2010, Vol. 5 No. 2, Article 62

Recent Concepts in the Aetiopathogenesis of
Foot Lameness in Cattle

U N Zahid*¹, Swaran S Randhawa¹, and M A Ganie²

¹Department of Clinical Veterinary Medicine Ethics and Jurisprudence
²Department of Veterinary Gynaecology and Obstetrics
College of Veterinary Sciences, GADVASU,
Ludhiana-141 004, Punjab

*Corresponding Author; e-mail address: [email protected]

ABSTRACT

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.

KEY WORDS

Lameness, Dairy cattle, Hoofase.

INTRODUCTION

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.
The aetiology of bovine laminitis is multifactorial and includes nutrition, trauma, physiological alterations around parturition and the type of flooring (Bergsten, 2003). The following paragraphs discuss widely accepted views about the aetiopathogenesis of laminitis.

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.
Phase 1 (Initial activation phase):
This phase is associated with a systemic metabolic insult. The reduction in systemic pH activates a vasoactive mechanism that increases digital pulse and total blood flow. Depending upon the insult that initiates the process, endotoxins and histamine can be released, which create increased vascular constriction and dilation and, in turn, cause the development of several unphysiological arteriovenous (AV) shunts, further increasing blood pressure. Histamine is believed to be an arterial constrictor and vasal dilator causing increase in blood pressure and flow towards capillary beds resulting in pooling, vessel rupture, serum seepage and hemorrhages. However, if reverse is true, then pooling would also occur due to constriction of veins rather than arteries. Damaged vessels then exude serum, which results in oedema, internal haemorrhage of the solar corium, and ultimately expansion of the corium, causing severe pain.
Phase 2 (Local mechanical damage, Vascular):
As a result of the initial insult, there is mechanical damage, which is associated with the vascular system. Once vascular edema has occurred, ischemia of the local internal digital tissue causes tissue hypoxia, resulting in fewer nutrients and less oxygen reaching the epidermal cells. Ischemia itself can trigger a further increase in AV shunting. Trauma, stress, and certain hormones and chemicals are released that can further aggravate the shunting process. This cycle continues. The local blood circulation gets deteriorated to such an extent that the results can be compared to a “heart attack” of the feet.
Phase 3 (Progressive local mechanical damage of bone and support structure):
Ultimately, after local vascular compromise a situation develops in which the epidermal junction is broken down, which results in the separation of the stratum germinativum and corium. This separation in turn results in a breakdown between the dorsal and lateral laminar supports of the hoof tissue. Ultimately, the laminar layer separates, and the pedal bone takes on a different configuration in relation to its original position in the corium and dorsal wall. As the bone shifts in position, it causes a compression of the soft tissue between the bone and sole, which is extremely susceptible to damage. The compression of this soft tissue results in hemorrhage, thrombosis, and further enhancement of edema and ischemia, resulting in a necrotic area within the solar region of the foot. Once this process is triggered, continued potential for tissue degeneration persists because cellular debris is incorporated into the cellular matrix and the production and integrity of new horn tissue layers are hindered. Ultimately, a variety of processes can occur as a result of the incorporation of scar tissue intervention, which includes double sole phenomenon, sole hemorrhages (red blood patches), bruises, diffuse lesions, in solar pulp.

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.
Biochemical explanation for these observations include the activation of matrix metalloproteinase through a novel ~ 52kD gelatinolytic protease (hoofase) which is followed by structural alteration and functional disturbances of the connective tissue that suspends the distal phalanx within the claw (Tarlton and Webster, 2002). Levels of this enzyme were highest in the claws of heifers from 2 weeks pre-calving to 4-6 weeks post calving. Interestingly, levels of metalloproteinase-9 (MM-9), the enzyme most consistently associated with inflammation, was not found in significant amounts in either the first lactation heifers or maiden heifers (Tarlton and Webster; 2002). This suggests that the classical form of rumen acidosis-induced laminitis was not a cause of foot lameness in first lactation heifers. On the other hand, there was marginal increase in “proMM-2” metalloproteinase (a metalloproteinase normally responsible for physiological and pathological remodelling of connective tissues) and significant increase in “activated MM-2” (a very important metalloproteinase normally involved in the mediation of collagen remodelling) in first lactation heifers (Tarlton and Webster, 2002). In addition to its ability to degrade corium matrix components, hoofase is also able to activate MM-2 which shows that hoofase may have a very important role in the cause of claw lesions especially in first lactation heifers or first calvers.
These effects appear to be mild when external stresses to the claws are low, but are exacerbated when they are accompanied by substantial external stresses, such as housing on concrete floors (Webster, 2002) which may set in motion the sequence of events that proceed to severe claw horn lesions, typically sole ulcers and white line disease, accompanied by marked lameness.

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).
The other school of thought suggests that sinking and rotation of P3 may be associated with a yet unexplained structural alterations occurring on the surface of P3 where the suspensory tissues are anchored (Mulling 2002). It is clear that despite the preponderance of information linking laminitis to feeding conditions and rumen acidosis, soft flooring surface and cow comfort cannot be overlooked as requirements for animals during the transition period.
In conclusion, there is clear evidence that the anatomical relationship between third phalanx and surrounding claw horn is altered significantly around the time of calving which is normal naturally occurring phenomenon. Remodelling of collagen that comprises the suspensory apparatus within the claws occurs constantly, so that by around 16 weeks after calving the support available to the third phalanx has returned approximately to the normal level that was present before the cow calved. 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.

REFERENCES

Bennett RM, Christiansen K and Clifton-Hadley RS. Estimating the costs associated with endemic diseases of dairy cattle. Journal of Dairy Research 1999; 66: 455– 59.

Bergsten C. Causes, risk factors, and prevention of laminitis and related claw lesions. Acta Vet. Scand. Suppl 2003; 98:157–166.

Callaghan O K. Lameness and associated pain in cattle – challenging traditional perceptions In Practice 2002; 24: 212–19.

Clarkson MJ, Downham DY, Faull WB, Hughes JW, Manson FJ, Merritt JB, Murray RD, Russell WB, Sutherst JE and Ward WR. Incidence and prevalence of lameness in dairy cattle. Veterinary Record 1996; 138: 563–67.

Esslemont RJ and Kossaibati MA. Incidence of production diseases and other health problems in a group of dairy herds in England. Veterinary Record 1999; 139: 486–490.

Garbarino EJ, Hernandez JA, Shearer JK, Risco CA, and Thatcher WW. Effect of Lameness on Ovarian Activity in Postpartum Holstein Cows. J. Dairy Sci. 2004; 87:4123–4131.

Hernandez J, Shearer JK and Webb DW. Effect of papillomatous digital dermatitis and other lameness disorders on reproductive performance in a Florida herd. In: Mortellaro, C.M., DeVecchis, L., Brizzi, A. (Eds.). Proceedings of the 11th International Symposium on Disorders of the Ruminant Digit. 2000; pp. 353–57. Parma, Italy.

Hernandez J, Shearer JK, and Webb DW. Effect of lameness on the calving-to-conception interval in dairy cows. JAVMA 2001; 218:1611–1614.

Holah DE, Evans KM, Pearson GR, Tarlton JF, Webster AJF. The histology and histopathology of the support structures in the laminated region of the bovine hoof in maiden heifers and around the time of first calving. In: Mortellaro, C.M., De Vecchis, L., Brizzi, A. (Eds.), Proceedings of the 11th International Symposium on Disorders of the Ruminant Digit and the 3rd International Conference on Bovine, 3–7 September 2000, Parma, Italy, 2000; pp. 109 111.

Mulling CKW and Lischer CJ. New aspects on etiology and pathogenesis of laminitis in cattle. Proceedings of the XXII World Buiatrics Congress (keynote lectures), Hanover, Germany, 2002; pp.236-247.

Nocek JE. Bovine acidosis: Implications on Laminitis. Journal of Dairy Science 1997; 80:1005 1028

Randhawa SS. Prevalence, biomechanics, pathogenesis and clinico-therapeutic studies on foot lameness in dairy animals. PhD Thesis Guru Angad Dev Veterinary and Animal Sciences University Ludhiana, India. 2006.

Sood P. Effect of lameness on reproduction in dairy cows. PhD thesis submitted to Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, India. 2005.

Sprecher DJ, Hostetler DE, Kaneene JB. A lameness scoring system that uses posture and gait to predict dairy cattle reproductive performance. Theriogenology 1997; 47:1179.

Tarlton JF and Webster AJF. 2002. A biochemical and biomechanical basis for the pathogenesis of claw horn lesions. Proceedings of the 12th International Symposium on Lameness in Ruminants, Orlando, Fl, p. 395-398.

Tarlton JF, Holah DE, Evans KM, JonesS, Pearson GR and Webster AJF. Biomechanical and histopathological changes in the support structures of bovine hooves around the time of first calving The Veterinary Journal 2002; 163: 196-04.

Tarlton, JF and Webster AJF. Biomechanical and biochemical analyses of changes in the supportive structure of the bovine hoof in maiden heifers and around the time of first calving. In: Mortellaro, C.M., De Vecchis, L., Brizzi, A. (Eds.), Proceedings of the 11th International Symposium on Disorders of the Ruminant Digit and the 3rd International Conference on Bovine, 3–7 September 2000, Parma, Italy, 2000; pp. 113–118.

Vermunt JJ. Herd lameness – a review, major causal factors and guidelines for prevention and control. In: Zemljic, B. (Ed.). Proceedings of the 13th International Symposium and 5th Conference on Lameness in Ruminants. 2004; pp. 3–18. Maribor, Slovenija.

Vermunt JJ. One step closer to unravelling the pathophysiology of claw horn disruption: For the sake of the cows’ welfare. Veterinary Journal 2007; 174:219–220.

Warnick LD, Janssen D, Guard CL, Grohn YT. The effect of lameness on milk production in dairy cows. Journal of Dairy Science 2001; 84:1988-97.

Webster AJF. Effects of housing practices on the development of foot lesions in dairy heifers in early lactation. Veterinary Record 2002; 151: 9–12.

Webster AJF. Effects of wet vs. dry feeding and housing type on the pathogenesis of claw horn disruption in first-lactation dairy cattle. In: Mortellaro, C.M., De Vecchis, L., Brizzi, A.(Eds.), Proceedings of the 11th International Symposium on Disorders of the Ruminant Digit and the 3rd International Conference on Bovine, 3–7 September 2000, Parma, Italy, 2000; pp. 113–115.