2010, Vol. 5 No. 2, Article 62
Recent Concepts in the Aetiopathogenesis of
U N Zahid*1, Swaran S Randhawa1, and M A Ganie2
1Department of Clinical Veterinary Medicine Ethics and Jurisprudence
*Corresponding Author; e-mail address: firstname.lastname@example.org
Foot lameness in cattle is caused usually due to damage to horn of hoof which produces severe pain when the sensitive laminae are involved. Nutrition, trauma, physiological alterations around parturition and the type of flooring constitute the main aetiological factors of foot lameness. The aetiopathogenesis of laminitis includes the disruption of peripheral vascular system of corium that can be best described as alternating phases of disturbances relating to metabolic and subsequent mechanical degradation of the internal foot structure. Systemic events associated with late pregnancy, calving and the onset of lactation compromise the structural integrity the support structures of the claw wall, predisposing the animal to the lesions of claw horn disease However if the housing and feed management of newly calved cows is such that their lying time gets reduced and rumen pH is lowered, then these adverse factors are superimposed on the normal biochemical changes occurring in the digits at the time of calving, and such animals are more likely to suffer claw horn disease in peak or mid lactation.
Lameness, Dairy cattle, Hoofase.
Lameness in cattle is a debilitating condition that challenges the sustainability of production systems (Vermunt, 2007). It causes decline in milk production by about 0.5 to 1.5 lts/day (Warnick et al, 2001) and also prolongs the calving interval by 35 to 50 days (Sood, 2005)., The annual losses due to lameness in cattle have been estimated at about £90 million (Bennett et al, 1999) in UK. About 90 to 99% of lameness incidents occur due to claw lesions (Clarkson et al, 1996). In India, the prevalence of clinical lameness in lactating cows and buffaloes is about 9 and 2 % respectively and 40-50 percent cases have subclinical lesions (Randhawa, 2006). Most of the lesions in the subclinical form have been associated with laminitis, which if not timely managed may produce clinical lameness.
DISRUPTION OF PERIPHERAL VASCULAR SYSTEM OF CORIUM
The pathogenesis of laminitis can be best described as alternating phases of disturbances relating to metabolic and subsequent mechanical degradation of the internal foot structure (Nocek, 1997). The process can be segmented into three phases.
ACTIVATION OF MATRIX METALLOPROTEINASES BY “HOOFASE”
Systemic events associated with late pregnancy, calving and the onset of lactation compromise the structural integrity the support structures of the claw wall, predisposing the animal to the lesions of claw horn disease ( Holah et al, 2000; Tarlton and Webster, 2000; Webster, 2000; Tarlton et al, 2002). Increased laxity, reduced rigidity, decreased load bearing capacity and a clear deterioration in the structural integrity of hooves has been seen in first lactation heifers during the peripartum period. Furthermore, these changes appeared to be progressive over a period of 2 weeks prior to calving until 12 weeks post calving.
PERIPARTUM HORMONAL EFFECTS
Another factor responsible for the weakening of the dermal-epidermal segment between the wall and P3is the result of hormonal changes that normally occur around the time of calving. Relaxin, a hormone responsible for relaxation of the pelvic musculature, tendons, and ligaments around the time of calving, is thought to have a similar effect on the suspensory tissue of P3 as well, however, housing of animals on soft surfaces during the transition period (4 weeks prior to calving through 8 weeks after calving), may be sufficient to reduce or alleviate the potential for permanent damage to these tissues. Clearly, cow comfort around the time of calving is important. First lactation animals in particular would benefit from softer flooring surfaces during the peripartum period (Tarleton and Webster, 2002; Webster, 2002).
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