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Sudden death due to probable urea toxicity

Unusual presentation:

100 of 3000 Brahman cattle found dead.

Brahman heifer in lateral recumbency

Above: Heifer in lateral recumbency with mild head and neck tremors

Time and location: August 2023, WA​​.

Case definition: Cows and bulls found dead in a paddock, some animals with sunken eyes and head down pre-mortem.

Disease mapping: The cattle were a mix of first round wet cows and bulls. They had been in the same paddock for two years prior and mustered and had been processed 3 months earlier. An annual botulism vaccination and phosphorus supplements had been given at the start of the year. A 30% urea lick had been started in the first week of August. Availability of dry matter in the paddock was low. The dead cattle were found spread throughout the paddock.

Gross findings: A two-year-old heifer lying in lateral recumbency with mild neck and head tremors and flaccid paralysis of her legs and tongue was euthanised. The only significant findings at postmortem examination was haemorrhagic mottling of the spleen and heart auricles. The rumen was full of dry grass feed material. The urine was clear. Samples submitted to the laboratory were pre-mortem bloods, aqueous humour, fresh and fixed tissue (heart, liver, kidney, spleen, lung, small intestine, forestomach, spinal cord, brainstem and brain), rumen contents and urine.

The prime field differential diagnosis was botulism because of the paralysis before death and predominately normal gross post-mortem findings. It was suspected that the vaccinations given earlier in the year may have been stored/administered incorrectly. Urea toxicosis was also a differential given the timing of starting the urea lick and the beginning of the mortalities.

Laboratory findings: The ammonia was markedly raised in both the aqueous humour (2788 μmoles/L) and blood plasma (964 μmol/L). ALT, total bilirubin, creatinine, CK, GGT and GLDH were all significantly raised in the serum biochemistry. Histopathology revealed severe, diffuse hepatic necrosis (consistent with the biochemistry results) indicating liver toxicity as significant pathology. Botulism C and D toxin ELISAs and botulism C and D toxin gene PCRs were all negative. The laboratory results confirmed that urea toxicity was the likely cause of deaths in these cattle, with plant hepatotoxins as a second differential.

Animal / management / environment risk factors: Urea toxicity normally first presents with ileus and bloat, aggression, muscle tremors, hyper salivation, polyuria and grinding teeth in distress. This progresses to stumbling and weakness, gasping then an acute death. Although not all these clinical signs were noted in these animals, they were not closely observed due to the extensive environment.

Urea toxicity can occur from a sudden increase in urea concentration or quantity. After an animal eats non-protein nitrogen the rumen microflora converts urea into ammonia which is absorbed by the blood stream. Urea poisoning then results in a rapid death due to high ammonia. The feed availability and palatability of the lick must also be considered as animals on fibrous pastures with low energy are more likely to suffer from urea toxicosis and a high palatability will increase consumption. After a period of three days off urea the rumen microbiome will need to be reintroduced slowly again.


  • Start non-protein nitrogen supplements with an 8% concentration and gradually increase up to 30% urea increasing by 4% every one to two weeks. Adapt this ration to feed availability in the paddock so that urea feed does not exceed 1% of dry matter consumed.
  • Monitor and keep a record of how quickly supplements are being consumed when initiated.
  • Don’t allow dry urea supplements to get wet as this can dissolve the urea and cause cattle to consume excess amounts quickly.