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Phillip Kemsley, District Veterinarian Casino, Jessica Hamilton, Final year Veterinary Intern, University of Sydney

Posted Flock & Herd July 2012


Tick fever is an important disease of cattle, caused by three organisms Babesia bovis, Babesia bigemina and Anaplasma marginale. These blood parasites share a common vector, the cattle tick (Boophilus microplus) (Angus 1996; Jonsson, Bock and Jorgensen 2008). Although the disease is fairly uncommon, it produces severe clinical signs including fever, depression, neurological signs and haemoglobinuria, often accompanied by jaundice and anaemia, with severity varying depending on the causative organism (McGregor 2006). Furthermore, the economic impacts of tick fever are significant, with losses to the producer due to mortalities, loss of productivity in chronic cases, costs of veterinary treatment, and costs to the industry as a whole arising from cattle movement restrictions (Jonsson, Bock and Jorgensen 2008).



A predominantly Brahman and F1 beef herd of 80 cattle were kept at a property in Grady's Creek, approximately 60km north of Casino, NSW. The property shares a border with a cattle tick premise, and its owner has experience with a tick fever outbreak on another property in the past.

Two of the cattle were found dead on April 25th, 2012. Post-mortems and examination of the remaining herd was conducted by the local veterinarian, and the District Veterinarian was alerted of the case.

A third cow began displaying signs of aggression and neurological abnormalities consistent with Tick Fever on April 26th, and was found dead alongside a fence the following morning. A post-mortem was performed by the District Vet, as well as examination of the property and remaining cattle.

Clinical findings

The sudden deaths of 3/80 cattle, following signs of aggression and neurological abnormalities, were observed. Ten of the surviving cattle were depressed, had pale mucous membranes and were showing signs of fever, such as isolating themselves from the mob, and seeking shade. A heavy cattle tick burden was also observed throughout the herd.

Post-mortem findings

According to the reports from the initial post-mortem performed by the local veterinarian, the cow was jaundiced, with dark kidneys, an enlarged liver, and haemoglobinuria.

The post-mortem performed on the third cow revealed a jaundiced carcass, dark (almost black) kidneys (Figure 1), an enlarged spleen (Figure 2), and a swollen liver with rounded edges and thickened bile, which was bronze in colour. Haemoglobinuria was also observed (Figure 3).

Image of bovine kidney and renal fat post-mortem
Figure 1. Dark kidneys and jaundiced carcass
Image of bovine post-mortem with large spleen
Figure 2. Enlarged spleen
Image of discoloured collected bovine urine
Figure 3. Haemoglobinuria, which is often termed 'red water' in cases of Tick fever

Laboratory Findings

The local veterinarian submitted a pot of ticks for identification, blood smears from the ear of the dead cow and from blood samples of surviving cattle, impression smears from the kidney, spleen, liver and heart, and blood samples from six cattle that were pyrexic, and had pale mucous membranes.

From the post-mortem conducted by the District Veterinarian (DV), three blood smears taken from the brain, spleen and tail tip were submitted for cytology, along with brain, spleen and liver tissue samples for histopathology.

Unfortunately, the blood smears submitted by the DV were non-diagnostic, due to advanced autolysis and heavy postmortem contamination with proliferating bacteria. The smears taken from the initial post-mortem however, revealed organisms consistent with Babesia sp. present in <1% of red blood cells. These smears were also examined by the Tick Fever Research Centre, Wacol, Queensland, and the presence of Babesia bovis in significant numbers was confirmed.

The ticks submitted to the Entomology section at the Orange Agricultural Institute were identified as Boophilus microplus.

Mild cerebral oedema, with organisms consistent with Babesia sp. visible within circulating erythrocytes was evident on histopathological examination of brain tissue sections, while the spleen was found to be markedly congested, with pigment laden macrophages. Centrilobular fatty degeneration in the liver was also evident, with a diffuse increase in circulating leukocytes in sinusoids and blood vessels, and portal areas containing abundant pale loose collagen with infiltrates of lymphocytes, plasma cells, macrophages and occasional pigment-laden macrophages.


Babesiosis, caused by Babesia bovis.


It was recommended to treat all surviving cattle with Imizol® (Imidocarb dipropionate) at a dose rate of 1ml/100kg body weight. Oxytetracycline was also prescribed prior to laboratory test results, as a treatment for Anaplasmosis.

For tick control, it was advised to treat all cattle with a Cydectin pour-on every three weeks, as well as overspraying with Barricade S® (Cypermethrin/ chlorfenvinphos) once weekly.

The property owners were also instructed to allow cattle into all areas of the property (following insecticidal treatment), in order to reduce cattle tick numbers.


The detection of Babesia bovis in the blood smears and organisms consistent with Babesia sp. in the brain tissue on histopathology confirmed the likely diagnosis of Babesiosis in this case. This was supported by clinical findings of sudden death in a small proportion of the herd, abnormal behaviour, depression and anaemia, as well as jaundice, enlargement of the spleen and liver, dark kidneys and haemoglobinuria on post-mortem. However, co-infection with Anaplasma marginale and Babesia bigemina, although not detected in the submitted samples, cannot be ruled out. It would be beneficial to continue sampling any cattle that die suddenly, develop clinical signs of Tick Fever, or remain clinically ill over the coming weeks to rule out involvement of the remaining two causal organisms of Tick Fever.

A bull of Queensland origin is the suspect carrier of Tick Fever onto this property. It will be worthwhile testing and culling this bull if necessary. The farmer may be better to purchase stock from NSW only in future.

Furthermore, Tick Fever can be a difficult disease to treat, as the prevalence of infection is determined by complex interactions between host animals, vectors and the parasites themselves (Jonsson, Bock and Jorgensen 2008). It is important that all contributing factors of the disease be considered in an eradication program. This was complicated in this case, as the property owner was unable to move cattle into the boundary paddocks along the side of the farm, due to neighbour complaints. This will not allow 'mopping up' of the tick population in this part of the farm and prevents adequate control of the disease from occurring.


  1. Angus BM. The History of the Cattle Tick Boophilus microplus in Australia and Achievements in its control. Int J Parasitol 1996; 26:1341-1355
  2. Jonsson NN, Bock RE, Jorensen WK. Productivity and health effects of anaplasmosis and babesiosis on Bos indicus cattle and their crosses, and the effects of differing intensity of tick control in Australia. Veterinary Parasitology 2008; 155:1-9
  3. McGregor P. Prime fact 80. Tick Fever. NSW Department of Primary Industries - Primefacts, NSW 2006, viewed 8 May 2012, ( www.dpi.nsw.gov.au )


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