Polioencephalomalacia in the Katherine region

Approximately 800 home-bred cattle aged six to 18 months were mustered and weaned at a property in the Katherine region in May 2019. The weaners and their dams were in good condition and mustered to the yards without issue. No chemical treatments were applied, there was no access to feed supplements (lick or salt) and no other processing was conducted at mustering; the weaners were separated from their dams into a clean, weed-free holding yard with access to freshly cut green Rhodes grass hay and fresh water.

The following day a single weaner in good condition was found dead in the yard; the remaining animals appeared normal. The second day, three animals in the yard were noticed to be wobbly on their feet and staggering, with some showing signs of drooling. The manager contacted the Katherine livestock biosecurity officer on the third day when a further six animals were noted to be showing similar clinical signs. The department’s biosecurity and veterinary officers attended the property that day. All affected animals were from the weaner mob; their unaffected dams were grazing in the paddock adjacent to the yards and adult animals in other parts of the property examined by the officers showed no evidence of disease.

On arrival, there were three dead weaners in the yard and two animals were collapsed, unresponsive and unable to rise. In the hours between the initial phone call and the livestock biosecurity and veterinary officers arriving at the property, a further 11 animals had developed significant neurological (nervous system) clinical signs, including head pressing, drooling, staggering, odd vocalisation and altered mentation. The two collapsed and unresponsive animals were euthanised and full post mortem examinations performed.

All affected animals were in good condition and the manager noted that the affected weaners were among the heavier individuals in the mob. Visible signs of organ malfunction in the two animals that were dissected was negligible; the younger animal had no abnormality visible to the eye and the other animal was found to have a number of firm red nodules in the left central lung lobe, which was considered incidental to the neurological signs.

Tissue and blood samples were submitted to Berrimah Veterinary Laboratory. Differential diagnoses for the nervous system signs included polioencephalomalacia, Bovine Herpes Virus 5, urea toxicity, lead poisoning, vitamin A deficiency, rabies, Australian Bat Lyssavirus and Aujesky’s disease. The lesions in the lung were tested to rule out a range of emergency and exotic respiratory diseases, including bovine tuberculosis, contagious bovine pleuropneumonia, Pasteurella and Mycoides sp infections.

The clinical findings, disease course and laboratory results pointed to a conclusion of polioencephalomalacia (PEM) as the cause of this morbidity and mortality event. PEM is a nutritional disease of well-fed, young growing animals in good condition, it is most common in animals between 6-18 months of age and occurs suddenly. In Australia, most cases are associated with a functional deficiency of vitamin B1 (thiamine). Cattle depend on the micro-organisms in the rumen to produce thiamine, and the level of daily production of this vitamin is close to the animal’s daily requirement. The most common cause of thiamine deficiency is the presence in the rumen of bacteria that produce thiaminase, an enzyme which consumes, degrades and therefore reduces the availability of thiamine to the animal. In pastoral production systems, a sudden change in feed from low quality dry feed to good quality hay or lush grass will cause a sudden change in the bacterial population of the rumen, which may precipitate PEM.

The visible signs of PEM are caused at a cellular level, and relate to the transport of water across the cell membrane. Lack of sufficient vitamin B1 results in reduced activity of an enzyme involved in the cell membrane pump that transports salt molecules in and out of cells. Dysfunction of this pump results in movement of water into cells, causing swelling. While this occurs in all tissues, the effects of cell swelling are particularly noticeable in the brain, which is limited in its ability to enlarge owing to the tightly protective skull bones. As swelling progresses, the cells are compressed against the inside of the skull, causing cell death and the development of neurological signs such as depression, apparent blindness, staggering and wobbling. Champing of the jaws, drooling and head pressing against fences and into corners are common. As signs progress, generally over 24-48 hours, animals fall and are unable to rise, with muscle tremors and convulsions becoming noticeable, and ultimately death may occur.

The likely cause of PEM in this case was the sudden change of diet from dam’s milk and dry paddock forage, to high quality hay. The rumen microflora are adapted to breaking down a particular type of food, and will take up to a week to adjust to a change. The observation that the larger, heavier animals in the mob were the worst affected speaks to the fact that these are likely to have been the greediest or earliest consumers of the high quality hay. In this instance, the high quality hay provided to the animals was the only available feed source, owing to the very poor preceding wet season in the Northern Territory and consequent lack of locally produced hay.

A presumptive diagnosis was made within 24 hours of investigation. The station manager was advised to limit the amount of high quality hay given to the weaners, slowly increasing the volume, to allow the rumen microflora to adapt to the change in feed. By day 5, no further cases had occurred and mildly affected animals were returning to normal without requiring medical intervention.  The veterinary officer also explained to the manager that if the same conditions were to occur again, the effects of a sudden feed quality and quantity change can be mitigated with the use of injectable Vitamin B complex for a few days after weaning. However, this may be a cost-prohibitive option when dealing with large mobs. Alternatively, close observation of the mob and injecting affected animals with Vitamin B1 early in the disease course, may lead to a remission of clinical signs within 6-24 hours.  A total of 15 animals died or were humanely destroyed; morbidity was approximately three per cent and mortality less than two per cent. Cases have been reported elsewhere of losses up to 10%.