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Polioencephalomalacia in Goats and Sheep

Polioencephalomalacia in Goats and Sheep

By Valens Niyigena and Maria Leite-Browning

Polioencephalomalacia (PEM) is a common metabolic disorder characterized by neuromuscular alterations of goats and sheep that are thiamine deficient.

Animals managed on nutrient-dense diets–such as with animals in feedlots–or animals on lush pasturage fed with highly concentrated rations are susceptible to this disease. During colder months, when producers rely heavily on feeding grain-based diets and use fewer forages, animals are at high risk of developing polioencephalomalacia. However, this disorder can occur at any time of the year, especially when sudden management changes occur with respect to the animal’s diet. This disorder may be acute or subacute in nature. Adults and young animals are equally at high risk for developing the disorder.

What is thiamine?

Thiamine deficiency usually implies the depletion of carbohydrates in brain cells that manifest as a neurological disorder. Thiamine (vitamin B1) is produced by the bacteria and protozoa of the rumen under normal environmental conditions. Any change in the ruminal environment will affect the natural production of thiamine by rumen microorganisms, increase the degradation of thiamine, or prevent thiamine from functioning properly in sheep and goats.

When sheep or goats are fed highly concentrated grain diets, thiamine produced in the rumen can be inactivated or degraded by thiaminases, the enzymatic proteins that break down thiamine. In the presence of excessive concentrated rations, thiaminase is excessively produced by Bacillus sp. and Clostridium sporogenes. Reduced thiamine production will result in a lower supply of carbohydrates to the nerve cells, causing central nervous system disorders, PEM, and death.

Increased thiaminase production can also result from prolonged treatment with antiprotozoa substances such as CORID® (amprolium), the administration of dewormers, animals grazing in recently fertilized pasture, and in animals exposed to high sulfur and/or zinc intake. For example, animals chewing on newly installed galvanized fences can provide enough zinc for animals to develop PEM. Diets with dried distillers grains (DDG) can at times contain extraordinarily high levels of sulfur due to the processes used to clean DDG drying and pelleting equipment. The first batch of DDG to be produced post cleaning may have much higher sulfur levels potentially leading to the development of PEM symptoms when included in the animal’s diet.

Clinical Signs of Polioencephalomalacia

In severe cases, polioencephalomalacia is fatal. Clinical signs of PEM are associated with the following:

  • Rapid loss of appetite, muscle tremors, seizures, increased aggression, and temporary blindness accompanied with walking in circles. These symptoms can last two to three weeks if nonfatal.
  • Frequent convulsions that occur in 2 to 5-minute intervals. Goats may be standing or lying down when having convulsions. Goats appear dull and depressed and unable to coordinate muscular movements.
  • Increased body temperature, pulse, and respiration rates, but rumen motility is maintained normally.
  • Other signs of PEM include opisthotonos–a condition of abnormal posturing where the head is thrown backward accompanied by rigidity– severe arching of the back, muscular contractions, and teeth grinding. As the conditions progress, the animal becomes recumbent with frequent convulsions, nystagmus (rapid involuntary movement of the eyeballs), blindness, and unaltered palpebral and pupillary responses.

Diagnosis

Diagnosis is based on clinical signs, herd management history, and laboratory analysis. Laboratory analysis shows that the levels of thiaminase, pyruvate in the urine, blood pyruvate, lactate levels, and pyruvate kinase levels are all increased. Transketolase activity values are lower in affected animals. Differential diagnosis consists of the exclusion of other diseases and disorders of the neuromuscular systems such as caprine arthritis encephalitis, listeriosis, enterotoxemia, pregnancy toxemia, grain poisoning, plant poisoning, rabies, and tetanus. It is important to consult with your veterinarian for a proper diagnosis.

Treatment and Control

If not well treated, polioencephalomalacia can cause significant losses in goat or sheep herds. The response to treatment depends on the condition and extent of brain lesions. In the early stages of thiamine deficiency, animals will respond promptly to treatment.

A dose of 10mg to 20mg/kg body weight of thiamine injected in the neck muscle (intramuscularly) or under the skin (subcutaneously) is administered every 4 hours for a total of six doses. A full recovery will occur in one day, but in severe cases it will take two days for goats or sheep to recover. If animals are not recovered within three days, they may never fully recover.

In more severe cases, where animals present blindness, thiamine should be given intravenously in 10 mg/kg BW dosages at 4 to 6-hour intervals until animals show improvement or every 3 hours for a total of five doses. The administration of Dexamethasone 1 to 2 mg/kg body weight intramuscularly or subcutaneously is recommended to decrease edema and inflammation of the brain. Fluid therapy with dextrose solution intravenously or subcutaneously, is also recommended. In severe cases the condition will be fatal if left untreated.

Note. Always consult with your veterinarian to ensure a proper diagnosis and treatment plan for your animals. When administering thiamine, dosage and timing of subsequent doses is critical to prevent anaphylactic shock and death of the animal.

Prevention

Frequent monitoring of sulfur concentrations in feed and proactively checking for early signs of any disease outbreak can help to prevent polioencephalomalacia and provide ample opportunity to treat animals before severe cases occur. If the disorder occurs in your flock, it is important to evaluate for recent management changes that may be responsible.

  • Observe sulfur intake (source of water and consumed dry matter).
  • Avoid rapid change in animal’s diet.
  • Provide feed with thiamine levels of 1.5 to 4.5 mg/kg of feed. Some commercial grain-based feeds have added vitamin packages, including thiamine.
  • Provide sufficient levels of roughage–such as high-quality pasture or hay–as part of the diet.
  • Monitor animals after you have administered levamisole (Prohibit®) and/or amprolium (Corid®). These drugs are competitive antagonists of thiamine in the rumen.
  • Check sulfur content on water source and forages.

More Information

Consult your local veterinarian before using any medications mentioned in this publication. You will need to know potential side effects and when to stop administering the medication. For additional information about sheep and goat production management, visit www.aces.edu.

Source : aces.edu

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