As the vitamin is water soluble and cannot be stored in tissues long-term, ruminants depend on having a healthy microbial population to produce their daily requirements of thiamine. Thiamine is essential in the production of energy for nervous tissue, especially the brain.
Should a rumen microbial population become disturbed, for example after a sudden change of feed or during a disease event such as acidosis, thiamine availability can be reduced either by a direct reduction in thiamine production as ‘good’ rumen bacteria numbers decrease, or as a result of an increase in ‘bad’ bacterial populations that produce thiaminase (an enzyme that breaks down thiamine).
Thiamine deficiency can eventually lead to a degenerative brain condition known as polioencephalomalacia (PEM), whereby energy and fluid imbalances cause the brain to swell and compress within the skull.
This leads to variable and non-specific neurological signs that can include dullness, apparent blindness, aimless wandering, incoordination, a high-stepping gait, teeth grinding, frothing at the mouth, muscle tremors and twitching.
Animals may then progress rapidly over 24 to 48 hours to having rigid limbs and stiff necks, seizures, paralysis and death. However, sometimes sudden death is the only sign.
Young, well-fed, thrifty cattle or cattle being fed large amounts of high-starch concentrates are most commonly affected.
Blood testing for thiamine is specific but expensive, while a post-mortem is also diagnostic but requires a dead animal and special laboratory testing (see image).
In a live animal, response to treatment provides one of the quickest and best methods of diagnosis, alongside a thorough neurological examination to determine specific clinical signs match suspicions and rule out other potential diseases.
Intravenous thiamine hydrochlorase (vitamin B1) in high doses is recommended for moderate to severe cases, and if response is promising treatment should be repeated frequently over the following days, alongside appropriate supportive care and nursing.
Cases are usually sporadic and outbreaks are uncommon, however even with prompt treatment 25 per cent of cases may progress to death, and in animals that are unable to stand mortality rate is closer to 100 per cent.
Prognosis is generally better for those animals that develop clinical signs slowly, and with less severity.
If treatment is not prompt, the degenerative changes to the brain can be permanent and neurological signs will persist or the animal will eventually die.
As PEM is usually nutrition-related and sporadic in nature, it is difficult to plan a good prevention strategy.
Good nutritional management with gradual transitions when adjusting feed rations and providing adequate roughage if feeding concentrates will go a long way.
Thiamine deficiency is not the only cause of PEM. Lead poisoning, sulphur and salt toxicity can also cause similar signs so as always, any cattle displaying unusual neurological behaviour should be examined by a veterinarian promptly to determine the best course of action before any treatment is administered.
Always be mindful of exotic diseases that may also present with similar signs, and if in doubt contact the Emergency Animal Disease Watch Hotline on 1800 675 888.
Lucy Collins is completing her Dairy Residency with The University of Melbourne. She works as an on-farm veterinarian for Apiam Animal Health, and alongside her partner on his family’s dairy farm in south-west Victoria. She is a 2021 Nuffield Scholar supported by Gardiner Dairy Foundation.
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