Goat Polio: Polioencephalomalacia in Goats
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Providing adequate nutrition is a staple of animal husbandry. However, there are times when, despite our best efforts, illness can result due to dietary inadequacies or disorders of digestion. A lack of thiamine, or vitamin B1, in goats can result in severe illness and, if left untreated, even death. The condition caused by thiamine deficiency, known as polioencephalomalacia (PEM) or goat polio, is not related to poliomyelitis, the viral disease in humans.
Thiamine is a water-soluble vitamin that’s imperative for appropriate brain function. The brain, an obligate user of glucose, requires thiamine to metabolize glucose appropriately. The lack of thiamine within the body results in severe neurologic disease. Goats in the early stage of goat polio may exhibit mild lethargy and decreased appetite. However, it progresses within 1 to 2 days to severe neurologic disease. Goats develop drooping ears, gait abnormalities, and even blindness. They can progress to recumbency, seizures, and death rapidly if left without treatment.
In ruminants, thiamine is produced by microbes within the rumen (or first stomach chamber) rather than by the animal itself or by direct intake within the diet. However, in young goats who are not yet utilizing their rumen, thiamine must be consumed within the diet. Because of this, deficiencies in thiamine are seen most commonly in those young animals transitioning to rumination or in animals with disruption of healthy rumen microbiota.
Though more commonly noted in cattle, goats can also experience thiamine deficiency as a result of elevated sulfur intake. Elevated sulfur can occur in feeds such as distiller grains, as well as rape, brassica, and seed oil meals. The excess sulfur in the diet increases the animal’s usage of thiamine, resulting in a more rapid reduction in the vitamin. Thiamine deficiency has also been seen secondary to treatment for coccidiosis with the medication amprolium. Amprolium prevents the transport of thiamine into the brain.
Goats with neurologic changes suggestive of possible polio should undergo treatment rather than awaiting diagnostics.
Diagnosis of thiamine deficiency is primarily based on history and clinical signs rather than testing. Tissue and blood sample tests often fail to reflect thiamine levels within the brain. The only definitive way to diagnose PEM is with an examination of the brain on necropsy. Goats with neurologic changes suggestive of possible polio should undergo treatment rather than awaiting diagnostics.
The primary treatment for PEM is the administration of thiamine. Thiamine is available in vitamin B complex, but when treating polioencephalomalacia, thiamine should be used by itself, as the concentrations of thiamine in the B complex are usually insufficient for treatment. However, frequent, high doses of B complex are better than nothing if you don’t have access to a vet who treats goats and you’re unable to get plain thiamine.
The initial dosage of thiamine should be administered intravenously. For following treatments, the medication can then be given intramuscularly. Treat twice daily for two days, then once daily for another five days. While animals can improve after the first dosage, complete resolution often takes several days. Animals with severe damage to the brain may not recover despite treatment.
Because animals affected by PEM can be blind and recumbent, they must also receive supportive care while recovering. It’s important to separate them from the herd and provide easily accessible food and water. They may also require assistance to stand. Your veterinarian may advise using anti-inflammatories to help reduce swelling of the brain secondary to the thiamine deficiency.
The occurrence of polioencephalomalacia is most commonly associated with changes in diet. Careful and slow diet transition can help reduce the incidence of this disease in goats. Slowly increase the feed in animals moving to a high-grain diet, such as finishing meat goats. Take care to provide sufficient amounts of neutral detergent fiber (NDF). NDF indicates fiber content, which can affect feeding behavior. Providing roughages of stem length greater than 3 inches will also help to encourage rumination. Appropriate rumen function encourages healthy microbiota and reduces the risk of polioencephalomalacia. While thiamine can be supplemented in feed, it generally isn’t cost effective. Closely monitor animals undergoing dietary changes or young animals transitioning from milk to forage. Careful management can reduce the risk of goat polio, but the disease can still occur sporadically despite best efforts.
Separate goats from the herd if they’re exhibiting neurological signs. Consult your veterinarian as soon as possible. Several other common conditions can appear similar to PEM. These include pregnancy toxemia, lead toxicity, listeriosis, clostridium perfringens type D enterotoxicosis, and salt toxicity. Polioencephalomalacia is a serious condition. Delayed or inappropriate treatment will result in a poor outcome for the animal.
Thankfully, treatment with thiamine isn’t harmful and can be initiated whenever goat polio is suspected. However, each animal should be evaluated carefully to avoid missing other serious neurologic conditions. Working closely with your herd veterinarian can ensure they’re available whenever serious illness arises. Having an established relationship with your veterinarian can also ensure you have access to helpful prescription medications such as concentrated thiamine. While thiamine deficiency may not be perfectly prevented, proper preparation allows you to care for your goats quickly and effectively.
DR. KATIE ESTILL DVM is a veterinarian consultant for Goat Journal and Countryside & Small Stock Journal. She works with goats and other large livestock at Desert Trails Veterinary Services in Winnemucca, Nevada
