The introduction of rabbit calicivirus disease (RCD) into Australia
has generated a great deal of controversy. Initially, the debate
centred on the use of a virus to control a mammal such as the
rabbit. More recently, concern has been expressed because the
virus has not been universally effective in all parts of Australia.
As the old adage goes 'It's never possible to please everyone'.
In reading about RCD in the press it would be easy to conclude
that the release of RCD had not been as successful as scientists
anticipated. However, that would be a total misunderstanding.
Following the successful release of myxoma virus as a biological
control in 1950, rabbits have been held at relatively low numbers
for nearly 50 years. Nevertheless, some parts of Australia continued
to be plagued by rabbits and this was particularly so in arid
areas where mosquitoes, the major vector of myxomatosis, were
rare. Rabbits continued to cause erosion and gnaw away at tree
seedlings, adding to the desertification of Australia's heartland.
RCD has effectively turned that problem around. It is now an additional
force helping to control rabbits in inland Australia. Experimental
sites such as the Nullarbor Plain in Western Australia, Erldunda
in the Northern Territory, the Flinders Ranges in South Australia,
Hattah-Kulkyne National Park in northwest Victoria and Muncoonie
Lakes in southwest Queensland have seen remarkable declines in
rabbit numbers. At many of these sites, the rabbit population
apparently fell by over 90 per cent when the disease first struck.
Furthermore, there is good evidence at many of these sites that
the virus is persisting and breaking out regularly, keeping rabbits
at about 10 to 20 per cent of their original numbers.
This reduction in the rabbit population has been enough to allow
significant regeneration of many arid zone shrubs. Shrubs which
were declining are now increasing again and a few rare species,
considered to have disappeared over wide areas, are being recognised
as they re-sprout from deformed, overgrazed stumps.
Other potential benefits from the spread of RCD are becoming apparent
too. A good example is the reduced use of '1080' poison for rabbit
control, which in some States has fallen by about two-thirds.
If this is a real result, it will not only mean lower costs for
farmers trying to control rabbits but also a reduced risk to other
wildlife species during rabbit poisoning. Of course, more information
is needed about the use of '1080' in the longer term. Initial
information of this type could be a little misleading if some
farmers are holding back on poisoning in the hope that the calicivirus
will resolve all their problems. On the other hand, farmers are
also being encouraged to capitalise on the initial impact of RCD
so, in some areas at least, rabbit control efforts have actually
increased.
The true benefits of RCD in terms of reducing the costs of rabbit
control in farming areas can only be estimated precisely over
time. Similarly, economic benefits such as better wool or beef
production and better land management will also take some time
to unravel from all those other factors such as drought, changing
markets and production costs which also influence productivity.
For those areas where RCD has not been so effective, more work
needs to be done to determine the reasons for the apparently poor
performance. Is it because the virus does not persist? Are rabbits
simply so productive in some areas that they can effectively re-coup
their losses to RCD? Are other factors involved?
If the problem is poor persistence of the virus, it may be possible
to remedy this. At present it is possible to release more virus,
but to improve its likely effectiveness this needs to be done
with a full understanding of the epidemiology of the disease.
For example, it is important to know that the virus has not been
recently active in a particular area and that the majority of
rabbits are susceptible to the disease. There is little point
in trying to introduce the virus into a population consisting
of immune survivors from an earlier outbreak. The timing of releases
is also important as RCD spreads best at moderate day-time temperatures
of between 15°C and 31°C (usually in spring and autumn), possibly
because insect vectors are most active under those conditions
too.
It is generally recommended that releases of the virus should
be in autumn, when conditions for spread are good and there are
few young rabbits in the population. Young rabbits are often doubly
protected against RCD as they have a better chance of overcoming
the disease than adult rabbits and furthermore may carry maternal
antibodies which protect them for the first 8 weeks of their life.
However, by the time they have reached about 10 weeks of age,
they have generally lost this protection and are fully susceptible
to RCD.
Beyond simple re-introduction of RCD, it will be necessary to
have a very good understanding of how RCD spreads in rabbit populations
if it is to be more closely integrated with existing rabbit control
measures. It will be some time before clear recommendations can
be made. In the meantime, normal rabbit control measures should
be continued: even if RCD does not reduce rabbit numbers in some
areas, it will certainly slow down the rate of recovery of rabbit
populations after other forms of control have been imposed. If
rabbit control can be more effective, or if it only needs to be
carried out once every 2 to 3 years, this is still a major saving.
To conclude, it is clear that RCD has been an immediate success,
particularly in arid Australia where rabbits were a major problem
and the costs of removing them were often too high to be justified
in terms of the economic returns from cattle and sheep production.
There have also been clear conservation benefits, particularly
in terms of shrubland vegetation.
RCD appears to complement myxomatosis, and the effects of both
diseases appear to be additive so that we should see rabbits held
at a lower level than myxomatosis was able to achieve alone. Because the RCD virus can be introduced on contaminated food and is spread by social contact or by biting and non-biting insects, it has greater potential for use as part of a coordinated control strategy than the myxoma virus, which must be injected and relies on the presence of fleas or mosquitoes for further spread.
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