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This paper reviews experiments investigating the responses of resistant and susceptible genotypes of sheep to gastrointestinal nematode infection under differential nutrition. Using faecal egg count as a measure of host resistance, differences between genotypes appeared to be greatest under conditions of low nutrient availability and under such conditions both resistant and susceptible genotypes generally responded to supplemental protein by reducing faecal egg count. However, when nutritional conditions were moderate to good, responses to additional protein tended to be observed only in susceptible genotypes. In general, host genetic resistance was associated with reliable reductions in faecal egg count of moderate to large magnitude, while nutritional intervention was less reliable at reducing faecal egg count, and induced reductions of smaller magnitude. The situation was very different when examining host resilience to infection, as determined by sheep productivity in the face of infection. Increased host resistance was rarely associated with improved growth or production during the period of infection. In contrast, nutritional supplementation reliably increased host productivity irrespective of infection status and prevailing nutritional conditions. A general model of the relationship between nutrient availability and host resistance and resilience in resistant and susceptible genotypes is postulated. Taken together, the studies reviewed in this paper suggest that selection for host resistance and strategic nutritional intervention have complementary roles in the integrated control of gastrointestinal nematode infection in sheep. The former will contribute primarily to the epidemiology of the disease by reliably reducing faecal egg output over a wide range of conditions, reducing host challenge and the number of treatment interventions required. The latter will reliably boost host resilience to infection, with lesser effects on resistance, and the economic rationale for use will require accounting for the full spectrum of production and disease responses |
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