Genetic correlations between endo-parasite phenotypes and economically important traits in dairy and beef cattle1

Abstract

Parasitic diseases have economic consequences in cattle production systems. Although breeding for parasite resistance can complement current control practices to reduce the prevalence globally, there is little knowledge of the implications of such a strategy on other performance traits. Records on individual animal antibody responses to Fasciola hepatica, Ostertagia ostertagi, and Neospora caninum were available from cows in 68 dairy herds (study herds); national abattoir data on F. hepatica-damaged livers were also available from dairy and beef cattle. After data edits, 9,271 dairy cows remained in the study herd dataset, whereas 19,542 dairy cows and 68,048 young dairy and beef animals had a record for the presence or absence of F. hepatica-damaged liver in the national dataset. Milk, reproductive, and carcass phenotypes were also available for a proportion of these animals as well as their contemporaries. Linear mixed models were used to estimate variance components of antibody responses to the three parasites; covariance components were estimated between the parasite phenotypes and economically important traits. Heritability of antibody responses to the different parasites, when treated as a continuous trait, ranged from 0.07 (O. ostertagi) to 0.13 (F. hepatica), whereas the coefficient of genetic variation ranged from 4% (O. ostertagi) to 20% (F. hepatica). The antibody response to N. caninum was genetically correlated with the antibody response to both F. hepatica (-0.29) and O. ostertagi (-0.67); a moderately positive genetic correlation existed between the antibody response to F. hepatica and O. ostertagi (0.66). Genetic correlations between the parasite phenotypes and the milk production traits were all close to zero (-0.14 to 0.10), as were the genetic correlations between F. hepatica-damaged livers and the carcass traits of carcass weight, conformation, and fat score evaluated in cows and young animals (0.00 to 0.16). The genetic correlation between F. hepatica-damaged livers in cows and milk somatic cell score was 0.32 (SE = 0.20). Antibody responses to F. hepatica and O. ostertagi had favorable genetic correlations with fertility traits, but conversely, antibody response to N. caninum and F. hepatica-damaged livers were unfavorably genetically correlated with fertility. This study provides the necessary information to undertake national multitrait genetic evaluations for parasite phenotypes.

Little genetic variability in resilience among cattle exists for a range of performance traits across herds in Ireland differing in Fasciola hepatica prevalence1

“…Despite the lack of widespread reranking for milk production and carcass traits in the present study, considerable reranking of sires was expected for the fertility traits across the different F. hepatica prevalence levels; nonetheless, the estimated genetic correlations were associated with large sampling variability attributable mainly to the low heritability of the fertility traits and also a paucity of data at the extremes. The presence of the G × E interaction for fertility traits in environments differing in F. hepatica prevalence was not unexpected given the known genetic association that exists between fertility traits and F. hepatica-phenotypes (Twomey et al, 2018). The larger extent of reranking for fertility traits in the present study suggests that sires that descended in rank as F. hepatica prevalence increased were not resilient to the environmental load of F. hepatica.…”

“…This conclusion is substantiated by a simulation described by Mulder et al (2006) who reported that maximum genetic gain can be achieved by using only 1 breeding program if genetic correlations between environments were >0.6. The minimal extent of reranking in the present study for milk production and carcass traits in environments differing in F. hepatica prevalence was somewhat expected as milk production and carcass traits are only weakly genetically (May et al, 2017;Twomey et al, 2018) and phenotypically (Mezo et al, 2011;Sanchez-Vazquez and Lewis, 2013) associated with phenotypes reflecting F. hepatica infection. Nonetheless, a noticeable weakening of the within-trait genetic correlations between milk productions traits in F. hepatica prevalence levels >0.8 and the rest of the F. hepatica prevalence levels, however, these were associated to larger standard errors.…”

Genome-wide associations and functional gene analyses for endoparasite resistance in an endangered population of native German Black Pied cattle

“…The SNP effect correlations between rFEC-GIN and rMY were negative for three of the five identified ROI, corresponding to the estimates from pedigree-based random regression models [15]. Twomey et al [20] detected genetic correlations close to zero between milk yield and antibodies for Ostertagia ostertagi , the most common GIN species in cattle. In our study, mostly negative SNP correlations were inferred between rMY and rFLC-DV.…”

“…In most cases, negative SNP effect correlations were observed between rFEC-FH and rFEC-GIN, implying that genomic selection on improved resistance to F. hepatica infections simultaneously increased the susceptibility to GIN. The pedigree-based genetic correlations ranged from − 0.10 to 0.17 between different GIN and liver fluke trait definitions [15, 20]. One explanation for the negative correlations on a genomic scale between rFEC-FH and rFEC-GIN and for the divergent marker associations as well as gene annotations might be due to the variations in immune response mechanisms for different endoparasite species.…”

“…In cattle, heritability estimates ranged from 0.04 to 0.36 for various definitions of GIN and D. viviparus infections [e.g., fecal egg count (FEC), antibody level], indicating a genetic component for pathogen-specific susceptibility [17, 18]. For the liver fluke F. hepatica , the heritabilities ranged from 0.09 to 0.33 [15, 19, 20]. The pronounced additive-genetic variances identified were stimuli to explore the underlying genomic architecture for endoparasite resistance in cattle and sheep, with a focus on GIN [21–23].…”