Polio, or polioencephalomalacia, in cattle is not considered infectious, but rather a pathological condition — a diagnostic term describing necrosis of the brain’s grey matter. Clinical signs include:
- depression
- animals found down or dead
- stupor
- muscle tremors
- head pressing
- strabismus (squinting)
- apparent blindness
- star-gazing
- convulsions
- recumbency and paddling
When first described, polio existed primarily as a thiamine deficiency but is now recognized as a metabolic disease involving several factors. Animals exhibiting signs of polio suffer a mortality rate of up to 90 per cent.
The most common cause of polio in ruminants is high-concentrate rations resulting in rumen acidosis and subsequent thiamine (vitamin B1) deficiency. As the rumen pH decreases, it becomes a less favourable environment for thiamine-producing bacteria and more hospitable for organisms that deplete thiamine. Available thiamine concentration is drastically reduced. Energy production is impaired. Loss of osmotic control results in swelling of nervous pathways. Any cause for alteration in rumen microflora may precipitate polio.
According to the Alberta Feedlot Guide, in an article prepared by Erasmus Okine, up to six per cent of Alberta feedlot cattle on barley-based diets may exist on low thiamine levels, borderline with subclinical polio and reduced productivity. It may be advantageous to add 200 to 400 mg of thiamine per head per day to feedlot rations, especially if wet-milled corn byproducts are fed. Thiamine pyrophosphate is essential for carbohydrate usage in the body. Thiamine is also important in the excitation of peripheral nerves by the central nervous system.
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Factors that complicate reduced thiamine effects in rations include:
- low-grade acidosis in high-concentrate rations
- mouldy feeds
- abrupt change in diets
- amprolium added to ration as an anticoccidial
- cobalt deficiency
- excessive sulphur intake (feed, water). Distiller grains can contain excess levels of sulphur.
The effects of sulphur are additive. Total sulphur intake from both feed and water must be determined to determine total sulphur intake. The National Research Council sets the maximum tolerable level of sulphur intake in cattle at 0.3 per cent for animals fed greater than 85 per cent concentrates and 0.5 per cent for animals consuming greater than 40 per cent forage.
Efforts to diagnose thiamine deficiency can be difficult. Cattle owners should contact a veterinarian at the first sign of nervous symptoms in groups of cattle, especially when yearlings are involved.
The first step is to rule out other causes of nervous signs:
- sulphur toxicity
- salt poisoning
- coccidiosis
- infectious thrombotic meningo-encephalomyelitis (hemophilus)
- vitamin A deficiency
- hypomagnesemia
- listeria
- Type D clostridial enterotoxemia
- rabies
- lead poisoning
Polio treatment is symptomatic. When animals with minimal clinical signs of central nervous system impairment are ambulatory and eating, removing the source results in recovery in most animals. Therapy includes thiamine administered at 10 mg/kg to 20 mg/kg intravenously or intramuscularly two to three times the first day followed by the same dose twice a day for two to three more days. When applicable, dexamethasone, at 1 mg/kg to 2 mg/kg, aids in the reduction of cerebral edema. Mannitol, furosemide, dimethyl sulfoxide, sedatives and tranquillizers may be used to control seizures.
End-stage lesions associated with polio include herniation of the cerebellum (posterior part of the brain controlling respiration and heartbeat) into the magnum foramen (spinal opening of the first spinal vertebrae) resulting from brain swelling. The brain becomes spongy in texture. Cerebral folds may flatten and turn yellow-brown. Brain tissue (grey matter) may fluoresce under ultraviolet light. Cerebral folds may also hemorrhage, and bubbles may form and collapse.
