In February 2019, sulphur toxicity was confirmed as the cause of death of approximately 200 of 1000 composite breed ewes in the Central West Local Land Services region. The source of sulphur was a pile of gypsum in the paddock in which the sheep were grazing. Initially, the case presented with history and clinical signs consistent with lactic acidosis, but this was excluded following post mortem examination and laboratory findings. Fluoride poisoning was also excluded following laboratory testing.
In late February, a producer reported 12 of 1000 sheep dead and another 20 animals sick. These were dry ewes running on cereal stubbles, supplemented with canola hay and pasture silage. Two days prior to the initial illness and losses, the ewes had been fed approximately 0.5kg wheat per head. The sick sheep were depressed, described as 'stiff', and some were recumbent and unable to rise.
Animals able to walk had been removed from the paddock. Of the remaining live sheep, those standing were depressed with hanging heads and a wide-based stance. Some had body tremors, but these did not involve the head. Recumbent animals were either sitting sternally, or in lateral recumbency with evidence of paddling. No affected animals appeared to be blind.
Two animals were necropsied. The rumens of both were largely full of roughage, with only a small amount of grain present. Rumen pH was 7. The abomasums contained a large amount of fluid, and a significant quantity of a sand-like substance. The mucosa near the pylorus of one ewe was reddish and swollen (inflamed), and the livers of both sheep were friable. The sand-like substance was consistent with the gypsum in a pile in the paddock.
Blood, aqueous humour and fixed tissues were submitted for laboratory testing, considering the differentials of lactic acidosis, polioencephalomalacia (PEM), and sulphur toxicity secondary to gypsum ingestion.
Deaths and new cases continued to develop, and by day 4, there was approximately 100 dead and 30 sick sheep. The producer had noted that illness progressed to death over 24 hrs - initial mild depression and a watery nose, developed to further depression and prominent mucoid nasal discharge. Sternal recumbency progressed to lateral, with paddling often to the extent of pivoting the animal in a circle.
A second property visit was conducted two days after the initial visit.
Post mortem examination was carried out on a further two freshly dead animals. Again, the rumens contained a large amount of dark green roughage, with a small amount of grain present, and a pH of 7. The contents of the ventral sacs were dry with the sand-like substance present. Rumen mucosa was light pink, suggesting inflammation, but there was no mucosal sloughing. In both animals, the abomasum contained a large amount of fluid, and the sand-like substance. The abomasal mucosa of the first ewe was slightly red (inflamed), but in the second sheep, inflammation was pronounced, and there were large areas of ulceration and associated haemorrhage. The kidneys of the first animal were soft and pale, and bulged on the cut surface, and the cortex and medulla were pale with prominent white cortical striations.
Further samples were submitted for laboratory testing.
Results from blood and aqueous humour testing ruled out lactic acidosis, with normal D-lactate levels, but samples from both submissions showed significantly elevated sulphate levels, ranging between 6.65 and 12.6mmol/L (0.70-2.00mmol/L reference range). Further blood and urine analysis findings were consistent with renal failure.
The most significant histological findings from both submissions were found in the rumen, abomasum and kidney.
Rumen wall changes were most pronounced in the samples from the first submission, and resembled the effects of a direct toxicity, with an acute, moderate erosive rumenitis described.
The abomasal changes in the second animal from the second submission were the most significant, and were described as an acute, marked necrohaemorrhagic abomasitis.
Kidney changes were significant in samples from both submissions, with marked acute tubular necrosis and degeneration, severe cast formation and occasional to abundant intraluminal oxalate crystals.
An interstitial suppurative pneumonia with mild alveolar necrosis was also described in the lung from the second submission.
Blood from three affected sheep was also submitted to the National Measurement Institute to evaluate fluoride levels. These were below the level of reporting, (<0.2mg/kg).
Gypsum (hydrated calcium sulphate), is commonly used in agriculture as a fertiliser or soil conditioner. It is found in naturally occurring deposits, and can also be produced industrially. It was the naturally occurring form involved in this case.
In our local area, gypsum is generally applied from summer to autumn, between winter cropping seasons. It is usually delivered on farm direct to the paddock, before being spread and incorporated into the soil sometime later. It would not be uncommon for livestock to graze in a paddock containing a pile of gypsum.
Excess dietary sulphur is more commonly known to cause PEM, but in this case, blindness - a classic clinical sign associated with PEM, was not seen in affected animals, and cerebrocortiocal necrosis was not seen during histological examination of the brain. Sulphur poisoning has also been described to cause fatal gastroenteritis and dehydration. Severe inflammatory lesions were seen in the rumen and abomasum of affected animals in this case.
The dramatic histologic changes in all kidneys submitted suggested exposure to a nephrotoxic agent. Potential nephrotoxins were considered, including plants, such as redroot pigweed (Amaranthus retroflexus), oak (Quercus spp.) and lesser loosestrife (Lythrum hyssopifolia), mycotoxins (ochratoxin), and heavy metals (lead, arsenic, mercury, cadmium). However, these were ruled out as the sheep had no access. The large amount of oxalate crystals present could have been due to ingestion of oxalate-containing plants such as redroot pigweed (Amaranthus retroflexus), fat hen (Chenopodium album) and Oxalis spp. but again, the sheep had no access to these plants. Fluoride was another potential toxin considered, as it can be present in synthetic gypsum as an impurity, and can cause gastrointestinal inflammation and changes in other tissues, including kidneys. Bourke and Ottaway (1998) have previously reported health problems in cattle associated with chronic gypsum fertiliser ingestion. Nevertheless, this was excluded, as fluoride was not detected in the blood of affected sheep.
The pathogenesis of the renal lesions is not known exactly. It is suggested they could be a consequence of the ingestion of high quantities of sulphur compounds, since these are oxidated and excreted through the urinary system. This reaction could potentially cause a direct renal toxicity. It was also suggested that the oxalate crystals could have been a secondary consequence of the renal lesion, the result of impaired calcium metabolism.
While problems associated with ingestion of gypsum dumped in paddocks are rarely reported, losses can be very significant, as in this case with 20% losses, and as reported by Dent (1997) with 25% losses. We can only speculate on why so many sheep in this mob decided to consume gypsum in this way. Hunger, greed, boredom and attempted self-correction of a mineral imbalance are all possible explanations.