock. This is illustrated for the case of gastro-intestinal paras itism in lambs. A model of the parasite infection was developed to include between-animal variation (genetic, permanent and temporary environmental) f or live-weight gain, food intake, larval establishment rate in the host, wo rn fecundity and worm mortality rate. Achieved live-weight gain was defined as the sum of potential live-weight gain under conditions of no parasite i nfection, a trait correlated with food intake and growth-rate reduction due to the infection. The reduction in growth-rate was calculated from cumulat ive larval challenge and cumulative worm mass in the lamb. Genetic paramete rs were then estimated for the output traits of observed live weight at 6 m onths of age, growth rate reduction and faecal egg count. Model parameters were chosen so that the output means and heritabilities for faecal egg coun t and live-weight gain mimicked field data for Scottish Blackface lambs and growth-rate reductions were proportionately 0.25, on average. The model pr edicted a weak phenotypic correlation (mean = -0.10) between observed live weight and faecal egg count, the indicator of resistance but a stronger fav ourable (negative) genetic correlation between these traits (mean = -0.27). The severity, or epidemiology, of the disease greatly influenced the resul ts - the genetic correlation between observed live weight and faecal egg co unt strengthened from -0.02 to -0.46 as the disease severity changed from m ild to severe. Selection for reduced faecal egg count resulted in large cor related increases in live-weight gain, more than twice that predicted by qu antitative genetic theory, due to the reductions in growth rate losses as t he disease challenge to the animals decreased. Conversely, selection for in creased live-weight gain resulted in reductions in faecal egg count close t o expectations. This asymmetry of selection response emphasizes the epidemi ological benefits obtainable from selection for resistance to infectious ch ronic diseases - such selection will result in improvements in both animal health and productivity not seen when selection is for improved productivit y, alone. Breeding goals should be designed to take account of such effects .