Claw horn disruption lesions (CHDLs: sole haemorrhage, sole ulcer and white line disease) cause a large proportion of lameness in dairy cattle and have a high rate of recurrence, yet their aetiopathogenesis remains poorly understood. Untreated CHDLs appear to be associated with trauma within and damage to the internal anatomy of the foot. Chapter 2 explored associations between abnormal bone modelling on the flexor tuberosity of the distal phalanx of cull cows and lameness during life, using a retrospective cohort study design. The hind claws of 72 Holstein dairy cows culled from a research herd were imaged using μ-computed tomography (CT) and lameness and lesion incidence data were available on cows throughout life. Four measures of bone modelling were taken from CT images from the flexor tuberosity of each distal phalanx, in plantar, distal and dorsal planes, and combined within claw. Bone modelling was greater in older cows, in cows with history of CHDL and in cows that had been lame at an increased proportion of locomotion scores during the 12 months preceding slaughter. Further, histological study demonstrated that the bone modelling resembled heterotopic ossification, also termed osteoma, which could have been due to either inappropriate force transfer through the distal phalanx or pathology in the soft tissues with lesion presence. Anatomical damage within the foot does appear to be associated with lameness and CHDLs, and may further predispose lameness. Preventing lameness constitutes a critical component of lameness control, and prophylactic foot trimming is a common management strategy for maintaining claw structure and function. However, over-trimming can cause damage to the foot architecture and lameness. Step 1 of the widely used Dutch Method of foot trimming states to cut the dorsal wall of the hoof to 75 mm. A vertical 5 mm step is left at the toe, therefore based on these recommendations, dorsal wall length would be 82 mm if the toe were trimmed to a point and the dorsal wall extended to the floor (at a toe angle of 50°). Chapter 3 used the CT data to assess the minimum dorsal wall length that would be suitable for trimming each claw. The median length was 76 mm (83 if the toe were trimmed to a point) and ranged from 59 to 86 mm; trimming all claws to 75 mm would have over-trimmed 55 % of claws. In a linear regression model, minimum dorsal wall length increased with age and carcass weight; older and larger cows had bigger claws. However, the vast majority of variation in claw length remained unexplained (only 22 % of the null variance was explained). In order to minimise the number of claws that are over-trimmed, recommendations for foot trimming dimensions should be based on the proportion of claws for which a measurement is suitable, rather than on population means. The minimum lengths that would have been suitable for all claws were 93 mm for cows aged ≥4 years and 86 for cows aged < 4 years; 7 mm could be taken from these measurements if a step is left at the toe. CHDLs appear to initially occur through trauma to the germinal epithelium of the sole, and Chapters 4, 5 and 6 present a longitudinal study of how the sole soft tissues (SST; i.e. the digital cushion and corium) alter throughout lactation. The digital cushion is a modified layer of the subcutis that is situated beneath the plantar and distal aspects of the distal phalanx and is considered to be important in dissipating forces during foot strike and to protect the germinal epithelium. The digital cushion contains depots of adipose tissue and recent work has identified that body condition loss is a risk factor for lameness. Previous work found that fatter cows had thicker SST and suggested that fat could be mobilized from the digital cushion and causes it to have decreased biomechanical function. The prospective cohort study assessed the SST of 179 parity 1, 2 3 or 4 cows at 5 assessment points, between 8 weeks pre- and 29 weeks post-calving of one lactation. Lesions present on claws and measures of body fat were recorded at each assessment point, and mobility scoring was performed fortnightly from calving. SST thickness at two sites beneath the distal phalanx were used as outcomes in 4-level mixed effects linear regression models (Chapter 5), and was positively correlated with back fat thickness. However, the effect size was much smaller than reported in previous cross-sectional work and only apparent under some circumstance. SST was thicker when a sole ulcer was present on a claw and was thinner immediately after calving (during the 4-10 days post-calving). The final model left 61 % of the null variance unexplained, of which 48 % remained between repeated measures of the same claw at different assessment points. Chapter 6 presents a series of logistic regression models of survival to first lesion or to first lameness (repeated lameness events were initially tested, but models were discarded due to the high rates of recurrence of both lameness and lesions). Lesion models demonstrate that claws were more likely to develop a lesion if SST was thin, and there was an additional effect of having thin back fat (all animals) or having lost back fat between previous assessment points (parity >1 animals only). Lameness models demonstrated that thin SST on the lateral claw increased the odds of a leg becoming lame, but SST on the medial claw had no effect on lameness. Change in SST thickness did not predispose lesions or lameness; only absolute thinness did. The work suggests that whilst loss of body condition loss may be one variable that contributes towards thinning of SST and subsequent claw horn disruption, many other variables also had a large effect on SST thickness, CHDL and lameness. This thesis presents a sequence of studies of how the anatomy of the foot is related to CHDL incidence, addressing recurrent lameness, mechanisms for the onset of new lameness and the appropriateness of prophylactic foot trimming guidelines as a management tool for lameness. The research literature is deficient in work demonstrating beneficial effects of interventions on lameness, and work throughout this thesis provides novel insights into the aetiopathogenesis of the claw horn disruption lesions. Based on this work, targeted interventions to reduce lameness can be tested.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:719405 |
| Date | January 2017 |
| Creators | Newsome, Reuben F. |
| Publisher | University of Nottingham |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://eprints.nottingham.ac.uk/34436/ |
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