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Tick Fever and Theileria Excluded From a Case of Copper Toxicity in a 7-Month-Old Brahman Poddy Calf

Kylie Greentree, District Veterinarian, Hunter Local Land Services

Posted Flock & Herd February 2022


The Hunter Region is a cattle tick free area, with tick fever and cattle tick (Rhipicephalus (Boophilus) microplus) being notifiable in NSW herds. As this case was a Brahman calf with 'red water' (red discolouration of the urine) and jaundice, it was important to exclude tick fever (Babesia bigemina, Babesia bovis or Anaplama marginale infection) as the cause of death. A thorough movement history of the livestock (primary and secondary hosts) onto this property was undertaken as soon as tick fever was identified as a differential diagnosis. There had been no movements of livestock from a cattle tick area onto this property. Studies have shown that Bos indicus cattle are quite resistant to the effects of Babesia bovis infections but susceptible to anaplasmosis.1

This calf was shown to have died from copper toxicity. There are two forms of copper toxicity. Primary copper poisoning occurs on diets high in copper or from treatment overdoses. Secondary copper poisoning occurs despite normal dietary intakes of copper, either from concurrent liver disease or, in the absence of liver disease, on subterranean clover-based pastures that are molybdenum deficient (more commonly seen in sheep).5 Primary copper poisoning can be acute, from an accidental administration of large quantity of copper (oral, parental, grazing pasture fertilised with copper) whereas chronic primary copper toxicity results from ingestion of smaller amounts of copper over a longer period with accumulation in the liver. When the liver capacity is overloaded, there is a release of copper into the blood stream that leads to intravascular haemolysis. Combined with liver damage, this release causes acute toxicosis and recumbency, with the animal dying within 24-48 hours. These animals show symptoms of severe depression, thirst, anorexia, pale or icteric mucus membranes and haemaglobinuria.3



In November 2021, the Lower Hunter District Veterinarian was called to a property at Bob's Farm, in relation to the death of a seven-month-old Brahman poddy calf. This calf had been a poddy since birth and was rotated between two small round yards with one other poddy calf that was approximately five months of age. One yard was covered in sawdust and had a cubby house for shelter while the other yard had green pick but no obvious weeds. These calves had no access to any other section of the property or the herd. Bracken fern (Pteridium esculentum) was noticed growing close to one of the round yards, but the producer had explained that the calves did not have any access to these plants and there was no bracken fern seen in either of the small holding yards. Bracken fern can cause acute haemorrhagic syndrome, anaemia and haematuria, so even though there was no known access to the plant it was on the differential diagnosis list.

The two calves had been given one clostridial vaccination (5-in-1) and had been drenched for internal parasites.

The calf became lethargic on Thursday (28/10/21) and anorexic on Friday (29/10/22). The producer had noticed the calf shaking its head and wobbly on its feet. The calf also appeared to be straining to defaecate and the producer thought it was constipated. The private veterinarian dispensed antibiotics and ear drops as they thought the calf had an ear infection. The calf did not improve with the medication. On Monday morning (1/11/21) the calf was found lying on its side with stiff legs and was unable to rise. The calf was euthanased, and the District Veterinarian was called.


Theileriosis, tick fever, bracken fern toxicity and copper toxicity.


Image of bovine post-mortem severe jaundice
Figure 1. Affected calf showing Jaundiced carcass

A necropsy was performed on the seven-month-old Brahman calf. The calf was in good body condition (BCS=3) and had no obvious external lesions except for the point of euthanasia (skull) and the conjunctiva was noticeably jaundiced. Once the carcass was opened it was found to be jaundiced throughout. The thoracic cavity had no abnormalities detected. The abdominal cavity contained a yellow rounded liver that was friable and had an obvious acinar pattern. The stomachs had no obvious lesions and no unusual stomach contents were detected. The small and large intestines had minimal intestinal contents with a small hard ball of faeces just inside the rectum. The intestinal contents were a normal green-brown colour and no obvious signs of blood in the faeces. The bladder was the size of a grapefruit and contained dark red urine. The kidneys were dark red throughout the cortex and medulla. There were no obvious lesions in the brain, sinuses or ear canal that could explain the head shaking and rubbing.

Image of bovine post-mortem jaundiced liver
Figure 2. Yellow friable liver
Image of bovine post-mortem jaundiced kidney
Figure 3. Dark red kidneys
Image of bovine post-mortem dark red urine
Figure 4. Large bladder with dark red urine


PCR successfully excluded tick fever, with Babesia bovis, Babesia bigemina and Anaplasma marginale not detected. Interestingly, on Theileria PCR there were no Theileria strains detected and 0 gene copies. This is very unusual in a Theileria endemic area in a seven-month-old calf.

Histologically the liver had acute, diffuse, moderate periacinar necrosis with bile accumulation and pigment-containing, portal macrophages. The presence of pigment-containing macrophages in the liver is consistent with subacute or longer-term exposure to copper. The periacinar hepatic necrosis could be due to a combination of causes, including copper toxicity and hypoxia due to the copper induced haemolytic anaemia. Acute copper toxicity could also be contributing.

The kidneys morphologically had acute, diffuse, and moderate haemoglobinuria.

The liver and kidneys both had elevated copper levels indicating that the calf had access to copper (oral and/or parental). At necropsy it is recommended to test both the liver and kidney for copper. In many cases the liver releases enough stored copper so that a non-toxic level of copper remains in the hepatic tissue. However, in these cases the released copper will have accumulated in the kidneys, resulting in markedly elevated levels of copper in the kidneys.2

Brahman Calf
Liver Copper (0.08-2.09) mmol/kg 8.70 High
Kidney Copper (0.00-0.20) mmol/kg 0.33 High


The cause of death in this case was copper toxicity, but unfortunately the source of copper is still unclear. All supplementary feeds (milk and pellets) were checked for copper levels and the sawdust in one of the round yards was also checked with the producing company. This calf was often observed sucking and chewing on part of the cubby house shelter. The cubby house was an older wooden structure that had been given to the family 16 years ago and they were unsure how old it was at that time. Given that wooden play equipment built before 2006 was treated with copper chrome arsenic (CCA) to prevent decay from damp rot and insect attack, this cubby house could be the source of the copper.

Some of the cattle on the property had been given regular copper injections, but apparently not to this calf.

The other poddy calf was clinically examined, and it appeared to be in good health with pink mucus membranes. This calf was taken out of the yard and put back with the herd. There have been no further problems. It was advised to check a sample of copper blood levels in the herd to check that there had not been excessive copper supplementation.

Bos indicus cattle have higher resistance to tick attachment. This may explain why this seven-month-old calf had not been exposed to any strain of Theileria in a Theileria endemic region.


Elizabeth Macarthur Agricultural Institute veterinary pathology teams for tissue examination, testing and interpretation of results.


  1. Carter P. Innate susceptibility of various cattle breeds to tick fever disease caused by B. bovis and A. marginale. 2011. QLD Government and MLA. www.mla.com.au
  2. Hammond J, Stephenson A, Rodgers J. Copper Poisoning in Sheep Grazing in a Vineyard. Riverland Veterinary Practice SA and Senior Veterinary Officer, PIRSA SA. www.flockandherd.net.au
  3. Radostits OM, Gay CC, Blood D and Hinchcliff KW. Veterinary Medicine 9th Edition Saunders, London. 2000 or Radostits OM, Gay CC, Hinchcliff KW and Constable PD. (2007). Veterinary Medicine, 10th Edition, pp 1820-1824
  4. Treated Timber NSW Health. www.epa.nsw.gov.au
  5. Watt, B. 2021. Secondary Copper Poisoning in Ewes on Subterranean Clover. www.flockandherd.net.au


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