Water deprivation and subsequent intoxication is not an uncommon occurrence in cattle and sheep and may be seen after transport, excessive heat or unexpected failure of water supplies. It is more appropriately called “water deprivation sodium ion toxicoses” (Kahn et al, 2005), as it is caused by dehydration leading to hypernatraemia and net movement of water extracellularly. When water is suddenly reintroduced, it rapidly moves back into the intracellular compartments, causing cerebral oedema in the CNS, as well as intravascular haemolysis from red blood cells (Parkinson et al, 2010). It can be difficult to establish a definitive diagnosis, with most cases diagnosed based on clinical signs and history, often with little further investigation. In this case, simple errors in management lead to the loss of 15 cattle, emphasising the necessity to familiarise stock with water supplies, especially when introducing stock to a new paddock.
District vets were initially called to investigate the deaths of 12 steers on a property near Wee Waa, North western NSW in August 2015.
A mob of 270 Angus x Hereford steers aged 7-15 months were grazing on native pasture in a 400Ha paddock. They were running as one mob, but half of the cattle (148 head – the “Blue Taggers”) had been moved to the property from a property near Narrabri 8 days earlier. The remaining steers (“Red taggers”), had been on the property for three months. All had been treated 3 months ago at weaning with 5-in-1 clostridial vaccination, and drenched with Cydectin pour on (Moxidectin, 5g/L, dose administered unknown). The pasture was largely wild turnip, with burr medic and galvanised burr, with thick stands of turnip up to 2m high. The water came from a single trough, fed from a bore via a tank. The water was treated with “Bloat Drench” oral bloat control (271g/L Alcohols C12-15 ethoxylated), at a rough rate of 7-8L per day poured into the trough, which was not regularly cleaned.
District vets were called when the caretaker checked on the cattle to find 6 dead steers scattered throughout the paddock. Upon finding the dead cattle, the caretaker decided to clean out the water trough, which hadn’t been cleaned in some time. He noted that once the trough was cleaned, the cattle rushed to the trough and were observed to be drinking enthusiastically. Three died around the water trough. The caretaker then opened a gate into an adjacent paddock, where there was a dam, fed by the same bore as the trough. The cattle mobbed around the dam, several walked into the dam, and three died in the dam.
The caretaker noted that the blue tag cattle had been looking “hollowed out” and have been losing condition since arriving on the property. He last observed them all alive 48 hours prior to discovering the deaths. The dead cattle were noted to have blood coming out of their noses.
On arrival at the property, multiple dead and recumbent cattle were observed in the vicinity of the water trough, and around the dam.
An Anthrax Immunochromotographic Test (ICT) was performed on a deceased steer who had a bloody nasal discharge (Steer 1) with a negative result. Aqueous humour was collected from a second steer (Steer 2), and a dipstick Nitrate / Nitrate test performed – also with a negative result. It was noted that it was very difficult to obtain aqueous humour samples from several dead steers as their eyes were dry and hard – no fluid was able to be obtained in several attempts.
A water sample was collected from the trough to test the suitability of the water for consumption by stock.
A recumbent steer (Steer 3) adjacent to the dam was examined. Its body temperature was 39.1, no audible lung or rumen sounds on auscultation. It was unable to rise, seemed unaware of our presence, and was bellowing. Its body condition score was 2/5. This steer was euthanased for post mortem, and blood was collected upon euthanasia.
The remaining cattle were mobbed around the dam. They were, as a whole, lethargic, easily approached, and not as flighty as expected.
Upon post mortem examination, the steer was noted to be a “dark cutter”: broadly, its skeletal muscle was dark red to purple.
The heart muscle was dark purple and flaccid, with thin ventricular walls. The Liver was enlarged and swollen with rounded edges and a distinct “nutmeg” pattern across the surface. On palpation the liver was friable and easily crushed between the thumb and forefinger.
The kidney cortex and medulla were dark purple and it was difficult to visually differentiate between the two.
The rumen was full of green, foul smelling fluid, with a relatively small amount of feed. The mucosal surface of the abomasum was red and congested. There was no evidence of a worm burden. The serosal surface of the small and large intestines were red with visible vascular patterns.
When the spinal cord was severed and the head was removed, it was noted that a large amount of fluid, containing white fat-like deposits with a jelly-like consistency flowed from the vertebral canal.
The rostral cerebrum was bilaterally grey when compared to the pink caudal cerebrum. The brain was damaged due to the use of a captive bolt gun.
Fixed and fresh samples of all major organs were collected and sent to Elizabeth Macarthur Agricultural Institute (EMAI) for analysis. Differential diagnoses at this stage included Polioencephalomalacia, salt toxicity and unknown plant toxicities.
Blood samples taken in the field were haemolysed on arrival at the laboratory, despite adequate refrigeration and care during transport. These samples were unable to be used for biochemical analysis.
Analysis of Aqueous Humour from steer 2 confirmed no nitrates or nitrites and no evidence of acidosis (D-Lactate within normal levels). Testing for Sodium levels in the aqueous showed that levels were elevated (180mmol/L), with levels of >172mmol/L associated with water / salt toxicity (H.Peam, EMAI Laboratory results).
Sodium levels in the haemolysed serum from steer 3 also showed hypernatraemia (158mmol/L, range 135-152mmol/L), with a level of >160mmol/L associated with salt toxicity (H.Peam, EMAI Laboratory Results).
Histopathology of the liver showed no evidence of a toxic hepatopathy. The kidneys showed “renal tubular degeneration without significant tubular necrosis. The lesions are unlikely to be severe enough to cause death through renal failure in this animal. Potential causes include haemolysis, myoglobinuria, toxins, reduced perfusion.” (E. Bunker, EMAI Laboratory results).
Histopathology on the brain showed “There was a diffuse mild increase in glial cells, and mild vacuolation of the superficial cortex. Vacuolation of the cortex can be an artefact of fixation, but given the increased sodium levels in aqueous humour and serum, cerebral oedema due to sodium toxicity cannot be ruled out.” (H. Peam, EMAI laboratory results).
Water salinity testing returned an EC of 460uS/cm, well within the safe limit of < 1600uS/cm recommended by the NSW DPI (Curran, 2014).
The laboratory results combined with the clinical picture, give a clear diagnosis of water / salt intoxication in this case. While it is the lack of water and subsequent influx of water that caused the problem, the pathology is due to the imbalance of sodium within the body.
Water deprivation leads to an increased extracellular osmolarity, most notably an increased extracellular sodium concentration (hypernatraemia). This provides an osmotic gradient for the movement of fluid. Of particular significance is the movement of fluid extracellularly from the Central Nervous System. Affected animals become hypernatraemic (Radostits et al, 2007). When water is made available again, extracellular osmolarity decreases, resulting in the rapid movement of fluid back into the intracellular CNS. As a result, potentially fatal cerebral oedema and increased intracranial pressure develop (Parkinson et al, 2010). Similarly, rapid intracellular influx of water into red blood cells often causes intravascular haemolysis, which may explain haemolysis of the submitted blood samples. From the explained pathophysiology, it is understandable that serum concentrations of affected animals may be hypernatraemic, normal or hyponatraemic, depending on the stage of the condition (Parkinson et al, 2010), and the time since water was reintroduced.
From literature reported clinical signs are similar to Polioencephalomalacia (PEM), which was a differential in this case , given the large amount of brassicas available in the pasture. Gross pathological changes generally include cerebral oedema, while other gross signs can include marked congestion of the abomasal mucosae (Parkinson et al, 2010), as was seen in this case. Haemoglobinuria is also a common finding when the condition progresses to the hyponatraemic stage (Radostits et al, 2007), however, urinalysis was not undertaken in this case.
The challenging aspect in this case was determining the cause of the initial water deprivation. Why was only the Blue Tag mob affected? What was wrong with the water or trough that prevented only the blue tag mob from accessing sufficient water, and had no affect on the red tag mob?
Further discussions with the owner revealed that the new cattle had been introduced to the paddock immediately after watering in the yards. They were then walked into the paddock, and were not shown where the single water trough was. Given the large size of the paddock, and the presence of thick stands of 2m tall turnip weed throughout, it is likely that many of the affected cattle simply could not find the water trough. It is also possible that they objected to the cleanliness of the trough, or that the water was more saline than they were used to. The use of bloat oil was considered to be an unlikely contributor as they were being given the same oil at the same dose, on the previous property.
The initial deaths in this case were likely due to water deprivation leading to severe dehydration. This would explain the loss of condition of the blue tag mob since their arrival, and their “hollowed out” appearance. Later deaths were likely due to the sudden intake of water causing cerebral oedema. Unfortunately, the time since death of the first animals found, and also a lack of daylight prevented useful post mortem examination, and attempts to collect aqueous humour were unrewarding. It would have been educational to compare the deaths prior to the change in water to those that occurred afterwards.
After the cattle were allowed into the paddock with the dam, they remained camped there for 2 days before spreading out across the paddock. There were two further deaths, bringing the total number dead to 15, with approximately 20 more noted to be lethargic and weak while camped around the dam. After this time, the cattle improved, and a week later the owner was not able to distinguish between those previously showing symptoms, and the rest of the mob. Owing to the change from a water trough to a dam, bloat oil was no longer administered to these cattle.
The recommendation for producers based on this case, is to always ensure that newly introduced cattle are shown the location of water sources on arrival at a new location.
My thanks to Patrick Staples, Pathologist at EMAI for his assistance interpreting test results and instigating further testing on the available samples.