Down and unable to move since birth, the calf was only 13 hours old when it was admitted to the Western College of Veterinary Medicine large animal clinic in Saskatoon.
This interesting case, reported in the Canadian Veterinary Journal, demonstrates the importance of neonatal calf care and it also illustrates an obscure disease of newborn calves.
The heifer had been calving for nine hours before the producer intervened. He reported that the calf was delivered with an easy pull. Because the calf was unable to get up and suck, the heifer was milked and the calf was tube fed a litre of colostrum four hours after it was born. Over the subsequent nine hours, the calf continued to deteriorate so it was taken to the veterinary college for assessment.
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The calf appeared comatose when it arrived at the clinic. Its body temperature was less than 32 C, which is the lowest reading on the digital thermometer. To combat hypothermia, it was warmed with heating lamps, and warm water bags were placed between its legs and on its abdomen.
To rehydrate the calf and give it energy, it was started on intravenous fluids and given a bolus of dextrose (20 millilitres or a 50 percent solution) through the intravenous line.
The calf’s temperature started to climb over the next 24 hours, but while it could prop itself up on its sternum, it was unable to stand.
Over the next day, it failed to improve further. Because of a persistent weak suckling reflex, tube feeding was still required.
The clinician in charge suspected the calf had a congenital form of nutritional muscular dystrophy. A blood test confirmed that the calf had elevated muscle enzymes, which reflected muscle damage, and that its blood levels of selenium and vitamin E were low. These abnormalities confirmed his suspicions and explained the calf’s weak muscles, stiff gait and dark urine, the result of the muscle protein myoglobin.
Once the diagnosis was made, the calf was given an injection of vitamin E and selenium under the skin.
The blood tests also revealed that the calf had low blood protein levels, suggesting it hadn’t received sufficient colostrum to ensure adequate maternal-derived immunity. To correct this, the calf was given a whole blood transfusion from a cow to boost its blood antibody levels.
Within 24 hours of the vitamin E-selenium injection, the calf was able to suck.
A day later, the calf could stand without assistance. When it walked, its gait continued to be stiff so another injection was given.
Improvement was echoed in repeat blood work that showed a reduction in muscle enzyme levels. After nine days of treatment, the calf was sent home. Two months later, the owner reported that the calf was normal.
Muscular dystrophy is caused by a deficiency of selenium, vitamin E or both. It occurs in lambs, kids, foals and calves. Though it strikes young animals, it is rare for a newborn to be affected.
Vitamin E is an antioxidant. Its role is to scavenge free radicals, the compounds that cause damage to cellular membranes.
Selenium plays a similar function. It is an integral component of an enzyme called glutathione peroxidase, which protects cellular membranes from peroxidative damage.
When these two nutritional components are deficient, cells die following degeneration of their outer membranes. Muscle cells are particularly susceptible to these effects.
Extensive muscle damage leads to the clinical signs of nutritional muscular dystrophy – stiffness, weakness and recumbency. On post mortem examination, these calves have pale muscles.
In older calves with chronic dystrophy, damaged muscle attracts calcium so it looks even whiter. For this reason, nutritional muscular dystrophy is commonly called white muscle disease.
Jeff Grognet is a veterinarian and writer practising in Qualicum Beach, B.C.
