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It was first field tested in 1938 and successfully released in Australia in 1950 (Fenner and Ratcliffe) and resulted in a estimated 99% mortality rate. In the first two years it reduced the rabbit population from 600 million to less than 100 million. However at Cowra rabbit numbers recovered to approximately half of premyxomatosis levels only two years after the first outbreak.
The innate resistance of rabbits to myxomatosis increased rapidly in the first few years after its release and the rabbits with a genetic resistance to the disease became more common. Resistance appeared to reach a plateau until 1968. Recent evidence suggests that rabbits in Victoria developed an increased resistance to the myxoma virus between 1975 and 1985, an by 1990 even the highly virulent Lausanne strain of myxoma (Willaims).
The impact of the disease was greatest in the semi-arid areas where the carriers (vectors) of the virus, mosquitos are seasonally abundant. Myxomatosis was not as successful in spreading in areas where there are few mosquitos, such as Tasmania, Western Australia and some tableland regions. The introduction in 1968 of the European rabbit flea (Spilopsyllus cuniculi), an alternative, more perennial vector, resulted in large reductions in rabbits populations in Tasmania, south-western Western Australia, on tablelands, and in parts of South Australia. The 1993 introduction of an arid adapted Spanish flea(Xenopsylla cunicularis) is intended to cause a similar reduction in the drier rangelands and its spread and efficacy are currently being evaluated (Williams).
Most field strains of myxoma are now of intermediate virulence and rabbits infected with these strains have relatively long survival times (>20 days) and have a high titre of virus in the skin; both of these factors promote transmissibility. Highly virulent strains do not transmit well because of short survival times and highly attenuated strains do not transmit well because they do not have a high titre of virus in the skin (Parer).
The efficacy of myxomatosis declined in the 1950Ős but has remained more or less constant since then and myxomatosis still plays a major role in limiting rabbit numbers. The present density of rabbits in Australia compared to the situation before myxomatosis is not known. On average, rabbit numbers are thought to be about 5% of premyxomatosis abundance in the higher rainfall areas and perhaps 25% in the rangelands. Although the resistance of the rabbits to the virus has increased, this has probably been balanced out by the evolution of more virulent strains of the virus. The effectiveness of the virus in the long term cannot be predicted, so no reliance should be placed on its continued effiacy (Fenner & Ratcliffe).
Rabbits with some degree of genetic resistance were selected for and populations became more resistant. Myxomatosis now kills about 50% of susceptible rabbits which are infected. In many areas this degree of myxoma mortality is sufficient to keep rabbits at low numbers. As rabbits become more resistant stronger myxoma strains are selected for to maintain transmissibility and the percentage mortality remains about the same. Until the virulence of the myxoma virus reaches some biological limit myxomatosis can be expected to exert about the same level of control in the future as it does at present.