This rabbit disease was introduced in the spring of 1950, in the Murray-Darling River Basin, with hope to control the growing population of this grazing feral animal, which had already reached plague numbers from the start of the 20th century.
The virus that causes Myxomatosis is called the Myxoma Virus. It is spread by a viral vector. That is an organism that carries a virus from one animal to another. The symptoms of Myxomatosis in the early stages is tiredness, slight elevation in temperature, increased consumption of water, decreases consumption of food;
After 4 days the rabbit resumes normal activity with a few exceptions including increased consumption of food (more so than normal), decrease in water consumption (less so than normal), normal temperature, may have eye discharge;
After 7 days the rabbit appears confused of irritated, stiff, ears may feel chilly, if it had a discharging eye then the lid has an increase in swelling, may have a clear nasal (nose) discharge;
After 10 days the rabbit has difficulty urinating and it may appear brown, may develop a musky “sick” scent, skin appears bruised, genitals, ears, anus, eyelids, nostrils, and lips swell; After 13 days the rabbit will die.
The suggestion of using Myxomatosis as a biological control agent was put forward by a Brazilian scientist called H. de Beaureparie Aragao in 1918. The Australian Government rejected the proposal due to it “wouldn’t work”. Finally in the 1920’s the Australian Government gave in and gave the authorisation of work on the myxoma virus to the CSIRO.
After the release of the Myxoma Virus in 1950, the decrease in the population of these pests was clearly visible. After 6 months of its release, it had killed out 80%-95% of the population in the non-arid areas. Since the spread of Myxomatosis is relied on vectors, and with the mosquito being the prime vector, the population of mosquitoes obviously effected the distribution of the virus, and mosquitoes cannot survive in arid conditions so, for a while the desert was a refuge for rabbits from Myxomatosis and eventually the population grew. Also the very small population that had natural immunity to the Myxoma Virus that didn’t die and bred with other rabbits that were immune and passed their genes onto their young built the population up as well. Eventually by 1955 the viruses’ effect wasn’t visible anymore.
In order to boost the virus back as an effective control agent, the CSIRO introduced the European Rabbit Flea in 1957 and again in 1966. This flea wasn’t as effective, as would have hoped, once again in the arid areas, but did give the virus a boost start again in the more temperate areas. In 1993 the Spanish Rabbit Flea was introduced to Australia by the CSIRO in hoping to spread Myxomatosis and the Myxoma Virus further inland. These fleas are more arid adapted than the other fleas and mosquitoes and they have spread inland, but it will take a few more years to calculate the effect that the flea has had in these arid areas and if the spread of the Myxoma Virus and Myxomatosis has had any effect on the rabbit population there.
Vaccines for Myxomatosis are banned by the Australian Federal Government. If a vaccinated rabbit escaped and became feral and began breeding, then it would pass on the immunity and eventually the disease would lose all effect.
Calicivirus was ‘accidentally’ released in 1995. It has had a massive effect on the population of feral rabbits, reducing the number by 95%. Calicivirus was first discovered in rabbits in China in 1984. The virus was given to the CSIRO in 1991 to develop it into a biological control agent, but then ‘escaped’ into the Australian Wilderness in 1995.
After the Calicivirus was detected in China, 1984, it was soon detected in Italy, in 1986, France, 1987, Switzerland and Spain, 1988, Germany, 1989, Denmark, 1990, and southern Sweden, 1993. Calicivirus has become established in many other countries since then, but these are the main milestones.
In July, 1991, a strand of the fatal Calicivirus that had plagued Europe was imported from the Czech Republic and was developed by the CSIRO, and it was ‘accidentally’ introduced under mysterious circumstances in 1995.
But just like Myxomatosis, the effect of the virus on the feral populations began to wear off after a period of time.
There are no noticeable symptoms of Calicivirus as it kills the rabbit within 24-48 hours of the animal contracting the highly fatal virus. During the ‘trial’ period at the CSIRO, post-mortems and autopsies revealed that the liver and spleen are swollen at the time of death; the liver is powdery and pale; and the lungs may fill up with fluid. The suspected cause of death is lack of oxygen and heart failure.
Calicivirus can be caught by rabbits of any age, but rabbits under 18 days old do not die from Calicivirus. Instead they excrete the virus and build up antibodies to fight it.