|Report disease signs in stock to protect market access and human health|
Whenever stock show unusual disease signs such as holding their head in an unusual position, blindness, or seizures, or higher than normal death rates, it is important to call:
The veterinarian may take samples for laboratory testing to rule out trade or human health diseases and provide you with management tools to prevent the disease recurring.
Other diseases that cause signs similar to polioencephalomalacia:
For information about subsidised disease testing, contact your local veterinarian or see the Significant Disease Investigation Program webpage.
Causes of thiaminase-induced diseases of sheep and cattle
Thiamine, also known as vitamin B1, is normally produced by bacteria in the rumen of cattle and sheep on well-balanced roughage diets. However, there are also bacteria in the rumen capable of producing enzymes, called thiaminases, which break down and inactivate thiamine. These bacteria are normally in the minority, but under some conditions they proliferate and produce an excessive amount of thiaminases. This results in thiamine deficiency. Thiamine deficiency reduces energy availability to the brain, which leads to a type of brain degeneration called polioencephalomalacia or PEM.
When does PEM occur?
Most outbreaks of PEM are sporadic and affect only a couple of animals in a mob, but death rates of up to 10% have been reported. In Western Australia, the disease occurs throughout the year, but it is most common when there is a sudden change to the feed composition such as during spring and autumn. All ages and classes of stock can be affected. Affected animals are generally in good condition.
PEM in feedlots
Feedlots present a special situation. Diets high in carbohydrates and low in fibre encourage the proliferation of thiaminase-producing bacteria in the rumen and increase the risk of PEM. On such diets, it may take as long as six weeks before thiamine levels drop sufficiently for sheep or cattle to show signs of the disease or die. When outbreaks of PEM occur in feedlots, the death rate is frequently higher than in grazing livestock.
Signs of polioencephomalacia
Whatever the initial cause, signs of the disease are similar. Usually, affected sheep or cattle display signs for 1–6 days before dying. However, sudden death can also occur only 12–48 hours after introduction into a paddock.
Progressive signs of the disease
- agitation and anxiety, making the animal difficult to handle
- muscle twitching, holding the head abnormally high and a high-stepping gait
- blindness and head pressing (the animal stands with its head pushed up against a solid object)
- lying down, seizures, paddling (legs thrashing back and forth on the ground) and drawing the head back stiffly so it is pressed against the spine
- death follows in 24–48 hours.
How is PEM diagnosed?
To diagnose PEM, the veterinarian needs to submit samples from a dead animal’s brain for microscopic examination at a laboratory. Levels of thiamine in the blood can also be measured to assist in determining the cause of the PEM.
Thiamine deficiency can also result in an ill-thrift syndrome, slowing the growth of younger sheep and cattle. In such situations, thiamine deficiency should be considered together with more common causes of ill-thrift, such as nutrition, parasitism and mineral or other vitamin deficiencies. Blood thiamine analyses are useful in this situation.
Treatment and control
The success of treatment depends on when it is given in the course of the disease. When animals are treated in the early stages, they may respond within six hours, although it may take up to 48 hours for full recovery. Animals treated later in the course of the disease may still recover, but may be left with nervous problems including blindness.
Consider euthanasia if a treated animal has difficulty eating, drinking or seeking shelter. Animals with permanent and extensive brain damage (those with severe signs) will not respond to treatment and should be euthanased immediately.
The treatment for PEM where the animal is able to swallow is drenching with thiamine. Just a single drench in the early stages of the disease can correct the imbalance of bacteria in the rumen.
Alternatively, treat affected animals immediately with an injection of thiamine. This treatment needs to be repeated three times a day for up to five treatments.
Thiamine injections treat the thiamine deficiency, but will not fix the problem of thiaminase-producing bacteria in the rumen, meaning there is the potential for relapse. Providing the animal with a high-quality hay diet and an oral supplement of thiamine will help significantly in returning thiamine availability in the rumen to normal.
Where multiple deaths from PEM have been diagnosed in feedlot animals over a short period, all other animals in the group are at risk. Prevention in feedlot outbreaks consists of switching the animals to a diet higher in roughage (at least 50% of the diet) and adding thiamine to the feed for 2–3 weeks. Slowly reintroduce more grain in the diet to re-establish required weight gains.
Other causes of PEM
Although thiamine deficiency is the most common cause of PEM in WA, there are many other causes.
PEM caused by sulphur poisoning has not been proven in WA yet, but is becoming common elsewhere in the world. It may occur when dietary sulphur exceeds 0.4% of total diet. For example, this might occur when gypsum or ammonium sulphate is included in a feedlot ration, especially when stock has access to water with high sulphur content.
Normal thiamine levels can be disturbed when animals eat plants containing thiaminases, the group of enzymes which break down thiamine in the rumen before it is available to the animal. Such plants include bracken fern, Nardoo fern and horsetail. However, this potential cause of the disease is rare in WA.
If you see any unusual signs or diseases in stock, call your local veterinarian, your local DPIRD field veterinary officer (see the Livestock Biosecurity program contacts page) or the Emergency Animal Disease hotline on 1800 675 888.