Vitamin A deficiency looms as calf risk in prolonged drought

Jon Condon, 17/11/2013


A phenomenon first observed in Northwest Queensland downs country cattle during prolonged drought in the mid-2000s is again being raised as a risk under current drought conditions.

Almost 170 young calves were mysteriously lost in 2004 in a beef herd on Toorak Research Station near Julia Creek. The full circumstances behind the event are spelt-out in a report published towards the bottom of this article.    

Vitamins are not usually a problem with grazing cattle in northern Australia as most vitamins are synthesized by rumen microorganisms, DAFF Queensland said in a recent extension alert. The exceptions are vitamins A and E which are readily available in high quality forage, but may become limiting during extended periods without green feed. Such conditions have been experienced in 2013.

Vitamin A is stored in the liver but after prolonged dry periods, reserves become depleted. This seldom occurs where cattle are in forest country or have access to browse because the green leaf will supply an adequate amount of vitamin A.

The first sign of vitamin A deficiency is often picked up when cattle are loaded at night time. This is because vitamin A causes night blindness. Other signs are a rough coat, reduction in fed intake and joint stiffness. Vitamin A deficiency in cows during early pregnancy can affect the development of their calf’s brain in utero resulting in calves dying soon after birth, research has shown.

The first, and to date only, reported case of gestational vitamin A deficiency in beef calves in northern Australia occurred on downs country on Toorak in north-western Queensland in 2004. This followed:

  • below average rainfall years from 2001 to 2003
  • an early end to the 2003-04 wet season in February
  • no effective rainfall for 10 months, and
  • an absence of any trees or shrubs to provide a source of vitamin A in green foliage (Hill et al 2009).

The cows were in better than average body condition before calving and showed no signs of vitamin A deficiency. They also had access to a protein-based supplement and the calving paddocks had a reasonable bulk of dry standing feed. However, at calving they experienced exceptionally high deaths of perinatal calves, i.e. calves up to 48 hours old.

Further investigation ruled out reproductive diseases (leptospirosis, pestivirus and neospora) or any vitamin deficiency in the cows. Affected calves showed signs of mild to severe ataxia (loss of muscle coordination), difficulty finding a teat and sucking, blindness and depression with prominent drooping of the head. Affected calves occasionally showed thickened carpal joints and a few had a head tremor.

Autopsies of affected calves also revealed abnormal brain development as a result of in utero vitamin A deficiency.

Here’s a Beef CRC summary of the Toorak episode, published in 2007 after a detailed investigation into the event:



Vitamin A deficiency blamed for cattle deaths

The loss of more than 100 calves during calving in 2004 initially baffled staff at Toorak Research Station near Julia Creek in Northwest Queensland.

What they eventually discovered could ensure that beef producers in future don’t suffer such a disastrous loss.    

“It was an economic disaster,” said Peggy Olsen, station manager at Toorak.

“We ended up losing about 40 percent of the entire calf crop. Everyone wanted answers.”

Of the 406 calves born in 2004, 168 died–most within the first 24 to 48 hours of birth.

The cattle at Toorak were part of a resource population put together by the Beef CRC as part of a research project looking at ways to improve the carcase and meat quality, adaptation and fertility traits of cattle in northern Australia.

The herd contained two breeds, Brahman and a Belmont Red/tropically adapted composite.

Mrs Olsen said there were numerous theories as to what was causing the deaths, but initial post mortems by station staff failed to find any obvious cause.

“We’d weigh the new-born calves, tag them and then release them back to their mums, but by the next day they were dead. We had no idea what was going on.”

“Some people put it down to heat-stress, others thought it was more sinister. Some believed we were stressing them when we tagged them.”

“We were pushing up dirt around the troughs so they had access to water as well as milk. We were offering them shade. We tried everything to prevent the losses.”

“You have to realise just how much contact we have with these cattle. Whether we’re weighing them, scanning their ovaries, measuring their rib fat, we’re dealing with them all the time. Even during pregnancy we checked them every day.”

Several QDPI&F vets, including Dick Holroyd from Rockhampton and pathologist Bruce Hill of the Animal Research Institute (ARI) spent time at Toorak investigating the deaths.

Dr Holroyd said post-mortems were carried out and samples tested for unusual viruses, bacteria or other signs of disease, but infection was ruled out.

During November they watched a number of calves just prior to their deaths. The calves were then placed in three broad clinical categories.

“In the first group, calves could follow their mother but had difficulty finding and sucking on a teat; the second group exhibited mild to moderate nervous system dysfunction, blindness and appeared mentally depressed and weak with prominent drooping of the head,” Dr Holroyd said.

“These calves could not follow their mothers, showed very infrequent and ineffective sucking and usually died about 24 hours after birth.”

“The third group showed depression and blindness. Some had severe nervous system dysfunction and their heads would shake. These calves could not suck, they spent periods lying on their side and usually died quickly.”

After extensive analysis, Dr Hill and his team at ARI found problems in the brain, the nervous system, the optical system and internal organs.

Eventually, the cause was discovered to be a vitamin A deficiency, which can prevent the skull from growing. “The brain was growing but the skull wasn’t. So as the brain got larger, it put immense pressure on the calf’s brain stem,” Mrs Olsen said.

A premature end to the previous wet season was also believed to have contributed to the phenomenon. Toorak had no rain for 10 months and as a result the Mitchell grass hayed off earlier than usual.

The cows were putting on weight and had good body condition, but had little or no access to green foliage, to provide vitamin A.

Désirée Jackson, a beef scientist and extension officer with QDPI&F (now DAFF), Longreach said vitamin A efficiency can be mistaken for other diseases.

“Some of the symptoms can look very similar to other diseases. Cattle can get a rough coat or decrease their feed intake, and many producers will think their cattle have worms,” Ms Jackson said.

“But the one sign that is most unique to a vitamin A deficiency is ‘night blindness’. Because people don’t usually work with their stock at night they don’t generally pick up on it.”

Ms Jackson said a calf receives all the vitamin A it needs from the colostrum of its mother’s milk. The cow stores vitamin A in its liver, but when the animals are grazing on dry pastures for extended periods, their vitamin A storage becomes depleted.

“They only need about an ounce of green feed per day, or if they can get a big dose of green feed the carotenoids will be converted and stored as vitamin A in the liver,” Ms Jackson said.

“Alternatively, when the season starts to dry off and if producers are feeding licks, it might be useful to include a pre-mix containing vitamin A,” she said.

Vitamin A is very susceptible to oxidation via contact with sunlight, so there will be some deterioration and not all of the vitamin will be available for absorption.

“Along with other nutrients, there is a higher demand for vitamin A at calving and during lactation so building up liver storage reserves of vitamin A to ensure there is plenty of vitamin A going into the colostrum for those calves makes good economic sense,” Ms Jackson said.

Following the event all cows at Toorak were subsequently routinely injected to increase body reserves of vitamin A.

They were usually injected once a year, but in seasons where the wet finishes early, two treatments are made, once in the first trimester and then again in the last trimester.

Injection might not be feasible for every producer but options might include shifting a fence or two, of shifting cattle into a paddock with some forest country. Cattle don’t need much.

Since the first reported deaths at Toorak, several other downs country properties have also reported similar issues.

“Although these reports could not be investigated, it would suggest that in dry years, vitamin A deficiency is possibly a significant cause of neonatal mortalities in northern beef herds,” Dr Holroyd said.

  • More information on potential for vitamin A deficiency can be obtained from Mick Sullivan, DAFF’s principal beef extension officer in Rockhampton. Contact Mick on Ph 07 4936 0239  Mob 0428 104 374 email





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  1. Denise Chambers, 12/08/2017

    I have a calf that showed Vit A defiency after birth. Due to lack of good feed over summer, autumn and into winter we have been supplementing and still are, our pregnant cows with Oaten hay and mineral licks. We have lost a couple of early calves prior to finding this one. We injected her with VitA,D & E as soon as we found her and again two weeks later due to the fact that her eye started to cloud over again. She hangs her head and has stiff legged gait but drinks well with a bottle. What is her long term prognosis?

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