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This article was published in 2000
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Cattle Mortality (Ergotism) on a Forbes Property

By JB Kemp, BVSc, DIPAH, MSc, Forbes Rural Lands Protection Board

On 16 December 1998 at 4.50 pm, I received a call from a manager advising 2 cows and some calves that had died, and a number of cows and calves were down. They were from a mob of 103 cattle consisting of cows and calves. The cows were on their first calves approximately 30 months of age and the calves were 2-4 months of age. The breed was Angus.

The property was visited at 5.37 pm. One calf was in lateral recumbency showing nervous signs — opisthotonus and tetanic convulsions and another animal charged the owner. The other animals that were down were in sternal or lateral recumbency and relaxed. Some of the animals had blood coming from the rectum. Temperatures were taken on 3 animals. Temperatures were very high — being over 43°C.

The cattle had a change of paddocks from an adjoining paddock at about 9.00 am that morning and cattle were found dead at approximately 4.30 pm that day. Both paddocks were similar consisting of natural pasture and the cattle had been in the previous paddock for 4-6 weeks.

Two post-mortems were done that evening—one on a cow and one on a calf.

Post-mortem of cow

Showed petechial haemorrhages on the epicardium, some subcutaneous petechial haemorrhages — but not a lot, petechial haemorrhages in the larynx: the lining of the abomasum showed inflammation — (pink colour); the small intestine showed inflammation, pink colour externally and showed enteritis with mayonnaise contents, the colon showed a small amount of bloody contents for a good length, the spleen was normal as were the kidneys and liver, a large amount of feed was present in the rumen and a small rope. Lungs congested.

Post-mortem of calf (a heifer)

Lungs were congested; petechial haemorrhages on the heart, particularly on the endocardium, small intestine showed marked changes similar to Pulpy Kidney plus mayonnaise contents, and a pink colour on the peritoneal surface, caecum showed very dry contents and some inflammation, kidneys congested on external surface, spleen normal, omasum - very dry contents, internal lining of the abomasum showed inflammation - pink colour.

Laboratory Tests

Test for anthrax was requested.

I also asked for tests for nitrate and cyanide and magnesium levels - on the aqueous humor.

Water samples were submitted for tests on Blue-green algae from a water trough - it was bore water.

Also requested were bacteriology, histopalbology, and tests for Salmonellosis and Pulpy Kidney.

When I left the property there were 5 cows and 9 calves that had died and one cow in sternal recumbency.

The following morning, I visited the property. Cattle in the mob appeared heat stressed showed panting, and they sought water but did not drink. Some cattle would put their front legs into water troughs. The neighbouring paddock from which the cattle came the previous day was inspected and ryegrass seeds were noted with black heads.

I recalled a case of hyperthermia in a cattle feedlot which had occurred in 1986 (April - May) where cattle had similar symptoms as these present cattle - but no deaths had been experienced on this occasion. Therefore ergotism was suspected in this last episode.

On 17 December 1998 three bags of plant material were collected for the laboratory from the paddock for examination in the ryegrass, and two containers of water for blue-green algae.

Laboratory Results - showed the following:

Anthrax smears negative

Bacteriology:

Calf lung - culture showed Pasteurells haemolytic

No other significant findings

Water examination for Blue-green algae negative

Biochemistry:

Eye - Aqueous humor (calf) Normal for Ca and Mg

Serum (calf) Normal for Ca and Mg

Examination of Intestinal contents for PK toxins - Clostridium perfringens Type D - negative

Histopathology - on a range of tissues

Histopathological examinations were done at the Regional Veterinary Laboratory at Orange on lung, liver, kidney, heart, small and large intestine in the cow and calf plus abomasum in the cow.

In the heart in the cow and calf, there was marked sub endo and epicardial haemorrhages and mild myocardial haemorrhage in the calf.

The laboratory comment was:- The histopathology is consistent with shock. These changes could be expected in a dehydrated/hyperthermic animal.

There were also mild changes in the liver, kidney and alimentary tract.

Sections were referred to Elizabeth McCarthur Agriculture Institute for histopathology to John Glastonbury.

A His comment was:-

Overall, the histological findings were relatively non-specific. Myocardial haemorrhage occurs terminally in a number of conditions resulting from endothelial damage or vasospasm. In his opinion, the laboratory examinations eliminated the possibilities of anthrax, blue-green algal toxicity and clostridial diseases. Considering the epidemiology, clinical signs and non-specific pathological findings corynotoxins / tunicaminyluracil toxicosis is worthy of consideration. They are produced by Clavibacter toxicus (Corynebacterium rathayi) which is carried to the seed heads of annual rye grass (annual ryegrass toxicity), annual beard grass (Polypogan monspeliensis) and blowaway grass (Agrostis avenacea) by a nematode (flood plain staggers).

Results of specimens collected on the second visit on 17-12-1998

1. Two water samples - from a trough and dam - negative for potentially toxic blue-green algae.

2. Examination of 3 plant samples:

These three samples showed no sign of ergot present. Blackening of rye grass heads due to smut infection.

In January 1999, I was on leave and Patty Paul from Forbes Veterinary Clinic was called out to the same property. Her report showed 40 head dead and 10 sick out of a mob of 200 calves, Angus bred, mixed sexes, 6 months of age. The weaners had walked about 2km's to the yards at 7.00 am. They had not been pushed. In the yards they were treated for worms with Eprinex pour-on. One died in the yards before being treated. Treatment was finished by 11.00 am, The calves were let out of the yard and moved off on their own to water troughs and shade. Then more died. Some attempted to jump in the trough. Others meandered off down the fence, collapsed and died. Some were panting with noisy respiratory effort and a few were salivating. One was noted with a high "goose stepping" gait which later died in approximately ½ hour. Calves would charge people without prompting; they would run out of the middle of the mob and attack, then run off again. Many were in sternal recumbency and unwilling to rise. Temperatures in those still alive but recumbent were 40°C plus.

Gross post-mortem changes:- There were subcutaneous petechial and echyemotic haemorrhages. Skeletal muscle was very dark. There was a large amount of haemorrhage on the endo and epicardium and within the heart muscle. There was haemorrhage into the spiral colon. All other organ systems appeared grossly normal.

All dead calves appeared to be on the heavier end of the weight range for calves in the mob.

Samples from four calves were submitted to Regional Veterinary Laboratory Orange on 5 January 1999.

Laboratory Results

Rumen contents were negative for arsenic.

Smears were negative for Anthrax.

Bacteriology was not significant.

Histopathology on a range of tissues

Examinations were done on liver, spleen, heart, kidney, lung and small and large intestines.

Regional Veterinary Laboratory Orange (John Seaman):-

Brain — mild diffuse vacuolation of the grey matter throughout the cerebral cortex. Scattered neurones appear shrunken and eosinophilic suggesting mild neuronal degeneration.

Comment on histopathology: from Orange

Histopathology non specific. The only changes of note would be those described in the brain (diffuse vacuolation and mild degeneration in the grey matter) but even some of these could be artefactual post death. Clinical signs described related to nervous system derangement. Overdosing with Eprinex could be a problem in stressed cattle but this appears to have been discounted based on history. At the moment there is no aetiological diagnosis for this significant mortality.

Again sections were referred to John Glastonbury, Regional Veterinary Laboratory — Menangle:

Brain — no significant findings.

Comment: Overall the histological findings were relatively non specific. Terminal struggling would account for the acute pulmonary lesions, the pulmonary haemorrhage possibly due to the method of euthanasia.

Myocardial haemorrhage occurs terminally in a number of conditions resulting from endothelial damage or vasospasm. The laboratory examinations have eliminated the possibilities of anthrax, blue-green algal toxicity and clostridial diseases. There was no evidence of viral encephalitis.

Considering the epidemiology, clinical signs and non-specific pathological findings, corynotoxins / tunicaminyluracil toxicosis is worthy of consideration.

Dr Chris Bourke of Orange Agricultural Insititue visited the same property in January 1999, after Patty Paul's visit. Ryegrass was submitted to RVL, Orange on 13/01/1999.

Results from the RVL (M Priest)

Ryegrass infected with ergot Claviceps purpurea.

The conclusion:- Ergot infection of ryegrass confirmed.

Then the subsequent comment on my original laboratory report came back as: "While first plant samples (DV Forbes) are negative for ergot, subsequent plant samples submitted by CA Bourke are positive for ergot. These investigations show ergotism as the cause of the mortalities" These samples were not found in the paddock where the cattle were and where the grass had been knocked down, but in an adjoining paddock with the pasture standing.

The conclusion of the reports stated —

"Deaths — ergotism implicated as the cause".

The comment and the conclusion for Patty Paul's laboratory report was similar to my original laboratory report with the added comment that there was no evidence of Clavibacter toxins.

The final mortality in the weaners affected in January, 1999 was 58 deaths aged 8 months plus 9 stillborn calves (and the deaths of 2 more cows during calving). This was in addition to the 14 head (9 calves and 5 cows) that died in December 1998, making a total number of deaths of 72 head, (excluding the death of 2 cows at calving and the 9 stillborn calves.)

On 10/05/1999, the manager rang me. He advised that a mob of 108 Angus steers 2 years of age were yarded two days previously on the Saturday. They had moved 1 ½ miles (or 2.4 km) to the yards, starting at 11.00 am. One or two were tongueing when they were moving and 5 minutes after they yarded, they all started to pant with a deep hollow noise, all showing signs of hyperthermia. The manager advised that the cattle had access to ergot prior to the rain on 05/04/199 on the same feed for 6 weeks consisting of ryegrass or clover and there was no sign of dry feed.

The manager also advised on 12/5/99 he had 50% live calves which were OK and 50% dead calves — out of a mob of 36 Angus cattle. All except one calf died at full term or 1-2 days after birth.

HYPERTHERMIA AND DEATH IN FEEDLOT CATTLE ASSOCIATED WITH THE INGESTION OF CLAVICEPS PURPUREA IN WESTERN AUSTRALIA. RL Peat et al. (1991)

Peat, McCarthy and Barbetti in 1991 were the first to report deaths in cattle associated with the ingestion of Claviceps purpurea. They reported a hyperthermia syndrome in yearling male cattle in a feedlot at Esperance in Western Australia. Eleven animals died, but the main effect was failure to gain weight.

Indicators of the disease appeared after approximately 3 weeks of feeding the steers in the summer and early autumn, 1990. About 35% of 1700 animals developed clinical signs which included hyperthermia with rectal temperature over 40°C, clear nasal discharge, excessive salivation, increased respiratory rate, inappetence, and a desire to stand or wallow in water and seek shade. The signs persisted and deaths continued to occur for at least 6 weeks with some clinical improvement occurring intermittently with cooler weather.

A sample of the feedstuff was found to contain 0.06% w/w ergot. The barley used in the feedmix was found to be contaminated with annual rye grass (Lolium rigidum) seed infested with Claviceps purpurea producing the black ergots. Six barley samples had np to 0.18% (w/w) ergot (range 0.05% to 0.18%). Screenings from the barley had 0.051% (w/w) ergot. The ergots were then sieved from the barley and clinical signs abated after 2 weeks. (The Jessep et al. (1987) outbreak contained levels of 0.02% to 0.8% (w/w) ergot).

After the diagnosis at Esperance, reports of similar cases in 3 other feedlots in different parts of south-west Western Australia were received. It was of interest that Bos taurus cattle were observed to be more severely affected than Bos indicus breeds. Lameness was unusual in affected animals, but some did adopt an unusual, cautious gait when moving to feed and water.

The cool and wet weather conditions from spring through to harvest in the previous year were ideal for Claviceps purpurea infection. These, and the failure to adequately control ryegrass in the barley crop, were local factors associated with the disease. Some feedlot managers reported apparent rodent faeces or "weevils" in the feedstuff. These proved to be the ergots of Claviceps purpurea.

COMPARISONS OF ERGOTISM IN CATTLE ON THE ABOVE FORBES PROPERTY WITH A COWRA PROPERTY. GA Bourke et al. (2000)

Bourke (et al) 2000 stated that ergot alkaloids in rats cause hypothermia when ambient temperatures fall between 20°C, whereas severe hyperthermia is caused when ambient temperatures are 30°C or greater. He contrasted outbreaks of lethal hypothermia ergotism in cattle — two in summer on the Forbes property at > 28°C following forced exercise and the other in winter, at < 19°C at Cowra in a cattle feedlot which occurred in the winter of 1999, following the introduction in mid June of barley grain containing up to 200mg/kg of ergotised annual rye grass seeds.

On the Cowra property, during the 33 days of ergot feeding the weekly death rate rose from 2 to 36 head. A total of 126 steers and heifers aged 9 to 12 months, died out of the feedlot population of 1565 head.

Barley comprised 60% of the total ration mix and eventually the stock owner noticed ergots in the feed and feeding of the contaminated barley was stopped. Within a week all cattle in the feedlot showed signs of an improvement, and within 3 weeks all surviving affected cattle had returned to normal. There was no shade on the feedlot and the weather conditions during the period of the outbreak were predominantly dry, cool and sunny.

It is of interest regarding the Forbes property that the difference between the paddocks for the fist mortality was that the second paddock that experienced the mortality had no shade trees whereas the paddock with trees had no deaths. Many of the paddocks on this farm were no longer cultivated and had been revegetated by self sown annual grasses.

Solar radiation decreases as the angle of incident sunlight decreases, but within any particular month the most significant cause of variation in solar radiation is cloud cover. The absence of shade on bright, sunny days is the factor common to all 3 outbreaks, and not ambient temperatures or total solar radiation intensity.

The New South Wales Grains Board, the state barley grain marketing organisation has a nil tolerance standard for ergot-of-rye contamination in barley grain delivered to New South Wales Graincorp by barley growers. However, the contaminated barley used by the Cowra feedlot had come out of storage sites belonging to New South Wales Graincorp, the state barley grain handling organisation. The barley contained up to 200mg ergots/kg. This equates with the current 200mg/kg national stock foods standard for ergot contamination tolerance in livestock feedstuffs.

The appropriateness of this standard for grain to be fed to shade-deprived livestock is now questionable. (Burke et al. 2000).

DEATHS AT TABBITA FEEDLOT, NEW SOUTH WALES FEBRUARY 2000. CA Bourke, pers com 2000

In February, 2000 at Tabbita feedlot, 35km west of Griffith 1250 cattle died within 24 hours out of 30,000 cattle. On the day of the deaths ergot was present in the feed. The environmental temperature was not excessivley hot (33°C).

In a group of 10,000 cattle that were in the shade, only 17 cattle died whereas in the remainder of 20,000 cattle which were out in the sun, over 1200 cattle died. It was likely that the cattle received a batch of feed with high ergot in it.

The grain had come from a 100 km radius of Tabbita — from Barellan between Griffith and Temora.

SPORADIC BOVINE HYPERTHERMIA (1986)

On 30/04/1986 I had a phonecall from an owner of a feedlot with 700 cattle, of Herefords and Angus, consisting of steers and a few heifers, 12-14 months of age. He said cattle were showing signs of heat stress. There was no shade; there was slight slobbering in the cattle, they panted quite quickly and the tongue protruded, the neck stretched out. It occurred in cattle with only 20% of grain in the ration. Visits were made to the property. It was seen that the cattle sought water and a number placed their front legs in water troughs. Cattle were reluctant to feed during the day but they returned to feed at nighttime. The symptoms showed signs within 4 days of going onto the grain ration, being first seen on 7/4/1986.

On 6/5/1986, the owner reported that the cattle had improved due to rain and cooler weather.

On 27/5/1986, another visit was made to the feedlot where many cattle were showing signs of hyperthermia and with a lot facing the sun to minimize their exposure to the sunlight and one animal had its front feet in the water trough.

On 30 May 1986, the owner rang and he advised that he had cattle in a yard at the back which were affected (with hyperthermia) and had been on grass and never had grain. Dr Lester Burgess of the University of Sydney was responsible for first identifying the ergot in grain in 1986 and in June of that year he and Wayne Bryden also from the University of Sydney came to the Forbes Pastures Protection Board District on 20/6/1986 and made a survey of a number of properties for ergot in pastures — particularly in ryegrass. Ergot in ryegrass was positively identified over a wide area, although the contamination was not found to be heavy. One sample of ryegrass in the paddock was found to have 0.06% by weight of ergot contamination. Ergot was seen in another pasture species known as "wheatgrass".

Prior to the identification of the ergot as being the cause of the problem, the condition in cattle was known as "Bovine Idiopathic Hyperthermia". Bourke (2000) states that hyperthermia associated with ergot of rye was first recognized in 1986 but probably is not a recent development. The first case of Bovine Hyperthennia seen was in January, 1986 when Veterinary Inspector Molong, Phil Ahrens, visited a Central West Dairy to investigate a case of unexplained "milk drop syndrome". Milk production was reduced by up to 75%. Subsequently, cows were reported in two dairies on the Illawarra coast and beef feedlots in the Central West. Until July 1986, the condition had been seen in four dairies and twelve feedlots in PP Boards of Molong, Forbes, Carcoar and Moss Vale. The Forbes episode was the most westerly reported case.

In all cases the morbidity was very high (75%-100%), often reached within two weeks and cattle remained affected for up to several months. The disease was characterized by high rectal temperatures (41°C to 42°C), excessive salivation, inappetance and increased respiratory rate. Affected cattle stood with their mouths open and tongues protruding. The condition was modified by the ambient temperature. During the warmer hours of the day or after forced exercise the condition was aggravated and cattle tended to stand in shade or in any available water. The condition of the cattle improved at night and in feedlots where food was available ad lib, cattle consumed nearly a full 24 hour ration during the night.

There was virtually no mortality associated with this condition in 1986 in contrast to the Forbes property with the mortality in December 1998 and January 1999.

At the time the first case was investigated the condition was thought to be associated with an infectious agent, but as more farms became involved and serology was continually negative, alternative causes were sought. Serological testing for IBR, leptospirosis, ephemeral fever and pestivirus revealed no significant findings. One dairy animal showing clinical signs was slaughtered and a line of mildly affected feedlot cattle were followed through an abattoir. Post- mortem examinations revealed no macroscopic lesions in any of the organs examined. Histopathology of tissues from these animals and liver biopsies from 4 clinically affected dairy cows revealed no abnormalities.

In 1986 nearly all cases were related to hand feeding of home grown grain (wheat, oats, barley and lupins) harvested in 1985 in the Central West of New South Wales. The coastal dairies involved had obtained grain from farms in the Central West.

Investigation of feed samples implicated in this condition revealed significant levels of ergot. This was done by Lester Burgess. The feed was contaminated with ryegrass seed that had been infested with Claviceps purpurea. [Annual (or Wimmera) ryegrass grows in the Forbes Rural Lands Protection Board district.]

Eighteen feed samples being fed to cattle affected with, or suspected of being affected with this condition contained levels of ergot in the range 0.02% to 0.8% (W/W) whereas 7 of 10 samples of feed being fed to unaffected cattle contained no detectable ergot and the other 3 samples had up to 0.02% (W/W) ergot.

The local factor was wet conditions in 1985 from spring to harvest, which would have greatly increased the content of ergot.

Tony (AD)Ross et al. in 1989 — describes the reproduction of the field syndrome of hyperthermia by feeding ergotised grain under simulated summer conditions.

Two groups of 4 Hereford steers were housed in a controlled environment room and exposed to simulated high summer temperatures. Both groups were fed barley grain and hay diet ad libitum. The barley in one diet contained 0.5% W/W ergots of Claviceps purpurea.

Within one week of feeding the ergot diet, mean rectal temperature was significantly elevated (P<0.05) each afternoon (up to 41°C) but returned to normal overnight. Elevated rectal temperature was accompanied by other signs of heat stress, reduced feed intake, body weight loss and depression of prolactin concentration. Symptoms disappeared within one week of ceasing to feed the ergot diet.

ERGOT OF RYE. Dr CA Bourke pers comm (2000)

Refers to an ergot fungus infection of the seeds of Annual rye grass (ie Wimmera rye), or Perennial rye grass or Cereal rye.

Rye grass seeds are a common weed seed contaminant of cereal grains grown throughout the wheat belt of NSW.

Barley grain harvesting tends to pick up more rye grass seeds, hence more ergot, than grains such as wheat.

Ergotised rye grass seeds look like rye grass seeds That have swollen up and turned dark black, they have the general appearance of mouse droppings.

Rye ergots reflect the size of the parent seed, in annual rye they are about 4 or 5 mm long and about 1 mm wide.

The following figures are a guide to levels of ergot contamination in grain:

0.5% 5000 mg per kg = about 1000 ergots in a 2 litre sample of grain (ie 1.3kg)

0.05% = 500 mg per kg = about 100 ergots in a 2 litre sample of grain (ie 1.3kg)

0.02% = 200 mg per kg = about 42 ergots in a 2 litre sample of grain (ie 1.3kg)

References

Radostits OM, Blood DC, and Gay CC — Veterinary Medicine — 8th edition p 1595-1596 Poisoning by Claviceps purpurea (ergotism)
Jessep TM, Dent CHR, Kemp JB, Christie B, Ahrens PJ, Burgess LW and Bryden WL (1987). Australian Veterinary Journal: 64,353: Bovine idiopathic hyperthermia
Bakau BJK, Bryden WL (1987) Proceedings of the Nutrition Society of Australia 12:170: Toxicity of ergots of Claviceps purpurea in chickens subjected to heat stress
Ross AD, Bryden WL, Bakau W, and Burgess LW, (1989) Australian Veterinary Journal 66,247-249. Induction of heat stress in beef cattle by feeding the ergots of Claviceps purpurea
Burgess LW, Bryden WL, Jessep TM, Scrivener CJ, and Barrow KD (1986). Proc. Nutr.Soc. Aust., 11,120. Role for ergot alkaloids in Bovine Hyperthermia
Cunningham GM, Mullham WE, Milthorpe PL, and Leigh JH (1981). Plants of Western New South Wales. p 114: Wimmera Ryegrass
Peat RL, McCarthy MR, and Barbetti MJ (1991) Australian Veterinary Journal 68:121: Hyperthermia and death in feedlot cattle associated with the ingestion of Claviceps purpurea
Plant Associated Toxins — edited by SM Colegate and PR Darling (1994) Chapter 69 (p387-392) by CA Bourke. The evidence against the existence of so-called convulsive ergotism in ruminants
R Moss (1999)Dairy R & D News (May/June) — Avoid sorghum ergot in dairy foods
Meg Ward (1999), Western Magazine, week commencing Monday, November 29, 1999 (page 1)
Blayney BJ, McKenzie RA, Walters JA et al. Australian Veterinary Journal 2000; 78:102-107: Sorghum ergot (Claviceps africana) associated with agalactia and feed refusal in pigs and dairy cattle
Bourke CA, Bailey GD and Kemp JB, (2000) Australian Veterinary Journal 78: 618-621. The case for solar light radiation being more significant than ambient temperature in producing lethal hyperthermia ergotism in cattle

Acknowledgements

Dr CA Bourke, Senior Veterinary Research Scientist (Poisonous Weeds), Orange Agricultural Institute, Forest Rd, Orange NSW 2800 for his collection of annual rye grass seed samples on the Forbes property which confirmed the diagnosis of ergotism and his providing me with both information on ergotism and references.
Dr Patty Paul of the Forbes Veterinary Clinic for her contribution on the Forbes Property.
Robyn Shea and Donna Newell for the typing.