Salt toxicity in ruminants occurs most frequently when salt-rich solutions are consumed during a period of restricted access to water, followed by unrestricted access to fresh water5. When water deprivation is not a factor, salt toxicity occurs due to high salt concentration in drinking water. This effect is compounded when the diet also has a high salt concentration8. High salt concentrations in the diet are usually tolerated if water is freely available. Salt toxicity has been reported in cattle with access to estuarine water8, 9 and waste products of oil and gas drilling10. Mortalities have been recorded in sheep2 and cattle3 drinking saline bore water which was concentrated due to evaporation in troughs.
This is the first published report of salt toxicity caused by saline dam water which had concentrated due to evaporation. The diagnostic challenges of this case are discussed.
Commencing on November 5th 2014, the death of 18 of 75, 12-30 month old mixed sex cattle on a property east of Jerilderie was investigated. The cattle had not been observed for six days so the time of death was unknown. The cattle had been moved into a 400 Ha paddock, which consisted of a mixture of mature annual grasses from an adjacent paddock, which contained similar pasture species with the addition of lucerne, 7 days earlier. The gate to the new paddock had been opened and the cattle were allowed to file in at their own pace. Mild lameness was noted in approximately 12 animals but was not considered significant at the time. A quick long distance observation was made the next day to ensure that they had found their way to the water source but a close examination was not made. The cattle had been born at a property in Broken Hill and had been agisted in The Gippsland before coming to the current property about 4 months earlier.
A private veterinarian from Jerilderie initially assessed the situation. He found that the deaths were staggered, of the 12 animals found dead, some animals had died recently and some were severely ill and unlikely to survive. The author and an LLS colleague examined the remaining stock the following morning. At that stage there were 16 dead. Two post mortem examinations were performed. One heifer remained in the previous paddock as she was considered too lame when the mob was moved and she appeared to still be in good health. Both paddocks carried approximately 1000 young, dry ewes which did not appear affected.
All cattle in the affected mob had lost significant condition. They were noticeably hollow in the left flank, depressed and most had diarrhoea or dysentery. They also sought shade or attempted to cool themselves in the dam. Several had a hypermetric gait when driven and two were aggressive when approached. Necropsies were unremarkable apart from varying degrees of enteritis. Handling facilities were not available but a moribund animal was examined and rectal temperature registered >42. The cattle that were well enough were moved back to the original paddock where they recovered over the next two weeks. Of the total of 18 cattle that died, only one death occurred after the animals were moved to their original paddock. One severely affected animal could not be driven to the original paddock for over a week and was much slower to recover. Both mobs of sheep were driven approximately five kilometres to new paddocks with no signs of illness.
Differentials of salmonellosis, clostridial enteritis, coccidiosis, Flood Plain Staggers, mycotoxicosis, blue green algae poisoning, lead poisoning, arsenic poisoning and nitrate poisoning were considered initially. Laboratory results from post mortem samples and water samples allowed the exclusion of most of these differentials except for mycotoxicosis which is hard to diagnoses from post mortem samples. A further property visit was carried out with the regional veterinarian Dan Salmon to investigate if there was a source of mycotoxins or any other possible cause. Samples of ryegrass and barley grass with signs of fungal growth were collected and sent to the state plant pathology lab. The dam water was examined and it was noticed to be remarkably clear with no plants or algae growing.
The dam water was found to have an electrical conductivity of 32 000 S/cm with sodium (3400 mg/L) and chloride (8600 mg/L) the most significant elements, while calcium (720 mg/L) and magnesium (810 mg/L) were also high. Industry water standards class electrical conductivity above 7800 S/cm as risky to beef cattle and over 30 000 S/cm as toxic to all classes of domestic livestock1. All clinical signs observed in the cattle were consistent with literature regarding salt toxicity and this was the final diagnosis. The dam in question had been filled from a bore eighteen months previously. The other dams on the property had been filled more recently from a surface water irrigation channel.
Mortalities from salt toxicity due to high salinity drinking water have only been reported in Australian literature twice in ruminants2,3 and both of these were due to bore water evaporating and concentrating in troughs. It has been proposed that significant production losses probably occur quite regularly but are not diagnosed4.
This case presented a difficult diagnostic challenge for several reasons. The stock were not observed for six days. . The variety of clinical signs and post mortem changes observed made it difficult to identify the changes that were significant to the disease process. Confounding factors such as lameness noticed when moving the cattle into the paddock with brackish dam water made the relevant clinical symptoms harder to determine. When other published cases of salt toxicity in ruminants were reviewed they were found to be similar to the findings of this case. Enteritis and CNS signs are the most common findings5 though this case was also signified by dehydration and hyperthermia which is consistent with the findings in two other studies6,7.
Surveys of bore water in the area have shown salinity levels above recommendations for stock water are not uncommon11. Bore water composition can change significantly within months and any analysis at the time of the disease outbreak would not reflect the water used to fill the dam 18 months previously (Adrian Smith, Murray Local Land Services, personal communication on 28th November 2014). Moule2 and Ohman3 both showed that the water made available to stock in troughs was more concentrated than the bore water supply due to evaporation. It is possible that the water in this dam had evaporated and become 10 times more concentrated since filling.
The sheep were consuming the same drinking water and were exposed to the same grazing conditions as the affected cattle and did not show any signs of toxicity. Though the sheep were not thoroughly examined, they were walked for approximately 5 kilometres to a new paddock and no signs of toxicity were observed. As the sheep were drinking the water while it was evaporating they would have been able to adjust to the increase in concentration12. This case appears to be the highest recorded salt concentration of drinking water where sheep did not show any signs of toxicity.