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An Update on Research into Lameness in Cattle


By Laura Randall , University of Nottingham, School of Veterinary Medicine and Science Laura.Randall@nottingham.ac.uk


Lameness is defined as the clinical manifestation of impaired mobility and is commonly stated as being one of the most significant, growing problems the dairy industry faces (Huxley, 2012). As global sustainability will undoubtedly drive the future of the dairy industry in the 21st


century with environmental, economic and social awareness


increasing; the way in which dairy cows are managed in the UK will also change. This inherently brings with it a set of issues that need to be understood and managed; lameness, in particular, presents as a problem in modern intensive dairy farming systems (Nelson and Cattell, 2001). Higher yielding cows are at greater risk of lameness and the economics of producing milk may drive farmers to retain lame cows within the herd (Barkema et al., 1994; Green et al., 2002; Archer et al., 2010). Yet the extensive impact of lameness on herd performance is likely to be more significant than any other disease of cattle currently seen. The literature describes the significant impact lameness has on production losses (Warnick et al., 2001; Green et al., 2002; Hernandez et al., 2005a; Cook and Nordlund, 2009), culling (Collick et al., 1989; Booth et al., 2004) and fertility (Garbarino et al., 2004; Hernandez et al., 2005b) in dairy herds. Currently, lameness in dairy cattle is considered to be at


unacceptably high levels; Cook and Nordlund (2009) highlighted that the literature suggests the prevalence in intensively managed dairy cows is approximately 20% worldwide. In recent years the UK dairy industry has developed standardized mobility scoring systems and the AHDB Dairy ‘Health Feet Programme’; to increase the level of awareness of lameness, increase the level of engagement with control on farm, and reduce its welfare impacts through improved diagnosis and management (AHDB Dairy, 2017). Causes of lameness may be infectious (e.g digital dermatitis) and


non-infectious (claw horn lesions). Claw horn lesions (which primarily includes sole haemorrhage, sole ulceration and white line disease) account for a large proportion of lameness in cattle (Manske et al., 2002; Capion et al., 2009; Green et al., 2014) and a major concern is that the aetiology and pathophysiology of these lesions is still poorly understood (Bicalho et al., 2007; Bicalho et al., 2009). Traditionally, claw horn lesions have been described in the literature as ‘subclinical laminitis’, implying a nutritional basis to the aetiopathogenesis. However, the literature raises challenges to the traditional ‘laminitis’ theory and subsequently nutritional risk factors for claw horn lesions are now being viewed in a different light (Logue et al., 2004; Bicalho et al., 2009; Schopke et al., 2013); the role of body condition score and the digital cushion in claw horn lesions has been a recent focus


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Laminitis and claw horn lesions; a historical perspective Since the 1960’s when the term ‘laminitis’ was first used to refer to disorders of the corium, it has continued to be used widely and broadly with considerable inaccuracy of nomenclature. Acute, chronic and subclinical forms of laminitis have all been described in the literature; acute laminitis is characterised by systemic signs alongside inflammation of the corium, whilst the chronic form refers to deformation of claws with disturbed horn growth pattern (Vermunt and Greenough, 1994). Subclinical laminitis was suggested to be associated with lesions of the sole horn; haemorrhage of the white line, apex of the sole and axial side of the sole bulb junction (Vermunt and Greenough, 1994). A common underlying disease process has been described for all forms of laminitis; loss of integrity of the laminae (the interdigitating tissues that suspend the distal pedal bone in the hoof capsule), thought to occur due to the release of vasoactive substances from the rumen impairing laminar vascular function, which ultimately causes movement of the pedal bone and damage to cells that form the claw horn. The initiating factor in cattle was believed to be associated with feeding high concentrate diets. Laminitis, by definition, refers to inflammation of the laminae.


Thoefner et al. (2004) highlighted that in studies regarding laminitis, authors frequently referred to sole haemorrhage and sole ulceration without evidence that the lamellae were directly affected. Whilst a small number of studies have induced an acute laminitis with inflammatory changes in the lamellae, this has only been achieved using readily available carbohydrates as an oligofructose overload (Thoefner et al., 2004; Danscher et al., 2009; Danscher et al., 2010). So far, studies have been unable to achieve these changes by feeding high concentrate diets (i.e. akin to the situation on farm) or show that there is an association between ruminal acidosis and development of claw horn lesions. Furthermore, where studies have induced an acute laminitis, no evidence of changes to the integrity or strength of the laminae have been demonstrated (Danscher et al., 2010). These conflicting findings provide considerable challenge to the laminitis theory especially with regards to claw horn lesions being a subclinical form of laminitis i.e. different from the acute laminitis theory originally proposed. Until there


for lameness research. This article aims to give an update into research investigating


the aetiopathogenesis of claw horn lesions with a particular focus on nutritional risk factors.


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