Lameness in calves

• What is the aetiology of septic arthritis in calves?

  > 3 weeks.

  May be subsequent to penetrating wounds - T.pyogenes (opportunistic pathogen).

  Mycoplasma bovis - typically BRD also present +/- otitis media/interna (head tilt). Often stifles affected.

  Circulating bacteraemia - intestinal origin e.g. Salmonella spp, respiratory origin e.g. H.somni, M.bovis.
• How do you diagnose septic arthritis?

  Clinical examination and history.

  Arthrocentesis - to culture bacteria in joint.

  • Clip and scrub area.
  • Large gauge needle. (16G or 18G)
  • Sedate if needed.

  Imaging -> rarely done, unlikely to add information to the examination.
• What are the presenting signs of septic arthritis in calves?

  Pain -> lameness (may be non-weight bearing), but if weight bearing doesn’t mean the calve is not in pain, if animal has polyarthritis calf won’t know which leg to stand on and can end up with even weight distribution.

  Affected joints painful and hot to touch, more chronic cases might not be.

  Joint swelling variable -> pyogenic bacteria = greatest swelling.

  Generalised signs variably present - pyrexia, inappetence.

  Co-morbidities may present.
• How do you do a clinical examination for septic arthritis?

  Acute cases are usually Pyrexic and dull.

  Observe the calf walking - lameness will be present, calf will be keen to lie down.

  If recumbent see if calf will stand - will be difficult or not possible, can examine joints when the animal is laying down.

  Examine joints - usually painful and a reduced range of motion.

  Hock, stifle and carpus are most commonly affected
• What are the post mortem findings of septic arthritis?

  A lot of fibrin, turbid synovial fluids, struggle to see the joint surface if there’s a lot of fibrin.

  PM findings are the same in calves and adults with chronic arthritis.
• What is the arthrocentesis for a healthy joint?

  Volume - small (~0.5-1ml)

  Quite difficult to obtain fluid.

  Gross appearance - colourless, clear, oily consistency (i.e. viscous).

  Leucocytes - Low numbers, few neutrophils.

  Protein - low

  Microbiology - no microorganisms.
• What is the arthrocentesis for a septic arthritis joint?

  High volume of fluid, that is usually easy to obtain.

  Gross appearance - turbid, yellow, may be prurulent, may be more watery (i.e. less viscous).

  Leucocytes - high numbers, predominantly neutrophils.

  High protein.

  Microbiology - bacteria (or other pathogens) might be cultured or visible on Diff Quik (although not always).
• What is the treatment for septic arthritis?

  NSAIDs (any that are licensed for cattle).

  Antibiotics

  • Selected based on likely organisms, penicillin, oxytet, TMPS.
  • Long course recommended -> 3 weeks, as penetration into the joint capsule can take a long time.

  Joint Lavage

  • Better results than just antibiotics + NSAIDs alone, due to flushing out a lot of the bacteria and some of the fibrin.

  Supportive care:

  • Feeding, soft bedding, good nursing, keep warm and dry.
• Why can’t you use penicillins for Mycoplasma?

  Penicillin works by targeting the cell wall of the pathogens, mycoplasmas do not have cell walls.
• What is the aetiology of white muscle disease?

  Vitamin E/selenium deficiency -> nutritional (AKA nutritional muscular dystrophy).

  • Dams fed diet insufficient in VitE/Se - so the calves do not get enough in utero and in colostrum.

  Young, fast, growing animals

  • Calves <6 months most often affected.
  • Lambs and kids as well as calves.

  Often following sudden expectation of exercise
• What are the clinical signs of white muscle disease?

  Recumbency and difficulty standing - inability to stand for more than a few minutes.

  Stiff, trembling legs. Weakness elsewhere (e.g. neck).

  May rotate distal hind limbs from hocks if able to walk.

  Gluteal, shoulder and dorso-lumbar musculature palpably enlarged and firm.

  Other signs related to (striated) muscle affected.

  • Intercostal mm = dyspnoea
  • Myocardium = cardiac arrythmias
  • Tongue mm = inability to suckle.
• How do you diagnose white muscle disease?

  Clinical exam and history - now deficient pastures.

  Clinpath:

  • Urinalysis = myoglobin present
  • Biochem (in house/at lab)= elevated creatinine kinase (CK) and aspartate aminotransferase (AST)
  • Biochem (at lab) = low selenium or glutathione peroxidase.
  • Liver biopsy (at lab) = low selenium and vitamin E.
• What is the treatment for white muscle disease?

  Vitamin E/Selenium:

  • Single dose usually sufficient but can be repeated after 2-4 weeks if needed.
  • Myocardial involvement = poorer treatment response.

  NSAIDs as needed.

  If there is myocardial involvement (arrhythmia) the prognosis is poorer.
• How do you prevent white muscle disease?

  Ensure adequate selenium intake of dams during late pregnancy.

  • Selenium -> transplacental and colostral.
  • Vitamin E -> colostral.

  Provide supplementation to dams if deficient pastures:

  • Long acting (bolus) injections
  • Intraruminal bolus
  • Oral dosing
  • Addition to ration

  Can also supplement calves.
• Distal metacarpal/metatarsal fractures in farm animals

  Excessive traction on rope/chain during calving.

  Typically a closed fracture.

  Manage with external coaptation (casting), surgical repair.

  The prognosis is excellent if closed but poor if open.
• Femoral fractures in farm animals

  Commonly caused by pressure from dam’s pelvis during breech presentation.

  Typically closed.

  Management is by surgical repair or conservative management.

  Prognosis for surgical repair is fair to good.

  Prognosis for conservative management is guarded.
• Growth plate fractures in farm animals

  Common caused by accidents.

  Can be an open or closed fracture.

  Management is external coaptation of closed, surgical repair or euthanasia of open,

  Excellent prognosis if closed, guarded to poor if open.
• Principles of cats/splints in calves

  Best candidates = transverse or short oblique fractures and Salter-Harris type 1 and 2 growth plate fractures.

  Closed fractures only -> examine skin carefully for wounds.

  Include the hoof in all casts.
• Cast application for calves

  use commercially available casting material and cotton wool/soffban for padding.

  Lay animal in lateral recumbency with fractured leg uppermost (sedate or GA aid fracture reduction).

  Carefully pad bony prominences and place cotton wool between claws.

  Cast limb in a neutral position starting at fracture site.
• Joint deformities - contracted tendons

  Large calves (tendons don’t have the chance to stretch out when the calf is in utero).

  Flexor tendons.

  Mild cases -> exercised and encourage weight bearing.

  More severe cases -> splint or cast.