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Arsenic toxicity in cattle given access to treated, burned vineyard posts

Jess Bourke, Central Tablelands Local Land Services, Mudgee


Arsenic is a metalloid element that is naturally present soils and is considered an essential mineral for some plant and animal species. It has a long history of use as a pesticide, medicine, pigment, timber preservative and homicidal agent. Although toxicity in livestock was once relatively common, it is now considered very uncommon (Parkinson et al., 2019). This case report describes a confirmed case of arsenic toxicity in a mob of cattle in the Central Tablelands of NSW.


On 13/06/2019, one unwell and one dead cow from a mob of approximately 20 were reported in the Central Tablelands. The cattle were grazing dry pasture and were approximately 5-6 months in calf. The owner reported no changes apart from burning some piles of old vineyard posts and wire in the paddock where the cattle were grazing. After the first death, the owner moved the cattle to a new paddock and removed the carcase.


On examination late in the afternoon, the unwell cow (cow 1) was in left lateral recumbency with a heart rate of 80bpm, respiratory rate of 40bpm and rectal temperature 38.6°C. Mucous membranes were pink and on rectal palpation of the uterus there was a foetus consistent with the reported stage of pregnancy. There was a moderate volume of dark diarrhoea present on the ground around her. Antemortem blood samples were taken. The cow died shortly after examination.

The owner of the stock observed several more cows that appeared unwell.

The following morning a post-mortem examination of cow 1 showed a slight reddening of the abomasal mucosa. Examination of the other cattle from a distance revealed ataxia, muscular tremors and depression in 4-5 cows.

Blood tests run privately though a local veterinary hospital showed elevated HCT of 58.3% (22.5-39.9), mild elevation of reticulocytes 5.2 (0.0-3.9), elevated glucose 8.2mmol/L (2.56-5.18), elevated urea 9.4mmol/L (2.5-6.1), low phosphorus 0.88mmol/L (1.39-2.55), elevated globulins 40g/L (27-38) and elevated total bilirubin 14µmol/L (0-12).

At this point the most likely differential appeared to be arsenic toxicity due to the history of access to burnt treated timber, with lead toxicity and nervous ketosis being less likely possibilities. Treatment was attempted with thiamine (Vitamin B1) (in case of lead toxicity) and propylene glycol Ceton® (Cetol, propylene glycol 892.0 g/L, choline chloride 75.0 g/L, cobalt chloride 0.75 g/L), but quickly abandoned as any stress led to dramatic worsening of clinical signs. One animal that was walked up the race progressed from being able to walk with mild ataxia to lateral recumbency and respiratory distress. After approximately half an hour, her condition returned to baseline (normal?).

Examination of the environment revealed the remains of burnt posts. There were piles of blue-green ash that appeared to have been licked by the cattle (see figures 1 and 2).

Image of ash from burnt posts
Figure 1: Remains of burnt posts
Image of ash showing lick marks
Figure 2: Ash showing lick marks

On 15/06/2019, a badly affected cow (cow 2) was euthanised by firearm as her condition had deteriorated. A post-mortem examination was conducted.

Significant findings in cow 2

Image of bovine kidney with brown plaque
Figure 4: Brown plaque within kidney

Pathology results

Testing on fresh liver and kidney samples at Elizabeth Macarthur Agricultural Institute demonstrated high levels of arsenic and normal lead levels.

Sample ID Tissue Lead Tissue Arsenic
<2.0 <1
1 Liver <0.5 8.8
2 Liver <0.5 5.8
1 Kidney <0.5 14.1
2 Kidney <0.5 8.8

Histology revealed a moderate multifocal acute to subacute erosive and necrotising abomasitis with focal fibrosis and mild multifocal acute mucosal haemorrhage in the colon. These changes are consistent with arsenic toxicity.

Additionally, there was an underlying mild to moderate multifocal chronic lymphoplasmacytic and eosinophilic abomasitis and severe diffuse subacute ulcerative and fibrinosuppurative pyelonephritis.

A sample of the ash from the burnt logs contained 4300mg/kg arsenic and 1600mg/kg chromium, confirming the source of the arsenic.


In this case, approximately eight out of 20 animals were affected, of which four died and four survived. Those cows that survived went on to deliver live, healthy calves with no problems reported in the calves.

The producer consulted the Environmental Protection Authority regarding site remediation. He was advised to consult local council. Contractors experienced in asbestos removal were used to remediate the site.

Following advice from the New South Wales Department of Primary Industries, a 72 day withhold on slaughter was applied, which, as the affected animals were five month pregnant cows, did not pose a problem.

Some media interest was generated by the case. Several print articles and a radio interview were utilised to raise public awareness.


Arsenic is a metalloid element with an atomic weight of 33. In its various forms, it has been used in medicine, engineering, agriculture and industry. Inorganic forms of arsenic, including oxides, trivalent or pentavalent compounds are more toxic than the organic compounds. Arsenic is indestructible and remains in the environment permanently (Radostits et al., 2007).

Copper chrome arsenate (CCA) contains up to 37% arsenic (NSW EPA). It is commonly used as a timber preservative and the compound is present as 1% of the timber. In 2005, the Australian Pesticides and Veterinary Medicines Authority advised CCA treated timber was not to be used for children’s playgrounds and high contact surfaces. From the July 1, 2012, "CCA products can only be supplied to and used by suitably trained and authorised people under the relevant state or territory law" (NSW EPA).

When CCA treated timber is burnt, the ash contains high levels of arsenic, which is palatable to cattle (Radostits et al., 2007). While ingestion is the most common form of exposure, percutaneous absorption has also been described (Radostits et al., 2007).

Trivalent arsenic inhibits oxidative phosphorylation, while pentavalic arsenic (the form contained in CCA) inhibits the release phosphate for ATP formation (Bertin et al., 2013). The pentavalent form can be converted to the trivalent form in the rumen (Bertin et al., 2013).

This effectively leads to a reduction of cellular metabolic activity and therefore those tissues with higher metabolic rates are those most affected by arsenic toxicity. Alimentary tract wall, liver, kidney, spleen and lung are commonly affected (Parkinson et al., 2019)

Capillary damage in the alimentary tract leads to increased permeability and exudation of serum. The mucosa lifts and is shed from the underlying muscle layer leading to massive fluid loss (Radostits et al., 2007). This contributes to the clinical signs of abdominal pain and severe dehydration. Degenerative changes are common in the liver and kidneys.

Toxic oral doses vary with the form of the arsenic, ranging from 1-25mg/kg for arsenite (trivalent) to 30-100mg/kg for arsenate (pentavalent).

Arsenic toxicity can present as peracute, acute, subacute or chronic cases.

In peracute cases, animals die within 3-4 hours of onset of illness. There may be depression and diarrhoea, followed by clonic convulsions and prostration (Radostits et al., 2007).

Acute cases are most common, and present 20-50 hours after the ingestion of arsenic. Severe abdominal pain, restlessness, groaning, complete ruminal stasis, increased heart rate, dehydration and oligura may be present (Radostits et al., 2007).

Subacute cases have similar signs to acute cases, but occur over a longer time period (2-7 days). Muscle tremor, incoordination and clonic convulsions are present (Radostits et al., 2007).

Cattle with chronic arsenic toxicity show reduced bodyweight, a dry, easily shed coat, bouts of indigestion, conjunctival erythema, and eyelid oedema. They may also exhibit buccal mucosal and muzzle ulceration, and as such chronic arsenic toxicity may be considered a differential diagnosis for foot and mouth disease (Radostits et al., 2007).

Treatment for arsenic is often unrewarding. The following antidotes are suggested by Radostits et al., (2007)

Supportive care includes fluid therapy to counteract dehydration, and charcoal to absorb residual arsenic.

In a review article, Bertin et al., (2013) noted that treatment attempts were not associated with increased survival, however, as only 2/156 animals survived, this finding is difficult to interpret. Interestingly, in this case four animals showing signs consistent with arsenic toxicity survived and went on to calve normally 4-5 months after exposure. This may be due to the ingestion of a sublethal dose, another cause of similar clinical signs or another unknown factor. Unfortunately blood or urine samples were not obtained from these animals to confirm arsenic toxicosis as any stress led to dramatic worsening of clinical signs.

Preventing stock from accessing potential sources of arsenic is important. Following this case, a media release and radio interview were used to raise awareness. In the wake of the 2019 bushfires, several resources warned of the risk of arsenic toxicity in burnt treated timber.

Despite being considered an uncommon occurrence, arsenic toxicity should remain a differential diagnosis when investigating cases of diarrhoea, abdominal pain and nervous signs in ruminants.


  1. Bertin FR, Baseler LJ, Wilson CR, Kritchevsky JE & Taylor SD. (2013). Arsenic Toxicosis in Cattle: Meta‐Analysis of 156 Cases. Journal of veterinary internal medicine pp997-981
  2. Ceton - Ketosis and pregnancy toxaemia treatment www.jurox.com
  3. Copper chrome arsenate treated timber www.epa.nsw.gov.au 20 May 2018, accessed 17/02/2020
  4. Parkinson TJ, Vermunt JJ, Malmo J & Laven R. (2019) Diseases of cattle in Australasia. 2nd edition, Massey University Press
  5. Radostits OM, Gay CC, Hinchcliff KW & Constable PD. (2007) Veterinary Medicine 10th edition, Saunders Elsevier


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