Genetic and Metabolic Aspects of Claw Horn Lesion Aetiopathogenesis in Holstein Cows

Sole haemorrhage (SH), sole ulcers (SU), and white line lesions (WL), collectively referred to as claw horn lesions (CHL), are important causes of lameness in dairy cattle. This thesis aimed to explore the aetiopathogenesis of CHL, with a focus on genetic and metabolic factors. A cohort of 2,352 Holstein cows was enrolled on four herds in the UK and each animal was assessed at four production stages. Data collected included detailed foot lesion records, ultrasound measurements of digital cushion thickness (DCT) and, on one herd, blood samples for analysis with proton nuclear magnetic resonance (1H NMR) spectroscopy. Pedigree records and genotypes were obtained for all animals. Single-step genetic analyses indicated sole lesions (SH and SU) had a moderate heritability, while WL had a low heritability. The genetic correlation was strong between SH and SU, moderate between SU and WL, and weak between SH and WL. The heritability estimates of DCT were low-to-moderate depending on the stage of production and location of DCT measurement. The genetic correlation between DCT and sole lesions was generally negative. The recovery of sole lesions between early and late lactation assessments was heritable and appeared only weakly genetically correlated with sole lesion susceptibility. Genome-wide association analyses of CHL and DCT traits revealed a polygenic background, with candidate genes identified relating to immunity and inflammation, as well as carbohydrate and lipid metabolism. Analysis of serum using 1H NMR spectroscopy indicated the serum metabolome could not accurately differentiate between healthy cows and those affected with sole lesions, but a small number of metabolites appeared to be associated with SU development. Finally, the potential of breeding for improved lameness resistance using national genetic indexes was assessed, and the Lameness Advantage index was significantly associated with SH and SU development. The additive genetic variance of CHL could be utilised to select for increased resistance to these lesions; novel traits such as DCT and sole lesion recovery may also be useful auxiliary traits to reduce CHL prevalence. The genetic relationships between investigated traits, in addition to the genomic regions and genes associated with CHL and DCT, provide further insights into the genetic background and potential aetiopathogenesis of CHL. The metabolic influence on CHL development is poorly understood with the results of this work suggesting the serum metabolome is not directly associated with sole lesion development, however, further metabolomic studies of CHL would be worthwhile. Breeding for reduced CHL by selecting on the Lameness Advantage index is likely to be effective, although more direct CHL traits would be more efficient. Genetic selection alongside management and environmental changes should be considered as the optimal approach to reducing CHL in dairy cattle