Bovis ISSN 2398-2993

Laminitis

Contributor(s): Nick Bell , Roger Blowey

Introduction

  • Cause: generalized inflammation of the laminar corium due to various mechanisms including several putative inflammatory mediators and vasoactive metabolites.
  • Signs: general tender-footedness.
  • Diagnosis: signs of inflammation of the laminae; exclusion of other causes of lameness; history of diet change or toxemia.
  • Treatment: resolve potential causes of physical trauma and any dietary disturbance; non-steroidal anti-inflammatory drugs and nursing in loose yard or paddock for very tender-footed animals.
  • Prognosis: good in cattle. Failure of the suspensory apparatus does not inevitably lead to more severe hoof lesions.

Pathogenesis

Etiology

  • The understanding of true laminitis is largely based on the old equine model of laminitis (prior to more recent theories on cortisol-mediated laminitis in horses).
    • This model in cattle involves inflammation triggered by ischemia, mediated by various putative vasoactive metabolites or inflammatory mediators.
    • Experimentally laminitis can be reliably reproduced with intravenous oligofructose infusion, but rarely with intra-ruminal infusion.
  • There have been many anecdotal cases and occasional case reports involving protein and urea over-feeding.
  • Starch and grain over-load is described as a cause of laminitis in feedlot beef cattle.
    • However, rumen acidosis and subacute rumen acidosis are not confirmed causes of laminitis in cattle despite the many references in the literature.
    • Many reports of severe acidosis have not been followed by development of claw lesions.
  • Endotoxin release following toxaemic conditions may be a trigger in some individuals but the evidence is weak
  • Historically several lameness conditions affecting dairy cows have been grouped together and termed laminitis based on a similar presentation, which has caused confusion.
    • True laminitis, periparturient corium dysfunction (coriosis) and uncomplicated traumatic bruising are conditions which affect many cows within the herd, with hemorrhage and altered claw shape appearing at some point on the sole surface. However, these conditions have a different underlying etiology (see differential diagnosis).

Predisposing factors

General

  • Major feeding errors.

Specific

  • Potentially high sugar diets based on experimentally induced laminitis, although this is not seen in practice e.g. spring grazing herds on sugar rich-grass.
  • Toxemic conditions, such as toxic mastitis, metritis and peritonitis. These conditions may also lead to a total cessation of hoof horn synthesis, and resultant horizontal fissures Hoof fissures.
  • High urea and protein diets:
    • The author has seen cases (yet to be published) whereby feeding errors resulted in herds receiving excess urea and protein. The affected herds suffered signs of laminitis which resolved once the dietary mistake was rectified. One affected cow suffered complete sloughing of the hooves.

Pathophysiology

  • Metabolites and toxins inducing ischemia within the laminar corium of the digit.

Timecourse

  • Tender-footedness and other signs of laminitis will persist for a few days after exposure to nutritional insult.
  • Signs may persist for longer if exposure is prolonged or if ischemia severe enough to cause sloughing (degloving) of the hoof.

Epidemiology

  • Can affect individuals, for example with toxic mastitis, or whole groups of cattle exposed to nutritional insults.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Randall L V, Green M. J, Huxley J. N. (2018). Use of statistical modelling to investigate the pathogenesis of claw horn disruption lesions in dairy cattle. The Veterinary Journal, Volume 238, pp 41-48.
  • Danscher A M, Thoefner M B, Heegaard P M H, Ekstrøm C T & Jacobsen S (2011) Acute phase protein response during acute ruminal acidosis in cattle. Livest sci 135, 62–69 VetMedResource.
  • Danscher A M, Enemark H L, Andersen P H, Aalbæk B & Nielsen O L (2010) Polysynovitis after oligofructose overload in dairy cattle. J comp pathol 142, 129–138 VetMedResource.
  • Danscher A M, Toelboell T H & Wattle O (2010) Biomechanics and histology of bovine claw suspensory tissue in early acute laminitis. J dairy sci 93, 53–62 VetMedResource.
  • Danscher A M, Enemark J M D, Telezhenko E, Capion N, Ekstrom C T & Thoefner M B (2009a) Oligofructose overload induces lameness in cattle. J dairy sci 92, 607–616 PubMed.
  • Danscher A M, Enemark J M D, Telezhenko E, Capion N, Ekstrøm C T & Thoefner M B (2009b) Oligofructose overload induces lameness in cattle. J Dairy Sci 92, 607–616 PubMed.
  • Donovan G A, Risco C A, Temple G M D, Tran T Q & van Horn H H (2004) Influence of transition diets on occurrence of subclinical laminitis in Holstein dairy cows. J Dairy Sci 87, 73–84 PubMed.
  • Offer J E, Logue D N, Offer N W & Marsden M (2004) The effect of concentrate composition on lameness and hoof health in dairy cows. Vet J 167, 111–113 PubMed.
  • Thoefner M B, Pollitt C C, van Eps A W, Milinovich G J, Trott D J, Wattle O & Andersen P H (2004) Acute bovine laminitis: a new induction model using alimentary oligofructose overload. J Dairy Sci 87, 2932–2940 PubMed.
  • Offer J E, Leach K A, Brocklehurst S & Logue D N (2003) Effect of forage type on claw horn lesion development in dairy heifers. Vet J 165, 221–227 PubMed.
  • Offer J E, Fisher G E, Kempson S A & Logue D N (2001) The effect of feeding grass silage in early pregnancy on claw health during first lactation. Vet J 161, 186 VetMedResource.
  • Anderson L & Bergman A (1980) Pathology of bovine laminitis especially as regards vascular lesions. Acta Vet. Scand 21, pp 559–566.
  • Andersson L (1981) An Attempt to Induce Laminitis in Cows by Intra-Ruminal Infusion of Lactic-Acid. Acta Vet. Scand 22, pp 140–142.
  • Bazeley K & Pinsent P J N (1984) Preliminary-Observations on a Series of Outbreaks of Acute Laminitis in Dairy-Cattle. Vet. Rec 115, pp 619–622.
  • Boosman R, Nemeth F & Gruys E (1991) Bovine laminitis: clinical aspects, pathology and pathogenesis with reference to acute equine laminitis. Vet. Q 13, 163.
  • Livesey C, Metcalf J, Marsh C, Johnston A & May S (1997) Comparison of high starch and high fibre diets and the development of subclinical laminitis syndrome in dairy heifers. Br. Soc. Anim. Sci. Br. Soc. Anim. Sci 96, pp 96.
  • Nocek J E (1997) Bovine acidosis: Implications on laminitis. J. Dairy Sci 80, pp 1005–1028.
  • Offer J E, Logue D N & Roberts D J (1997) The effect of protein source on lameness and solear lesion formation in dairy cattle. Anim. Sci 65, pp 143–149.
  • Ossent P & Lischer C (1998) Bovine laminitis: the lesions and their pathogenesis. In Pract 20, pp 415–427.

Other sources of information

  • Greenough P (2007) Bovine laminitis and lameness. Saunders Ltd.
  • Offer J E, Logue D N & Mason C (2004a) Effect of an incident of overfeeding of concentrate on claw horn lesion development in first lactation dairy heifers. In: 13th international symposium and 5th conference on lameness in ruminants. Maribor, Slovenija. pp 175–176.
  • Blowey R W. Cattle lameness and hoofcare. 3rd edn. 5M.


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