Myxomatosis (sometimes shortened to "myxo" or "myxy") is a disease that affects rabbits and is caused by the myxoma virus. It was first observed in Uruguay in laboratory rabbits in the late 19th century. It was introduced into Australia in 1950 in an attempt to control the rabbit population (see Rabbits in Australia). Affected rabbits develop skin tumors, and in some cases blindness, followed by fatigue and fever; they usually die within 14 days of contracting the disease.
The disease is spread by direct contact with an affected animal or by being bitten by fleas or mosquitoes that have fed on an infected rabbit. The myxomatosis virus does not replicate in these insect hosts, but can be physically carried by an insect's mouthparts, i.e. from an infected rabbit to another susceptible animal. Due to the potential of insect vector transmission, pet rabbits may be susceptible in enzootic areas and vaccination is highly recommended.
Effects of the disease
In rabbits of the genus Sylvilagus (cottontail rabbits) living in the Americas, myxomatosis only causes localized skin tumors, but the European rabbit (Oryctolagus cuniculus) is more severely affected. At first, normally the disease is visible by lumps (myxomata) and puffiness around the head and genitals. It then may progress to acute conjunctivitis and possibly blindness; however, this also may be the first indication of the disease. The rabbits become listless, lose appetite, and develop a fever. Secondary bacterial infections occur in most cases which cause pneumonia and purulent inflammation of the lungs. In cases where the rabbit has little or no resistance, death may take place rapidly, often in as little as 48 hours; most cases result in death within 14 days.
In pet rabbits, myxomatosis can be misdiagnosed as pasteurellosis, a bacterial infection which can be treated with antibiotics. By contrast, there is no treatment for rabbits suffering from myxomatosis, other than palliative care to ease the suffering of individual animals, and the treatment of secondary and opportunistic infections, in the hopes the treated animal will survive. In practice, the owner is often urged to euthanize the animal to end its suffering.
Use as a population control agent
After its discovery in 1896 in imported rabbits in Uruguay, a relatively harmless strain spread quickly throughout the wild populations in South America.
In Australia, the virus was first field-tested for population control in 1938. A full-scale release was performed in 1950. It was devastatingly effective, reducing the estimated rabbit population from 600 million to 100 million in two years. However, the rabbits remaining alive were those least affected by the disease. Genetic resistance to myxomatosis was observed soon after the first release and most rabbits acquired partial immunity in the first two decades. Resistance has been increasing slowly since the 1970s, and the disease now only kills about 50% of infected rabbits. In an attempt to increase that number, a second virus (rabbit calicivirus) was introduced into the rabbit population in 1996.
Myxomatosis was introduced to France by the bacteriologist Dr. Paul Armand Delille, following his use of the virus to rid his private estate of rabbits in June 1952 (He inoculated two of the rabbits on his land). Within four months the virus had spread 50 km; Armand suspected this was due to poachers taking infected rabbits from his estate. By 1954, 90% of the wild rabbits in France were dead. The disease spread throughout Europe.
The disease reached the UK in 1953. The first outbreak in the UK to be officially confirmed was in Bough Beech, Kent in September 1953.  It was encouraged in the UK as an effective rabbit bio-control measure. This was done be placing sick rabbits in burrows, which it is not illegal in the UK. By 1955, about 95% of rabbits in the UK were dead. Hunters would specifically target infected rabbits to mercifully dispatch the animal.
However by 2005 - fifty years later - the UK Land Registry surveyed 16,000 ha (40,000 acres) of its land. It reported that the rabbit populations had increased three-fold every two years – likely as a result of increasing genetic resistance to the Myxomatosis virus.
Myxomatosis was introduced in New Zealand the early 1950s as a form of pathogenic control but, unlike Australia, it failed to establish through lack of a suitable spreading organism.
Use of vaccine
A vaccine is available for pet rabbits (ATCvet code: QI08). The vaccine is not allowed to be used in Australia because the live virus in the vaccine has the potential to spread into the wild rabbit population which could result in wild rabbit immunity to myxomatosis. If this happened, there would be a dramatic increase in the number of wild rabbits in Australia, which would cause major damage to the environment and economic losses. Many pet rabbits in Australia continue to die from the disease due to their lack of immunity. There is at least one campaign to allow the vaccine for domestic pets.
In the UK a live combination vaccine, Nobivac Myxo-RHD, made by MSD Animal Health, has recently become available. Its active ingredient is a live myxoma-vectored RHD virus strain 009 and it offers a duration of immunity of 1 year against both RHD and myxomatosis.
The development of resistance to the disease seems to have taken different courses. In Australia, the virus initially killed rabbits very quickly, about 4 days after infection. This gave little time for the infection to spread. However, a less virulent form of the virus has become prevalent there, spreading more effectively by being less lethal. In Europe, many rabbits are genetically resistant to the original virus that was spread. The survival rate of diseased rabbits has now increased to 35% when in the 1950s it was near zero.
Hares are not affected by the myxomatosis virus but can still be hosts of the flea vector.
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|Wikimedia Commons has media related to Myxomatosis.|
- An interview with Frank Fenner
- Society & Animals Journal of Human-Animal Studies, Volume 9, Number 2, 2001
- Possible windborne spread of myxomatosis to England in 1953