Cattle - Myopathies

Question 1

Describe the aetiology of hypokalaemic myopathy in dairy cattle.

Answer 1

• Occurs when serum K+ concentrations are

Question 2

List the clinical signs of hypokalaemic myopathy in dairy cattle.

Answer 2

• Severe weakness.
• Recumbency.
• Abnormal position of the head and neck.
• Rumen hypomotility or atony.
• Abnormal faeces.
• Anorexia.
• Tachycardia.

Question 3

List diagnostic test findings in dairy cattle with hypokalaemic myopathy.

Answer 3

• Serum K+

Question 4

Outline the treatment of hypokalaemic myopathy in dairy cattle.

Answer 4

• Tx difficult as serum K+ conc do not necessarily reflect muscle K+ conc.
• KCl IV 16g/100Kg - do not exceed 0.5mEq/kg/h.
• KCl PO 26-42/100Kg - do not exceed 230g PO q12h.
• Tx to resolve primary cause of ketosis and anorexia.

Question 5

What is the prognosis for survival in dairy cattle with hypokalaemic myopathy?

Answer 5

22-79%.

Question 6

Describe the epidemiology of clostridial myonecrosis in cattle.

Answer 6

• Cattle: 4-24mo; young colostral ABs, older acquired IR.
• Animals on high planes of nutrition in excellent body condition most likely to develop dz.
• C. sordelli most common in older feedlot cattle.
• C. chauvoei most common in warm weather; spring to fall.
• C. septicum, C. novyi and C. perfringens type A usually assoc w skin wounds e.g. inj sites, punctures, castration.
• Infections in genital area can occur post-dystocia.

Question 7

Outline a vaccination program for prevention of clostridial myonecrosis in cattle.

Answer 7

• Multivalent bacterin toxoids containing antigens against multiple clostrididial spp incl chauvoei, septicum, novyi, sordelli, perfringens.
• Initial vacc at 4-6mo, repeat, then q6-8mo.
• Usually only nec up to 3yo but continue if high-risk area.

Question 8

Describe the aetiology of nutritional myodegeneration (a.k.a. NMD, white muscle dz).

Answer 8

• An acute myodegenerative dz of cardiac and skeletal muscle caused by a dietary deficiency of Se or Vit E.
• Most common in young, rapidly growing calves, lambs, kids and foals, esp if dam was on Se-deficient diet.
• In utero form –> CSx after birth.
• Adult forms in cattle and horses also reported.
• Se and Vit E synergistic but Se def more important.

Question 9

Describe the clinical signs of NMD.

Answer 9

1. Cardiac form: acute signs of myocardial decompensation - depression, weakness, rapid irregular heartbeat, severe degeneration and often death within 24 hours.
2. Skeletal form: slower onset, muscular weakness, stiffness, trembling, recumbency, painful muscles on palpation; if diaphragm and intercostal involved animals may show resp distress, inc abdo effort; if tongue muscles may show dysphagia.

Question 10

List clinicopathologic abnormalities associated with NMD.

Answer 10

• Significantly elevated CK, AST and LDH and myoglobinuria during acute phase.
• Foals: hyperK, hyperP, hypoNa, hypoCl.
• Whole blood Se

Question 11

Describe the pathophysiology of NMD.

Answer 11

• Destruction of cell membranes and proteins –> loss of cellular integrity.
• Se and Vit E are biologic antioxidants.
• During normal cellular metabolism highly reactive forms of oxygen (free radicals) are produced.
• There is an important interrelationships b/w the Se and Vit E status of the animals and the level of polyunsaturated fatty acids (PUFAs) in the diet and NMD.
• Full relationship not understood as no dz/dz can occur with deficiencies of Se +/- Vit E.
• Active pasture growth –> high PUFAs e.g. calves just turned out on pasture –> inc risk.

Question 12

Describe the epidemiology of NMD.

Answer 12

• Se-deficient areas found worldwide esp acid soils, those originating from igneous rock or with high sulfur content.
• Different forage varies in Se content e.g. legumes take up less Se than grasses; lowest during rapid growth.
• Vit E defic most common in animals fed poor-quality hay, straw, root crops, grain tx w propionic acid.
• Vit E defic also in calves fed milk replacers containing fish oil, linseed oil, sybean oil, corn oil –> inc PUFAs.

Question 13

Describe the necropsy findings in animals that die of NMD.

Answer 13

• Bilaterally symmetric myodegeneration charac by pale discolouration and dry appearance of affected muscle, white streams in muscle bundles, calcification and IM oedema.
• White streaks coagulation necrosis or fibrosis and calc.
• Cardiac form: LV and septum in calves, RV+LV lambs.

Question 14

Describe treatment and prognosis for animals with NMD.

Answer 14

• Cardiac form: usually incompatible with life.
• Skeletal form: px guarded, depends if complications.
• Injectable Se IM or SC at label doses.
• Oral Vit E: natural greater bioavailability than synthetic; 15-60mg/kg dry feed calves; 600-1800mg/day horses.
• Supportive tx e.g. ABs for secondary pneumonia and decubital ulcers, nutrition, fluids.

Question 15

How can NMD be prevented in large animals?

Answer 15

• Total ration Se up to 0.3ppm.
• Salt/mineral mixes Se 90ppm for sheep, 120ppm for cattle.
• Max intake Se 0.7mg/head/day for sheep, 3mg/head/day for cattle.
• Se boluses not in USA, but can do 30d inj of Se/Vit E.
• Horses: Se 1mg/day inc blood Se above NMD levels; recomm to supp preg mares in Se defic areas.
• Periodic blood/tissue sampling for Se q 60-90d.