Implications of Host Genetic Variation on the Risk and Prevalence of Infectious Diseases Transmitted Through the Environment

Previous studies have shown that host genetic heterogeneity in the response to infectious challenge can affect the emergence risk and the severity of diseases transmitted through direct contact between individuals. However, there is substantial uncertainty about the degree and direction of influence owing to different definitions of genetic variation, most of which are not in line with the current understanding of the genetic architecture of disease traits. Also, the relevance of previous results for diseases transmitted through environmental sources is unclear. In this article a compartmental genetic–epidemiological model was developed to quantify the impact of host genetic diversity on epidemiological characteristics of diseases transmitted through a contaminated environment. The model was parameterized for footrot in sheep. Genetic variation was defined through continuous distributions with varying shape and degree of dispersion for different disease traits. The model predicts a strong impact of genetic heterogeneity on the disease risk and its progression and severity, as well as on observable host phenotypes, when dispersion in key epidemiological parameters is high. The impact of host variation depends on the disease trait for which variation occurs and on environmental conditions affecting pathogen survival. In particular, compared to homogeneous populations with the same average susceptibility, disease risk and severity are substantially higher in populations containing a large proportion of highly susceptible individuals, and the differences are strongest when environmental contamination is low. The implications of our results for the recording and analysis of disease data and for predicting response to selection are discussed

Synthesis of direct and maternal genetic compounds of economically important traits from beef breed-cross evaluations

Published information on relative performance of beef breed crosses was used to derive combined estimates of purebred breed values for predominant temperate beef breeds. The sources of information were largely from the United States, Canada, and New Zealand, although some European estimates were also included. Emphasis was on maternal traits of potential economic importance to the suckler beef production system, but some postweaning traits were also considered. The estimates were taken from comparison studies undertaken in the 1970s, 1980s and 1990s, each with representative samples of beef breeds used in temperate agriculture. Weighting factors for breed-cross estimates were derived using the number of sires and offspring that contributed to that estimate. These weights were then used in a weighted multiple regression analysis to obtain single purebred breed effects. Both direct additive and maternal additive genetic effects were estimated for preweaning traits. Important genetic differences between the breeds were shown for many of the traits. Significant regression coefficients were estimated for the effect of mature weight on calving ease, both maternal and direct additive genetic, survival to weaning direct, and birth weight direct. The breeds with greater mature weight were found to have greater maternal genetic effects for calving ease but negative direct genetic effects on calving ease. A negative effect of mature weight on the direct genetic effect of survival to weaning was observed. A cluster analysis was done using 17 breeds for which information existed on nine maternal traits. Regression was used to predict breed-cross-specific heterosis using genetic distance. Only five traits, birth weight, survival to weaning, cow fertility, and preweaning and postweaning growth rate had enough breed-cross-specific heterosis estimates to develop a prediction model. The breed biological values estimated provide a basis to predict the biological value of crossbred suckler cows and their offspring

Suboptimal herd performance amplifies the spread of infectious disease in the cattle industry

Farms that purchase replacement breeding cattle are at increased risk of introducing many economically important diseases. The objectives of this analysis were to determine whether the total number of replacement breeding cattle purchased by individual farms could be reduced by improving herd performance and to quantify the effects of such reductions on the industry-level transmission dynamics of infectious cattle diseases. Detailed information on the performance and contact patterns of British cattle herds was extracted from the national cattle movement database as a case example. Approximately 69% of beef herds and 59% of dairy herds with an average of at least 20 recorded calvings per year purchased at least one replacement breeding animal. Results from zero-inflated negative binomial regression models revealed that herds with high average ages at first calving, prolonged calving intervals, abnormally high or low culling rates, and high calf mortality rates were generally more likely to be open herds and to purchase greater numbers of replacement breeding cattle. If all herds achieved the same level of performance as the top 20% of herds, the total number of replacement beef and dairy cattle purchased could be reduced by an estimated 34% and 51%, respectively. Although these purchases accounted for only 13% of between-herd contacts in the industry trade network, they were found to have a disproportionately strong influence on disease transmission dynamics. These findings suggest that targeting extension services at herds with suboptimal performance may be an effective strategy for controlling endemic cattle diseases while simultaneously improving industry productivity

Estimation of variance of maternal lineage effects at the Langhill dairy herd

Evidence to support the existence of a maternal lineage variance component for production and food intake traits at the Langhill experimental dairy herd was investigated. Maternal pedigree records of the herd were traced back to the points of cytoplasmic origin using herd book records. Cytoplasmic origin was defined as the earliest maternal ancestor of a cow and used to assign cows to maternal lineages. This was either a grade-up cow or an ancestor traced back to 1920. The tracing resulted in the cows being assigned to 56 maternal lineages, ranging in size from one to 72 cows. A total of 1118 records of 517 cows, all with a first lactation record, were used in the analysis. Traits analysed were daily milk, fat and protein yield, fat %, protein %, food dry-matter intake, net energy of milk production, a measure of milk production efficiency, average condition, and calving condition, all averaged over the first 26 weeks of lactation. The analysis was performed using a residual maximum likelihood animal model with and without a random component for maternal lineage. Possible bias, due to the fact that the sires were a select sample from the population, was also examined. No significant effect was found in the analysis of the full data set that could be assigned to maternal lineage. Fat yield was the only trait to show a variance component approaching a 5% significance level with a magnitude of 4% of phenotypic variance. However, when maternal lineages of at least five cows were considered, a significant 4% maternal lineage component of phenotypic variance was found for fat yield. The power of the analysis to detect a variance component of less than 4% was shown to be poor. No evidence was found for a maternal lineage component of food intake traits or condition score. Treating sire as a fixed effect or regressing data on sire EBV made little difference to the maternal lineage component