Introduction/Causative Agent: Polioencephalomalacia (PEM) is a central nervous system (primarily brain) disorder caused by a lack of thiamine (vitamin B1) in body tissues. This deficiency is most commonly associated with a rapid dietary change to high levels of concentrates. A high concentrate to fiber ratio alters the bacteria in the rumen, producing enzymes that break down (metabolize) thiamine before it can be utilized by essential body organs. Other causes of polioencephalomalacia may include dietary deficiencies in young animals, poisoning by eating plants that contain thiamine-metabolizing enzymes (bracken fern, rock fern, nardoo, and Kochia scoparia), ingestion of moldy feed, and the intake of high amounts of sulfur-containing products such as molasses. Problems are most often noticed in lambs and kids that are between 2 and 6 months of age.
Clinical Signs: Thiamine is essential in producing glucose for energy. When a lack of thiamine exists, the biochemical processes necessary to produce energy for brain cells cannot be completed. Hence, the nerve cells within the brain begin to swell and deteriorate, resulting in neurological defects such as isolation from the herd/flock, depression, and staggering. Diarrhea, going off feed (anorexia), and weight loss can also occur. If it remains untreated, the disease may progress to include abnormal eye placement with the eyes positioned upward. This condition has been termed "star gazing." Progression of the disease may lead to head-pressing and blindness.
When the cause of PEM is related to a rapid change in dietary concentrates, decreased rumen contractions and a distended, fluid-filled rumen may also be present. This may also be accompanied with a watery, foul-smelling diarrhea. If the cause is related to the intake of high amounts of sulfur-containing feeds, a rotten egg, sulfur-like smell may be detected on the breath. In the latter stages of the disease, the animal may be unable to stand and may exhibit seizures. Death usually occurs within 3-4 days after clinical signs begin if no treatment is undertaken.
Disease Transmission: Polioencephalomalacia is not contagious between animals. However, when the causative agent is feed-related, more than one animal within the herd/flock may develop the disease.
Diagnosis: The diagnosis of this disease may be obtained by measuring blood thiamine levels. However, the more practical diagnosis is obtained from past history of feeding and clinical signs, in addition to the response to thiamine therapy. If the animal is dead, specialized microscopic evaluation of the brain by a pathologist can provide a precise diagnosis of thiamine deficiency.
Treatment: Polioencephalomalacia is a medical emergency and should be treated immediately following the observation of clinical signs. Affected animals should be isolated and treated with thiamine hydrochloride at the dose of 45 milligrams (mg) per 10 pounds of body weight (10 mg per kg of body weight). The first dose should be administered intravenously (IV). It is recommended that this initial IV dose be diluted with 5% dextrose or 0.9% saline solution and administered slowly. Following this initial IV dose, the same amount of thiamine hydrochloride should be given intramuscularly (IM), or subcutaneously (SQ) every 6-8 hours for the first day of treatment. The same treatment dosage should be continued, IM or SQ, 2-3 times daily for at least 3 days. In severe cases, medication to control seizures and reduce pressure within the brain may also be required. Valium (diazepam) is often used to control seizures and should be administered under the direction of a veterinarian. To reduce pressure within the brain, furosemide or mannitol may be beneficial. The recommended dose of furosemide is 4.5 milligrams (mg) per 10 pounds of body weight (45 mg per 100 pounds) given IV, IM, or SQ twice daily. Mannitol may be given at 1-2 grams (g) per 2.2 pounds of body weight. Mannitol must be administered IV as a 20% solution. Due to the intense monitoring required when administering furosemide or mannitol, direct administration and monitoring by a veterinarian is highly recommended.
Recovery: The rate of recovery is directly related to the promptness of diagnosis and treatment. Some animals may respond to treatment within 24 hours. If clinical signs are not severe, normal function should be restored within 1-2 weeks. However, if clinical signs have advanced to blindness and seizures, long-term supportive care including supplementing the diet with thiamine and feeds high in fiber, while decreasing the amount of dietary concentrates, may be required. Other animals that have not responded to treatment after 3 days may need to be euthanized. Recovery to normal vision and function may take up to 8 weeks. Some blind animals may never recover their vision.
Prevention: To aid in preventing polioencephalomalacia, gradual introduction of feeding high concentrate rations (at least 2 weeks) is recommended. Supplementing high concentrate diets with Brewer’s yeast or thiamine (3-10 mg/kg/day) may also be beneficial. Where possible, frequent pasture rotation to avoid the need for concentrate supplementation can control outbreaks of the disease.