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This article was published in 1958
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Grain Poisoning with Sheep Nuts

D. J. WALKER, B.V.Sc., Veterinary Inspector, Armidale


Reference to grain poisoning invariably brings to mind death of animals from engorgement with wheat or other cereal grain; the result of failure to ensure that each individual eats its proper share of a large quantity of feed placed before a proportionately large number of animals. It is generally assumed that once a mob of sheep has learned to feed on nuts and grain the risk of trouble is past. Though this may be the general rule, losses have been experienced in this District after months of trouble-free feeding, at less than minimum drought maintenance levels.

Since the inference might be drawn, from lack of description or reference to lesions in the scanty literature upon this subject, that poisoning with grain or wheat is without macroscopic lesions, it is possibly of interest and value to record the spectacular lesions observed in a series of outbreaks believed due to grain poisoning.


In early June, 1957, hand-feeding of 620 Merino ewes, which were in near-fat condition, was commenced. From early in May till trouble commenced in August they had been running in the same 600-acre paddock of trap country. They were due to lamb at the end of September. Hand-feeding was carried out in spite of their condition because, though sufficient roughage was available, it was of low quality and a hard winter was anticipated. Two ground tanks were available for watering but stock mainly used a creek which had ceased to flow except through gravel beds.

Throughout the period a proprietary brand of sheep nuts, comprised mostly of crushed wheat and containing not less than 12 per cent of protein, was fed. The ration was 1½ lbs. per head per week, fed in equal parts bi-weekly. No loss or difficulty was experienced in the early stages of hand-feeding.

On 6th August a routine drench of phenothiazine was administered. Count and apparent health was then satisfactory. On 12th August the mob was fed. Sheep appeared to be in satisfactory health; the mob was grazing normally and no sick sheep were noted. There was an extremely heavy frost that night. On 17th August, two days after sickness was first noted, the mob was seventy short by count after muster, the deficiency being assumed due to deaths.


General lassitude was the main symptom in the early stages. Odd sheep, not seen by the writer, were reported to be affected with bloodstained faeces and evidence of abdominal pain. The mob was scattered, sheep grazing in groups of threes and fours or standing singly or in groups under trees. In later stages of the outbreak, numbers of sheep were noted to be affected with diarrhoea. Temperatures were recorded as 101.8, 102.8, 105.5 and 103.0°F. There was a break in the wool at the skin. When in extremis there was generally a discharge of sour-smelling rumen contents from the mouth and nostrils.

A considerable amount of Rockfern (Cheilanthes tenuifolia) was found growing in the paddock. This was dry, with a few green shoots. No evidence of this plant could be found in rumen contents.


Autopsy findings were recorded for six sheep, all but one of which had eaten freely of sheep nuts as gauged by examination of rumen contents. All were freshly dead or destroyed. Macroscopic lesions were highly spectacular and variable.

Lesions were consistently present in the forestomachs in some form. Large patches of inflammation and necrosis frequently were present in the walls of the ventral curvature of the rumen, to which area they were confined. Only two of those for which auotpsy findings were recorded carried rumenal lesions.

However, subsequent investigations, on another holding, suggested strongly that early stages of lesions, to be found only by very careful examination, may have been present but overlooked on the mucosa. Examination of the peritoneal surface of the rumen gave no evidence of these early lesions. Considerably more than the six were examined and in about half of all of them spectacular ruminal lesions occurred.

A highly constant lesion (5 out of 6) was necrosis, in a patch on one or more of the laminae of the omasum. An area half an inch in diameter in one single lamina was involved in one. Others carried lesions involving almost the whole of a number of contiguous laminae. In two, hyperkeratosis in the form of a brown cornification of ridges continuing the laminae was noted.

The necrotic patches in the rumen were observed as sulphur-yellow areas of generally circular outline varying in size from about three inches to half an inch in diameter, with an area of surrounding intense inflammation, the colour of arterial blood, about half an inch wide surrounding the necrotic area. On the peritoneal surface of the rumen the lesions appeared as diffuse dark red blotches. Lesions on laminae of the omasum were of similar macroscopic appearance, half an inch to an inch and a half in diameter.

Lesions in the abomasum took the form of a relatively mild gastritis, with ulcerations which were bright scarlet. The periphery of ulcers was raised. Some had necrotic centres. Ulcers were up to about 18 in number and from one-quarter to an inch and a half in diameter. These were mostly on the free folds of the abomasum and consequently, on occasion, were arranged in linear fashion. In cases showing most severe lesions there were diphtheritic ulcerations surrounding the anterior orifice of the abomasum.

The free borders of the cells of the reticulum were noted to be inflamed in two cases.

Inflammatory change in the small intestine was comparatively slight and inconstant.

Typhlitis and colitis were present generally and were notable features of this outbreak. Ulceration present in the caecum appeared to be more chronic than lesions elsewhere in the carcase. Erosion of the mucosa appeared to be part healed. Longitudinally on the ridges of the mucosa and extending into the rectum, inflammatory change was intense, with much free blood in some cases.

At times an especially foul odour as of gangrene was present. This was particularly noted in the caecum but also occurred in forestomachs. It was not specially noted on first opening the carcase; but was remarkably persistent on the hands.

No lesions worthy of note were observed other than in the gastro-intestinal tract.


Toxicological examination for nitrite, nitrate and phosphorus was negative. Bacteriological examination revealed no significant organisms.

Histological examination of tissues confirmed the necrosis of epithelium observed macroscopically, but threw no additional positive light on the aetiology of the condition.

The Botanist's report on ruminal contents showed that among other plant material a species of Trifolium, a species of Eucalyptus, Triticum aestivum, Avena sativa, and Rosa rubiginosa were included in the diet.


Six sheep which were treated with 1½ mil. units each of penicillin were alive next morning, as against only one of a similar number of controls. However, all treated sheep eventually succumbed, possibly as a result of pregnancy toxaemia; symptoms of which developed later.

On 17th August the whole mob was placed on grazing oats, Losses ceased within two days; or about a week after the last feed on sheep nuts.


Shortly after lambing and shearing it was noted by the owner that about two-thirds of those which had lost lambs or failed to lamb were affected with a break in the fleece at a position corresponding in time with the outbreak. With very few exceptions the wool of those with lambs at foot was sound. No abortions are known to have occurred.

On the evidence of information supplied by local colleagues concerning deaths where stock were being fed sheep nuts or grain, of our investigation of a number of other outbreaks and of work on cattle reported by Rue Jensen et alia (1954), the conclusion was reached that the cause of sickness and death was poisoning by grain; the main constituent of the sheep nuts.


At least four deaths occurred in a mob of 104 fat Romney Marsh ewes which were due to commence lambing in three weeks. From April to September they had been fed; the ration toward the end of the period being 3 oz. per head per day of sheep nuts, fed each third day. Lesions corresponded with the general post-mortem picture described for outbreak No. 1.


Two hundred and eighty (280) poorly grown, but strongly conditioned, Merino weaners on very poor native pasture were fed a ration of lucerne, oaten grain, sheep nuts and crushed wheat with cereal chaff ad lib; followed by maize and chaff. Within the ingredients referred to there was considerable variation in composition and amount of the ration, except as regards cereal chaff which was always available.

Twelve became sick with a thin watery scour and were removed to grazing oats, where they recovered. Other odd cases continued to develop. After inflammation from abomasum to caecum.(sic) Three other sheep were examined. Ruminal lesions as described were present in all. The peculiar, offensive smell, as of gangrene, was strong.


Six died and at least four were sick in a mob of two-hundred (200) young Merino wethers which were being fed sheep nuts at the rate of 10 oz. per head per day on alternate days. Though they were well accustomed to hand-feeding, on the first feed after a change to a fresh paddock trouble started. This was apparently an "acute" outbreak, with insufficient time between feeding and death, i.e., less than 24 hours, for development of the more spectacular type of lesions. There were large quantities of finely triturated grain in the forestomachs, the contents of which had a strong sour odour. The mucosa of the forestomachs was abnormal, with the appearance of being macerated. The laminae of the omasum were tender.


Deaths occurred in three-hundred and twenty (320) Merino wethers which had been fed sheep nuts since May. The ration had been one pound per head per week and was increased to two pounds, half fed on Mondays and Fridays, three weeks prior to the start of trouble.

On 9th September the mob was fed after moving to a fresh paddock. Eight were dead next morning. By nightfall on the first day following feeding, there were 22 dead and approximately 30 very sick; by the second day 44 deaths had occurred and by the third day 52 deaths. The total loss was approximately 70 head.

Late on the first day following feeding, such of the mob as could be driven were placed on improved pastures, shortly after which no more deaths occurred. Treatment of sick sheep with doses of up to one ounce of sod. bicarbonate was without effect.

Most noteworthy features of this outbreak were the frequent marking of muzzles with regurgitated ingesta, profuse diarrhoea of a yellowish colour, in most cases, and odd cases of lameness, a feature not seen in other outbreaks.

Autopsy of five sheep on the second day of mortalities revealed no lesions in the forestomachs. The surface mucosa of the abomasum was necrosed and small intestines were distended, having a diameter of approximately one inch. The mucosa of the whole of the alimentary tract of these sheep gave the appearance of being parboiled.

At the fourth day after mortality commenced, in three sheep examined obvious ruminal lesions were found in the usual position. Additional to the more frequently observed type of lesion, in one of them were about SIX insignificant whitish spots on the peritoneal surface of the rumen. On lightly scraping the mucosa it was evident that beneath the spots was necrotic epithelium; this being confirmed later by histological examination. In one of these three sheep, patches of lighter tissue were found in the liver; being observed on the diaphragmatic and visceral surfaces.


This involved six-hundred (600) store conditioned Merinos, gummy to hoggets, which were being fed a generous ration of good quality wheaten hay. Grain in the heads was very pinched and not plentiful.

On the day before deaths commenced, the mob was drenched with 2 ml. Carbon tetrachloride in paraffin oil.

Macroscopically there was a diffuse rumenitis with gas in the sub-mucosa. No necrotic plaques were found in the rumen. The sour smell of acute grain poisoning was not noted. Liver lesions, though not marked, were present. Sheep destroyed some days after the first examinations were found to present a post-mortem picture typical of later stages of the condition.

Three untreated sick sheep made uneventful recoveries.

Histological examination showed mild subserous inflammation of the rumen, and in the liver centrilobular losses of cell substances suggesting previous necrosis and lysis.


Little reference has been found in literature to the condition of grain poisoning in sheep. Belschner (1953) refers to the fact that digestive disorder may be caused by a ration which is too concentrated and lacking in bulk but gives no details of symptoms, lesions or pathology.

Annual reports of C.S.I.R.O. during the period 1950-53 state that in toxicity there is development of a predominantly lactobacillary type of fermentation in the rumen, a sharp fall in pH to about 4, and a rise in ruminal lactic acid to 1 per cent. or more. Ruminal changes are soon followed by a rise of blood lactate, a fall of blood pH and plasma bicarbonate and a severe fall of blood volume with eventual death. Ruminal atony may supervene even 54 hours after a large toxic dose. No description of the clinical condition is given.

Extensive observation upon the rumenitis-liver abscess complex in beef cattle has been conducted by Rue Jensen et alia (1954). Apparently this condition in cattle is of importance, not so such because of sickness, death or failure to thrive, but rather because of condemnation of livers at slaughter. The disease is associated with finishing off or fattening in feed-lots. In this work the acute rumenitis of cattle is so described as to enable the rumenitis in sheep to be recognised.

These authors produced rumenitis at will by feeding barley, at the rate of six pounds per day for two days, to cattle unaccustomed to it. Though evidence suggests that production of acetic acid by fermentation is responsible, five gallons of acetic acid at pH 4.3, or of sodium acetate at pH 7.0, daily for two days, with a ration of straw, failed to produce it.

Subsequent work by Rue Jensen et alia demonstrated that the incidence of rumenitis in cattle was proportionate to the amount of concentrate in the ration and also to the rate of change to a ration high in concentrate.

A feature of the disease in cattle would appear to be absence of lesions in the lower bowel; which in sheep, in the series reported, were rather constantly present.

Liver lesions were infrequent in sheep, and such as occurred were possibly attributable to biochemical damage. They certainly were not abscesses due to Spheropherus necrophorus. Had the sheep which came under observation been subjected to high bacterial challenge, as in intensive hand-feeding conditions, abscesses may then have been a feature of the condition seen.

Association of mortality with change of paddock suggests that under such conditions the risk is increased. It is more than likely that portion of the mob is enticed away from the nuts, leaving the remainder to gorge themselves.

In outbreak Number 6 it was almost astonishing that the amount of grain in the hay and its type, i.e., very pinched and small, could cause trouble. In addition, though grain could be found in the ingesta, it was not in what were considered to be large amounts. As in the case of one sheep examined post mortem in outbreak No. 1, it is assumed that offending ingesta had passed on from the rumen and that only in cases where antony of the rumen had occurred was there to be found the high proportion of concentrate resulting from over-eating.

As far as is known, none of the sheep nuts involved contained urea.


1. Six outbreaks assumed to be poisoning with grain are described. Particular attention has been given to description of macroscopic lesions found at autopsy. Necrosis, with both discrete and diffuse inflammation on the ventral curvature of the rumen, ulceration in the abomasum, typhlitis and colitis are all frequent post-mortem findings.

2. Deaths occurred after months of trouble-free feeding on the same material. In some cases it was associated with movement of sheep to a fresh paddock.

3. In deaths which occurred very shortly after gorging, no major macroscopic lesions were found. Two or three days later large patches of inflammation and necrosis were found on the mucosa of the rumen.

4. Feature of the rumenitis-liver abscess complex of cattle were compared with the near-equivalent disease of sheep.


Histopathological and bacteriological examination of specimens was carried out by staff of the Glenfield Veterinary Research Station. Permission of the Director of Veterinary Research, Mr. Grahame Edgar, B.V.Sc., for publication of these results is acknowledged with thanks.

It is a particular pleasure to acknowledge the assistance of Miss L. C. Lawrence, Librarian in Charge, C.S.I.R.O. Regional Pastoral Laboratory, Armidale, who, with her staff, has always been most helpful.


  1. Belschner, H. G. (1953)-"Sheep Management and Disease". Angus and Robertson, Sydney
  2. Rue Jensen, H. M. Deane, L. J. Cooper, V. A. Miller & W. R. Graham (1954) - Amer. J. Vet. Res. 15:202-216
  3. Rue Jensen, W. E. Connell & A. W. Deem (1954) - Amer. J. Vet. Res. 15:425-428

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