22.5.1: Lameness in calves Flashcards

1
Q

What causes White muscle disease?

A
  • Vitamin E/ selenium deficiency
  • These two nutrients come as a pair

White muscle disease is also known as nutritional muscular dystrophy

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2
Q

When do animals present with signs of White muscle disease? Which animals are affected?

A
  • Affects young, fast growing animals
  • Most commoly calves <6 months, has been reported up to 2 years old
  • Lambs and kids can be affected too
  • Often following sudden expectation of exercise e.g. reared indoors then turned out at 6-8 weeks old; also reported in housed animals
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3
Q

Clinical signs of White muscle disease

A
  • Recumbency and difficulty standing -> inability to stand for more than a few minutes
  • Stiff, trembling limbs, weakness elsewhere (e.g. neck)
  • May rotate distal hindlimbs from hocks if able to walk
  • Gluteal, shoulder and dorso-lumbar musculature palpably enlarged and firm
  • Other signs related to (striated) muscle affected e.g. intercostal muscles -> dyspnoea; myocardium -> cardiac arrhythmias; tongue -> inability to suckle
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4
Q

Which of the following is a poor prognostic indicator in White muscle disease?
* Dyspnoea
* Cardiac arrhythmias
* Inability to stand

A

Cardiac arrhythmias

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5
Q

Diagnosis of White muscle disease

A
  • Clinical exam and history -> known deficient pastures
  • Urinalysis: myoglobin = muscle injury
  • Biochemistry: elevated creatine kinase (CK) and aspartate aminotransferase (AST)= muscle injury/ myocyte damage
  • Biochemistry (at lab): low selenium or glutathione peroxidase
  • Liver biopsy: low selenium and Vitamin E
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6
Q

What is glutathione peroxidase and why would it be low in a calf with White muscle disease?

A

Glutothione peroxidase (GSH-Px)
* Delayed increase in response to selenium administration (4-6 weeks)
* GSH-Px is a selenium protein
* Collect sample in lithium heparin (green) or EDTA (purple) tube (check with lab)
* This is the preferred test for WMD in the UK

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7
Q

Treatment of White muscle disease

A
  • Vitamin E/ selenium - single dose usually sufficient but can be repeated after 2-4 weeks; poorer prognosis if myocardial involvement
  • NSAIDs as needed
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8
Q

Prevention of White muscle disease

A
  • Ensure adequate selenium intake of dams during late pregnancy
  • Provide supplementation to dams if deficient pastures e.g. long acting injection, intraruminal bolus, oral dosing, addition to ration
  • Can supplement calves
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9
Q

How do Vitamin E and selenium pass from dam to calf?

A
  • Vitamin E - colostral transfer
  • Selenium - transplacental and colostral transfer
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10
Q

Causative agent of Blackleg

A

Blackleg = clostridial myositis
* Causative agent: Clostridium chauvoei

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11
Q

Clinical signs of Blackleg

A
  • Sudden death☠️
  • Can look like White muscle disease but Blackleg is typically unilateral
  • Lameness and upper limb muscle swelling
  • Often die soon after clinical signs appear (12-36hrs)
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12
Q

Aetiology of clostridial myositis (Blackleg)

A
  • Soil-borne infection that enters through lesions of the skin or mucosa
  • Calving/ lambing injuries, fresh navel etc. are risk factors
  • Causes severe necrotising myositis
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13
Q

Diagnosis of clostridial myositis (Blackleg)

A
  • ⚠️Take care at PM exam - anthrax is a ddx!⚠️
  • Once anthrax is exposed to oxygen, starts to sporulate -> must test first before cutting it open
  • Blackleg: affected muscles are dry and dark on cut surfaces
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14
Q

Treatment of clostridial myositis (Blackleg)

A
  • High dose penicillin
  • Double dose every 12-24hrs
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15
Q

Prevention of clostridial myositis (Blackleg)

A
  • Vaccination: monovalent and multivalent vaccines available
  • Initial course at 3-6 months old followed by annual boosters
  • Vaccines are cheap so definitely cost-effective even if one animal lost to Blackleg
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16
Q

Which animals are affected by osteochondrosis dissecans (OCD)?

A
  • Youngstock (7-10 months), especially high performing beef units
  • Overall OCD is rare
17
Q

Clinical presentation of osteochondrosis dissecans

A
  • Multiple young animals going lame
  • Some are seriously affected but milder cases can be seen throughout the herd
  • Stifles and hocks most commonly affected
  • Animals show stiffness, reluctance to stand/move ± joint swelling
  • Lesions are usually bilateral but lameness may be in one leg only
18
Q

True/false: in animals with OCD, you should give NSAIDs early to try and reverse the changes that have occurred within the joint.

A

False
NSAIDs can be given for pain relief, however OCD is irreversible

19
Q

Pathogenesis of OCD

A
  • Focal defect in the articular cartilage resulting from failure of development of blood supply during ossification (-> focal ischaemic necrosis)
  • There is chronic lameness with stifles and hocks most commonly affected
  • Cause unclear, possible genetics/ demands on fast-growing breeds, possible Ca, P deficiency also plays a role