Cases of superphosphate poisoning are reported as rare in the literature.? The fact that I have seen two of these cases in seven years seemed unusual and also both the producers and in the first instance, myself, were completely unaware of the risks of stock gaining access to superphosphate even in relatively small quantities. I provide the following case studies as a reminder of the potential danger of stock accessing even relatively small amounts of this common agricultural product.
On 29/3/12, a ewe was presented in lateral recumbency with severe depression, injected mucous membranes and with a temperature of 38.4. This was the seventh sheep out of a mob of 200 that had presented similarly in the past few weeks with four mortalities. The ewe mob had been on this paddock approximately two weeks; it was a red grass/ clover pasture and they had been drenched onto the paddock with Naphthalophos/Benzimidazole/Levamisole combination drench. The mob was generally in good body condition score and had just finished joining.
On necropsy, the kidney was large and soft (Figure 1). Obvious white pellets were visible in the rumen contents (Figure 2). The GIT was generally filled with fluid content. No internal parasites were found.
Serum biochemistry results from this ewe showed significant renal insufficiency.
Histopathology of the kidney showed multifocal distal and proximal tubules dilated with attenuated epithelial cells. Dilated tubules contained hypereosinophilic fluid admixed with sloughed epithelial cells and debris. Bowman's capsule was variably dilated and contained eosinophilic globules. The pathologist commented that the high level of phosphate was consistent with the ingestion of the pellets found in the rumen. The high sulphate (leading to polioencephalomalacia (PEM)) and the hypocalcemia are likely factors in the clinical presentation.
In September 2005, three of 80 ewes were found down after yarding for 24-36 hours and weaning the lambs. Hypocalcemia was suspected but the ewes showed no or only an initial partial response before progression of clinical signs occurred. On necropsy of one ewe, the kidneys were enlarged and soft with a yellow discolouration. The cortex appeared to bulge on the cut surface.
Histopathology of the kidney showed multifocal acute tubular necrosis and degeneration. No crystals were found. The changes reflected a nephrotoxic cause, most likely to be superphosphate poisoning or oak toxicity.
References suggest that superphosphate is not particularly palatable but that sheep will eat it when it is in the granular form where the size and texture resembles grain (Radostits et al. 2007). The poisoning is mainly due to the fluorine present although calcium pyrophosphate and calcium orthophosphate also contribute. The typical result of the toxicoses is proximal renal tubular necrosis. The LD50 is reported to be 100-300 mg/kg bodyweight for sheep.
In the first case, some left over superphosphate had been discarded by the producer in the paddock where the sheep gained access. In the second case, the holding yards where the sheep were kept was also the place that the superphosphate had been stockpiled for spreading.