For much of Australia, spring is associated with warmer temperatures and reliable rainfall, resulting in a relatively sudden change in diet for many grazing animals.
Any change in diet especially from poor, stalky grass to good, lush pasture can increase the risk of polioecephalomalacia (PEM).
What is PEM?
PEM is a disease which affects the nervous system of ruminants and is caused by a low level of vitamin B1 (also known as thiamine).
Thiamine is required to maintain normal fluid balance within body tissues.
A deficiency in thiamine results in dysfunction of fluid balance leading to swelling of cells in the brain and subsequent cell death.
Long-term storage of thiamine in the body is not possible, which means that cattle depend on daily production of this vitamin by bacteria in the rumen. In healthy cattle daily thiamine requirement is usually balanced by daily thiamine production.
Most commonly, PEM occurs when there is an overproduction of enzymes called thiaminases which break down and inactive thiamine, leading to an overall deficiency.
These thiaminases can come directly from overgrowth of bacteria in the rumen or indirectly from plant sources. PEM is also associated with high levels of dietary sulphur in the water or feed.
Signs of PEM
In pastoral animals, PEM predominantly occurs in well-fed, thrifty, young animals typically between six and 18 months of age, although adults can infrequently be affected.
In Australia, PEM is common in weaned calves in early summer. It is usually sporadic, affecting only a couple of animals in a mob, although occasionally outbreaks can occur.
In feedlot cattle, the disease is associated with diets high in carbohydrates and low in fibre, resulting in ruminal acidosis and over-production of thiaminase-producing bacteria.
Signs of the disease usually develop suddenly within 12 to 48 hours after a change in diet.
Blindness, depression, staggering, agitation, frothy salivation and head pressing are commonly seen. In some cases, affected animals may simply be found dead.
If left untreated, the neurological signs progress to twitching, muscle tremors, collapse with extended head and neck, seizures and eventual death.
Diagnosis and treatment
Your veterinarian should be consulted in any suspected case of PEM. There are other diseases which can cause similar signs and a full veterinary clinical examination is necessary to exclude these conditions.
History and clinical signs alone may be sufficient to initiate treatment but in some instances your veterinarian may wish to collect samples from affected animals to assist with a definitive diagnosis.
Other diseases which need to be considered include lead poisoning, salt/water toxicity, listeriosis, vitamin A deficiency and bacterial meningitis.
Treatment with vitamin B1 should be initiated as quickly as possible with the response to treatment often being diagnostic of PEM. Repeat treatments may be required.
If treated promptly in the early stages of disease, animals can respond within six hours of treatment.
Animals affected in the later stages of the disease may partially respond and suffer permanent signs such as blindness. Severely affected animals should be euthanised.
Always consult with your veterinarian if your cattle are displaying neurological signs of disease. Further testing, including post-mortem sampling, may be required to reach a diagnosis.
Dr Gemma Chuck works for Apiam Animal Health in the dairy operations team where she writes technical service programs for farmers and vets.