The Lismore District Veterinarian was contacted in December 2011 following the sudden death of three steers on a Wooyung property near Murwillumbah. These steers had been introduced six months ago as part of a larger herd of 200. The steers had been grazing low lying country and had received two doses of 5 in 1 vaccine and a Moxidectin pour on drench since arriving at the property.
The District Veterinarian visited the property and performed a post-mortem on a single dead steer and submitted samples for pathology. A tail hair sample was also obtained for pestivirus testing.
A follow up visit by the District Veterinarian in January 2012 found abundant Setaria sphacleta in the paddock of concern. Bloods were collected from five of the remaining steers for further testing.
As the three steers were found dead it was not possible to determine whether they exhibited clinical signs prior to their death. The farmer did not observe any signs before the steers died. No obvious signs of disease were present in the remainder of the herd.
The fresh carcass of a single dead steer, considered small for its age, was necropsied. The findings were as follows;
|Skeletal||Undershot lower jaw|
|Vascular||Petechial and echymotic haemorrhages throughout the carcass
Slight bloody discharge from the nose
|Lungs||Adhered to the chest wall
Cranioventral lung fields diffusely thickened
Diffuse purple/red colour change
Cut surface gritty with increased clear fluid
|Kidneys||Swollen and pale with multifocal pinpoint red dots
Loss of distinction between medulla and cortex
|Liver||Thickened billiary ducts
High liver fluke burden
Initial visit - December 2011
Lung, liver and kidney samples were collected during necropsy and sent away for histopathology. The following results were reported:
|Lungs||Patchy moderately severe pulmonary oedema, mild congestion and mild mononuclear interstitial inflammation.|
|Kidneys||Large amount of biorefringent crystalline material within the tubules and collecting ducts, patchy moderately severe non-suppurative interstitial nephritis, tubular necrosis and increased protein within tubules and collecting duct lumens. Scattered prominent parenchymal and extra-renal haemorrhage.|
|Liver||Mild lymphocytic cholangiohepatitis without significant hepatocellular necrosis.|
The tail hair sample was found to be pestivirus antigen negative.
Follow-up visit - January 2012
During the follow-up visit blood samples from five of the remaining steers were collected and sent away for calcium, urea and creatinine testing. One steer was found to have a mild azotaemia, the results were otherwise unremarkable.
The large amounts of crystalline material within the tubules and collecting ducts of the kidneys established the probable diagnosis as oxalate toxicity. This was supported by the post-mortem findings of degenerative changes to the kidneys, widespread petechiae and ecchymoses and congestion and oedema of the lungs. These changes have been described in prior cases of oxalate toxicity (Groenendyk et al., 1970). The liver changes were most likely from a high liver fluke burden, not related to the oxalate toxicity.
In this case the abundance of Setaria sphacelata within the paddock of interest identified it as the likely cause. Setaria sphacelata has previously been identified as containing sufficient levels of oxalate to cause toxicity within livestock (Groenendyk et al., 1970). However, despite the abundance of Setaria sphacelata in the region, toxicities remain rare. It is assumed homebred cattle quickly adjust to grazing high levels of Setaria, developing a resistance to the oxalate levels within the plant. Newly introduced naive cattle are at the greatest risk of poisoning. The history of the case supports this (with 200 newly introduced steers placed on oxalate containing pastures).
On follow-up five of the remaining steers were tested to exclude subclinical oxalate toxicity within the herd. The two most important parameters to determine oxalate toxicity are calcium levels and kidney enzymes. Oxalate competitively binds with calcium, acutely producing hypocalcaemia, and more chronically forms calcium oxalate crystals within the kidneys, causing kidney damage and elevated kidney enzymes. In this case only one of the five tested steers exhibited a mild azotaemia. From this it was concluded that the remaining steers on the property had most likely adjusted to the oxalate pastures and were unlikely to develop disease. The farmer was informed of this.
It was suggested that in the future the farmer purchase homebred stock or place naive stock on pastures containing low levels of oxalate containing plants, particularly Setaria sphacelata. The farmer was also informed of the high liver fluke burden on his property, and it was suggested that he use an effective registered drench three times annually.