Grain Poisoning in Merino Ewes on Wheat Stubble

Katharine Marsh, District Veterinarian, Central West Livestock Health and Pest Authority

Posted Flock & Herd August 2009


Approximately 20 of 1000 ewes died following yarding. They had previously been grazing stubble since mid December, were yarded for 12 hours, then put onto fresh wheat stubble following yarding. The owner was unaware of any large grain spills in the paddock (which was supported by the relatively small amount of grain found in the rumen), so the only grain available was that left in the any remaining heads and normal spillage from the header. Some heliotrope (Heliotropium europaeum) and black grass (Eragrostis cilianensis) had grown underneath the stubble following some minor rain received in December.

The deaths started the night after being in the yards and continued the next day (3/2/09). Some ewes were found dead, but others seemed to look very lethargic and depressed before going down and eventually dying. When the mob was examined, some ewes appeared depressed, some had a very 'proppy' gait and others had pasty, grey diarrhoea. Most of the ewes that died had evidence of this diarrhoea.


A ewe examined on 3/2/09 was recumbent and very depressed. The mucous membranes were dark red/ purple but without evidence of jaundice. The ewe's temperature was not taken. As she had been sitting in full sun it was unlikely to be of value. The ewe was sacrificed for post-mortem


The post-mortem was largely unremarkable. Some grain was noted in the rumen but there was not a large quantity (approximately 30% grain at most, 70% roughage) and the contents did not smell sour as would be expected with grain poisoning. The rumen pH was approximately 6 on a dipstick. The rumenal mucosa did not appear damaged and there was no evidence of inflammation. The ewe did not have evidence of diarrhoea.

A limited post-mortem was conducted on another ewe found dead. This ewe had scours as described above. The post-mortem of this ewe revealed a small hole in the rumen (although this may have occurred following death, as the carcass was very bloated, or by me getting a little vigorous with my knife). The mucosal surface of the rumen was sloughing, although this was most likely a post-mortem change. There was no evidence of inflammation and similar amounts of grain were seen in the rumen as the sacrificed ewe. The rumen pH was 5.5-6 on a dipstick. Sections of rumen wall and liver were collected. Further samples were not collected as the tissues had literally cooked in the heat (the carcass was found lying in full sun).


D-lactate levels of the sacrificed ewe were 18.6mmol/L (normal 0.0-0.5mmol/L).

Histopathology of the rumen of both ewes revealed extensive oedema within epithelium with scattered necrotic foci infiltrated with neutrophils. These lesions are typical of those seen in grain poisoning, with the elevated D lactate confirming the diagnosis. There were no significant findings in other tissues or on haematology. Hypocalcaemia had been considered as a differential, but calcium levels were normal. Heliotrope poisoning had also initially been considered, but ruled out as there was no evidence of jaundice or gross liver damage.


At the time of the farm visit, the owner had already moved the sheep onto a browned off pasture paddock. In addition to this, I recommended feeding hay if possible. However, the owner only had silage available. It was not recommended to feed this as it may be reasonably readily fermentable, which could worsen grain poisoning if this were the cause, and was less likely to act as effective roughage anyway. No additional treatment was undertaken at the time of the visit, as, given the small amounts of grain in the rumen, grain poisoning seemed a remote possibility. No further deaths occurred.


Given the small amount of grain seen in the rumen of both ewes and the reasonably limited access to grain, this seemed an unusual presentation of grain poisoning. I suggested to the owner that the heat experienced at the time of the deaths could have played a role in the course of the disease. On the day of the farm visit it was 42°C in Nyngan and probably hotter on this property. Since death in lactic acidosis is ultimately due to dehydration and circulatory shock, the heat would have exacerbated this and quite possibly led to the animals' deaths. In normal weather conditions, I feel that it is likely that the affected animals may have experienced only mild grain poisoning, from which they would have likely recovered.

It was suggested that an explanation for the limited amount of grain in the rumen of the post-mortemed ewes was that it had previously been passed in the faeces. This can be at least partly discounted, as the sheep had congregated around the few trees in the paddock so had mostly defaecated in these areas. The owner had later driven around these areas, and although they noted many pasty faeces, they did not notice the presence of much grain.


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