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Phillip Kemsley, District Veterinarian Casino

Posted Flock & Herd July 2012


A large vertically integrated rabbit farm on the north coast of NSW experienced heavy losses of over 1,000 growers and breeders in early 2012.

The enterprise is well run, turning off 1,000 - 1,200 meat rabbits per week at 12 weeks of age. The property has a high calibre of general management, nutrition, genetics and use of artificial insemination. It is vertically integrated with breeder sheds, grower sheds and abattoir all on the one site. Growers are also grown out in a leased facility off site. The company also manages marketing and distribution to over 100 outlets, mainly restaurants & butchers in NSW and QLD.

The breeders are routinely vaccinated with 1ml Cylap® on an annual basis in September.

A sharp rise in mortalities started on 11th February, initially in 11 week old rabbits in one shed. All rabbits died suddenly and few were seen sick. This was despite the daily observation of individual pens and pick up of any dead being increased initially to three times a day at the time of the first visit and then to two-hourly in response to the mortalities. Rabbits that died were all in good condition, with evidence of epistaxis observed in 10-20% of the dead.

At the time of the outbreak there were a large number of midges in the sheds and low numbers of house flies. There was also a low level of rat predation on the dead rabbits.

At the time of the first property visit on 15th February on day 6 of the outbreak, over 100 had died. Deaths at this time were predominately in the 10-12 week age group. 38 dead from the this morning's pick up and one sick rabbit were presented for autopsy (Figure 1).

Image of dead white rabbits
Figure 1


The sick rabbit was near death with moderately pale mucous membranes, teeth grinding, groaning, low temp of 32.8 degrees celcius and coarse lung sounds.

Post-mortem findings

All 39 rabbits were autopsied. About 10% had epistaxis. 60-70% had petechial and ecchymotic haemorrhages in the lungs (Figure 2). 30% had changes to the liver including: marked zonal pattern, sinusoid congestion, swollen with rounded edges, raised cobblestone surface or petechial haemorrhage. 10% had blood tinged pleural/peritoneal fluid (Figure 3). One had ecchymotic haemorrhage over the longissimus muscle (Figure 4). Two had background Pasteurella lung changes.

Image of rabbit lungs on <em>post-mortem</em>
Figure 2. Haemorrhages in the lungs Figure
Image of rabbit abdominal cavity on <em>post-mortem</em>
3. Blood-tinged pleural/peritoneal fluid
Image of rabbit musculature <em>post-mortem</em>
Figure 4. Haemorrhage over the longissimus muscle


From three of the rabbits liver was submitted fresh, liver and lung fixed for histopathology and clotted blood collected from the caudal vena cava for serology. Two of the three livers were Rabbit Calicivirus Antigen ELISA positive. The livers from the same two rabbits also had random, multifocal, moderate, peracute hepatic necrosis. Lungs from all three rabbits had interstitial and alveolar, multifocal, moderate, acute pulmonary haemorrhage. The Rabbit Calicivirus Antibody ELISA results were negative for all three rabbits.

The pathologist comment from the NSW State Diagnostic Laboratory was: 'Liver histopathology of moderate to marked, random necrosis is consistent with an infectious aetiology (viral or bacterial). Consequently, reduction of hepatic coagulation factors can lead to secondary haemorrhages in other tissues including lung. Rabbit Calicivirus infection is confirmed by antigen ELISA'.


Rabbit Calicivirus.


Vaccination of growers, insect and rodent control in sheds and emergency slaughter of growers that were of a marketable weight were the control measures undertaken. Breeders were also given a booster vaccination.


Grower rabbits from seven weeks of age were vaccinated, commencing 15th March. Mortalities in the vaccinated rabbits dramatically decreased from 27th March, 12 days post vaccination. By this time approximately 1,000 rabbits had died.

As the outbreak progressed the disease spread into younger age groups, with growers as young as seven weeks of age affected.

The disease also progressed into a group of does that were vaccinated as maiden replacements in November 2011. Management suspected that this break may have been due to vaccine mishandling.

Mortalities attributable to Calicivirus in the breeders that had been vaccinated in September 2011 were low.

Following the epidemic peak a second but significantly smaller wave of mortalities occurred in mid March, in 11 - 12 week old rabbits that had been vaccinated at seven weeks age.

Concurrently a small, self limiting outbreak of colibacillosis occurred in the offsite grow out facility. This occurs periodically in growers during wet, humid conditions.


Calicivirus has the potential to cause significant losses in farmed rabbits. In this outbreak it was evident that the industry practice of only vaccinating breeders was insufficient to prevent deaths in growers. The cause of this apparent failure of maternal colostrum derived immunity is not clear. One possible explanation is an antigenic shift in the strain of the virus.

The cause of the biosecurity breakdown in this outbreak is also not clear. Calicivirus is known to circulate in the local wild rabbit population. Deaths in wild rabbits were confirmed approximately 35 km away in October 2011. Wild rabbits have been sighted as close as two km to the facility. Flying insects may have been the vector.


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