Project description:Claw horn disruption lesion (CHDL) is the collective term used to describe non-infectious foot lesions such as sole ulcers (SU), sole hemorrhage (SH), and white line disease (WLD) that commonly affect dairy cattle. The potential role of the bovine digital cushion, an anatomical structure located under the pedal bone and composed mostly of adipose and connective tissue, in the aetiopathogenesis of CHDL has recently been the subject of several studies. The aim of this prospective cohort study is to identify risk factors associated with the development of CHDL and to add further evidence regarding the role of the digital cushion. In order to achieve that we collected data from 500 lactations; 455 dairy cows from 3 farms were enrolled in this study. Data were collected from each animal on three occasions: 3-4 weeks before expected calving date, 1 week post calving, and 8-10 weeks post-calving. At each occasion, sole soft tissue thickness (the combined depth of the digital cushion and corium, SSTT) was measured using B-mode ultrasonography. At 8-10 weeks post-calving foot trimming was undertaken and the presence of CHDLs was recorded. Univariable analysis was undertaken between variables of interest, before multivariable regression models were constructed. Mixed effects multivariable linear regression models were created to describe the changes in SSTT and associations with various explanatory variables. Multivariable logistic regression models with the presence of SU, SH, or WLD as an outcome were also built. SSTT was shown to decrease from calving to early lactation (EL). Primiparous animals were found to have smaller SSTT, than multiparous animals. Animals with greater BCS had greater SSTT. Cows with a SU in early lactation had lower SSTT both at pre-calving and calving inspections comparing to cows without a SU. Cows that developed mastitis within 30 days of calving had approximately four times higher odds of developing SU compared to cows that did not develop mastitis. Our study advances our understanding of animal level risk factors associated with the development of CHDL and highlights the importance of the periparturient period.

Project description:Sole ulcers (SUs) and white line disease (WLD) are two common noninfectious claw lesions (NICL) that arise due to a compromised horn production and are frequent causes of lameness in dairy cattle, imposing welfare and profitability concerns. Low to moderate heritability estimates of SU and WLD susceptibility indicate that genetic selection could reduce their prevalence. To identify the susceptibility loci for SU, WLD, SU and/or WLD, and any type of noninfectious claw lesion, genome-wide association studies (GWAS) were performed using generalized linear mixed model (GLMM) regression, chunk-based association testing (CBAT), and a random forest (RF) approach. Cows from five commercial dairies in California were classified as controls having no lameness records and ≥6 years old (n = 102) or cases having SU (n = 152), WLD (n = 117), SU and/or WLD (SU + WLD, n = 198), or any type of noninfectious claw lesion (n = 217). The top single nucleotide polymorphisms (SNPs) were defined as those passing the Bonferroni-corrected suggestive and significance thresholds in the GLMM analysis or those that a validated RF model considered important. Effects of the top SNPs were quantified using Bayesian estimation. Linkage disequilibrium (LD) blocks defined by the top SNPs were explored for candidate genes and previously identified, functionally relevant quantitative trait loci. The GLMM and CBAT approaches revealed the same regions of association on BTA8 for SU and BTA13 common to WLD, SU + WLD, and NICL. These SNPs had effects significantly different from zero, and the LD blocks they defined explained a significant amount of phenotypic variance for each dataset (6.1-8.1%, p < 0.05), indicating the small but notable contribution of these regions to susceptibility. These regions contained candidate genes involved in wound healing, skin lesions, bone growth and mineralization, adipose tissue, and keratinization. The LD block defined by the most significant SNP on BTA8 for SU included a SNP previously associated with SU. The RF models were overfitted, indicating that the SNP effects were very small, thereby preventing meaningful interpretation of SNPs and any downstream analyses. These findings suggested that variants associated with various physiological systems may contribute to susceptibility for NICL, demonstrating the complexity of genetic predisposition.

Project description:Sole ulcers (SU) and white line disease (WLD) are noninfectious claw lesions that arise due to compromised horn production and are common causes of lameness in dairy cattle, imposing welfare and profitability concerns. The low to moderate heritability estimates of SU and WLD susceptibility indicate that genetic selection could reduce their prevalence. To identify loci associated with SU and WLD susceptibility, generalized linear mixed model (GLMM) regression and random forest (RF) genome-wide association studies (GWAS) were performed. Cows from five commercial dairies in California were classified as sound controls having no instances of lameness and above six years of age (n = 102) or cases having SU (n = 152), WLD (n = 117), SU and/or WLD (SU+WLD, n = 198), or any type of noninfectious claw lesion (n = 217). Top SNPs were defined as those passing Bonferroni-corrected suggestive and significance thresholds in the GLMM analysis or those that a validated RF model considered important. Effects of top SNPs were quantified using Bayesian estimation. Linkage disequilibrium (LD) blocks defined by top SNPs were explored for candidate genes and previously identified, functionally relevant quantitative trait loci. The GLMM GWAS revealed regions of association on BTA8 for SU and BTA13 common to WLD, SU+WLD, and noninfectious claw lesions. Bayesian estimation of effect sizes indicated that these SNPs had effects significantly different from zero, indicating their small but notable contribution to susceptibility. Promising candidate genes identified in these regions were involved in wound healing, skin lesions, bone growth and mineralization, adipose tissue, and keratinization. The LD block defined by the most significant SNP on BTA8 for SU included a SNP previously reported to be associated with SU. The RF models were overfitted, indicating that SNP effects were very small and thereby preventing meaningful interpretation of SNPs with the highest importance values and downstream analyses. These findings suggested that variants associated with a variety of physiological systems may contribute to susceptibility for noninfectious claw lesions, demonstrating the complexity of genetic predisposition.

Project description:BackgroundLameness in dairy cattle is primarily caused by foot lesions including the claw horn lesions (CHL) of sole haemorrhage (SH), sole ulcers (SU), and white line disease (WL). This study investigated the genetic architecture of the three CHL based on detailed animal phenotypes of CHL susceptibility and severity. Estimation of genetic parameters and breeding values, single-step genome-wide association analyses, and functional enrichment analyses were performed.ResultsThe studied traits were under genetic control with a low to moderate heritability. Heritability estimates of SH and SU susceptibility on the liability scale were 0.29 and 0.35, respectively. Heritability of SH and SU severity were 0.12 and 0.07, respectively. Heritability of WL was relatively lower, indicating stronger environmental influence on the presence and development of WL than the other two CHL. Genetic correlations between SH and SU were high (0.98 for lesion susceptibility and 0.59 for lesion severity), whereas genetic correlations of SH and SU with WL also tended to be positive. Candidate quantitative trait loci (QTL) were identified for all CHL, including some on Bos taurus chromosome (BTA) 3 and 18 with potential pleiotropic effects associated with multiple foot lesion traits. A genomic window of 0.65 Mb on BTA3 explained 0.41, 0.50, 0.38, and 0.49% of the genetic variance for SH susceptibility, SH severity, WL susceptibility, and WL severity, respectively. Another window on BTA18 explained 0.66, 0.41, and 0.70% of the genetic variance for SH susceptibility, SU susceptibility, and SU severity, respectively. The candidate genomic regions associated with CHL harbour annotated genes that are linked to immune system function and inflammation responses, lipid metabolism, calcium ion activities, and neuronal excitability.ConclusionsThe studied CHL are complex traits with a polygenic mode of inheritance. Most traits exhibited genetic variation suggesting that animal resistance to CHL can be improved with breeding. The CHL traits were positively correlated, which will facilitate genetic improvement for resistance to CHL as a whole. Candidate genomic regions associated with lesion susceptibility and severity of SH, SU, and WL provide insights into a global profile of the genetic background underlying CHL and inform genetic improvement programmes aiming at enhancing foot health in dairy cattle.

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A prospective cohort study examining the association of claw anatomy and sole temperature with the development of claw horn disruption lesions in dairy cattle

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