22.5.1: Lameness in calves Flashcards
What causes White muscle disease?
- Vitamin E/ selenium deficiency
- These two nutrients come as a pair
White muscle disease is also known as nutritional muscular dystrophy
When do animals present with signs of White muscle disease? Which animals are affected?
- 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
Clinical signs of White muscle disease
- 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
Which of the following is a poor prognostic indicator in White muscle disease?
* Dyspnoea
* Cardiac arrhythmias
* Inability to stand
Cardiac arrhythmias
Diagnosis of White muscle disease
- 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
What is glutathione peroxidase and why would it be low in a calf with White muscle disease?
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
Treatment of White muscle disease
- Vitamin E/ selenium - single dose usually sufficient but can be repeated after 2-4 weeks; poorer prognosis if myocardial involvement
- NSAIDs as needed
Prevention of White muscle disease
- 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
How do Vitamin E and selenium pass from dam to calf?
- Vitamin E - colostral transfer
- Selenium - transplacental and colostral transfer
Causative agent of Blackleg
Blackleg = clostridial myositis
* Causative agent: Clostridium chauvoei
Clinical signs of Blackleg
- 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)
Aetiology of clostridial myositis (Blackleg)
- 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
Diagnosis of clostridial myositis (Blackleg)
- ⚠️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
Treatment of clostridial myositis (Blackleg)
- High dose penicillin
- Double dose every 12-24hrs
Prevention of clostridial myositis (Blackleg)
- 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
Which animals are affected by osteochondrosis dissecans (OCD)?
- Youngstock (7-10 months), especially high performing beef units
- Overall OCD is rare
Clinical presentation of osteochondrosis dissecans
- 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
True/false: in animals with OCD, you should give NSAIDs early to try and reverse the changes that have occurred within the joint.
False
NSAIDs can be given for pain relief, however OCD is irreversible
Pathogenesis of OCD
- 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
