Rabbit Biocontrol Advisory Group

Rabbit Biocontrol Advisory Group

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The IPM Story

IPM = Integrated Pest Management.

This involves the integration of biological, chemical and management practices to improve the effectiveness of a control programme. In the world of insect control, there has been increasing emphasis on an integrated approach, following the emergence of insects resistant to pesticides.

With the world-wide increase in concern on the long-term effects of some agricultural chemicals, and the increasing demand of consumers in affluent countries for residue-free fresh produce, there is a major increase in effort to develop integrated pest management systems, particularly for insect pests and weeds.

In the United States, there has been a resurgence in interest in IPM over the last three years, following President Clinton’s announcement that 75% of US farms would use IPM methods by the year 2000. This will be extremely difficult to achieve, but it’s important to New Zealand in that it’s indicative that our trading partners, and competitors, are taking this integrated approach for sound ecological and market demand reasons.

In New Zealand, in the world of insect control, there are some excellent examples of evolving IPM systems. Entomologists working with orchardists have for some years been developing pheromone trap systems to lure insects such as the codlin moth away from developing fruit. Pheromones are chemical signals emitted by insects which can be detected in minute concentrations at considerable distances. Their purpose is to get the insects together for mating.

Pheromones can be synthesised, incorporated into slow-release materials and then placed strategically around an orchard. The result? Confused mating behaviour and fewer moths infecting fruit. The end result; a significant reduction in the use of sprays.

The use of several biological or pheromone agents in an orchard, combined with sophisticated monitoring of insect pests, enables a major reduction in the use of pesticides, which has significant cost advantages, as well as ecological and market ones.

An integrated approach to insect management in pastures has also been developed extensively in New Zealand. An excellent example is the approach to the reduction of Argentine stem weevil damage to ryegrass pastures.

In the 1970s, a compound called lolium endophyte was discovered in ryegrasses and found to protect them from stem weevil attack. Cultivars have subsequently been selected with higher endophyte levels, thus providing protection.

The second method of reducing Argentine stem weevil damage involved searching in South America, the home of the weevil, for natural parasites and predators. An effective parasitic wasp was identified, imported and tested extensively in quarantine, and is now being released in the field. The combination of these two methodologies has considerably reduced Argentine stem weevil damage and hence losses to ryegrass pastures.

History’s lesson

History has taught us again and again that any single method of controlling pests, be they insects, weeds or animals such as rabbits and possums, will usually decline in effectiveness with time. Most pest management research, world-wide, is indicating that greater attention needs to be paid to the natural controls of species that become pests

The development of systems that encourage natural enemies and diseases is essential. Species-specific biocontrols, biocides (organisms that need to be applied to the pest, weed or plant disease) are needed. These systems encourage putting in place effective monitoring of the pest species’ population and breeding rate and assessing accurately the need for action.

Biocontrols: Some New Zealand History in the Weed and Pest Camp

New Zealand has had over 150 years of introducing a vast array of plants and animals; most of our food, fibre and forestry industries are based on introduced plants and animals. From an ecological and crop damage perspective, a number of the introductions were clearly major disasters. The rabbit was certainly one of these! Attempts to remedy the first mistake led to additional introductions, as early efforts at biological control, e.g. ferrets, stoats, weasels for rabbit control. These early mistakes, both in terms of the introduction of species such as the rabbit and possum, and subsequent introductions in attempts to control them, tend to colour our thinking about the potential value of biological controls.

There is no question that the introduction of rabbit predators (which, in the case of ferrets, have ultimately been very important limiters of rabbit populations) have also had disastrous impacts on many of our native birds. These predators, combined with unwanted introductions such as the three rat species, all helped to create concern regarding introductions.

Leaving predators aside, there have been a large number of beneficial control introductions, particularly for insect management. In the last 30 years, there have been over 230 introductions. These have been made following increasingly sophisticated checks on the potential risks to beneficial insects and our native species.

The search for viral and bacterial controls for rabbits and possums is a more recent phenomenon, as it has become increasingly apparent that current control methods are not sustainable long-term, for both biological and financial reasons.

Rabbit populations that have been subjected to regular poisoning for 20 to 30 years have now developed avoidance behaviour of both the baits and, in some cases, the poison, usually 1080. This bait and toxin-avoidance behaviour parallels the insecticide resistance that emerged in frequently-sprayed insect pest populations over three to four decades ago.

Currently, biological control research on possums and rabbits is focusing in two areas. The first involves searching for organisms that will kill them, while the second involves molecularly modifying an organism that will, when it infects the rabbit or possum, cause infertility of either males or females or both. This approach is termed immunocontraception.

New Zealand, in partnership with Australia in some cases, is currently investing millions of dollars in research and development in these two areas for possums and rabbits. Given the threat that possums pose to both conservation and animal health in New Zealand, it’s crucial that this research is undertaken and that there is wide appreciation of the benefits and risks of any subsequently-discovered control agents or developed technologies.

RCD and Mutations

Summary:

Viruses are minuscule parasites, consisting essentially of a core of a single nucleic acid surrounded by a protein coat, that transmit between cells and hosts as particles or virions.
Caliciviruses are a family of viruses that have small, round, non-enveloped virions that contain RNA as their genetic material.
Caliciviruses are named because of the presence of cup-shaped (calici-, from calex meaning cup or goblet) depressions on the surface of their virions.
Many different caliciviruses have been isolated from a wide range of species, including humans, a chimpanzee, calves, pigs, mink, skunks, rabbits, hares, sea lions and dolphins.
Mutations occur in caliciviruses as they do in all viruses and other living things.
There is no evidence that mutations in caliciviruses have resulted in host-switching.
Some caliciviruses C such as the San Miguel sea lion virus C have a broad host range, but the rabbit calicivirus affects only European rabbits.
There is no reason to suspect that rabbit calicivirus is likely to switch hosts.
Mutation is more likely to lead to weakening of the virus.

What are Viruses?

Viruses are parasites (technically described as obligate cellular parasites) that move between cells and hosts as particles known as virions. The virion consists of:

a protein, and sometimes
an additional lipid coat (a fat-like material) that
surrounds a nucleic acid genome (the set of genes characteristic of each species).

The genome is either DNA [D(eoxyribo)N(ucleic) A(cid)] or RNA [R(ibo)N(ucleic) A(cid)], never both.

This virion, when it enters a cell, strips the coating off the cell and uses the cell=s structures and enzymes to make many thousands of copies of itself. In this process the normal functioning of the cell is disrupted, and the cell usually dies.

The new virions produced go on to infect more cells and the symptoms of the disease that we see in the plant or animal are the result of accumulated damage. This can lead to the death of the host, but more often in an animal the infection is fought off by the immune system and the animal recovers.

A wide range of diseases are caused by viruses in animals. This is because the animal is made up of many organs and cell types. Most viruses tend to infect only a certain cell type in the animal and diseases are often confined to only one organ or tissue type. This is because each virus is adapted to a particular cell type.

There are exceptions such as the rabies virus, which has evolved to be able to infect nervous tissue of most warm-blooded animals. However, most viruses are maintained in nature in one species of host, called maintenance hosts. If the host is eliminated, the virus becomes extinct, even if it is able to infect other hosts.

There are also subtle interactions between hosts and viruses that go beyond mere adaptation to cells, and involve host behaviour and environment as well.

Viruses can be classified into two groups depending on whether their genome is DNA or RNA.

They are further subdivided into families based on a range of characteristics such as:

shape and size of virions,
whether or not they have a lipid coat,
their host range,
the type of disease they cause,
whether or not they replicate in insects,
the reaction of their protein coats with antibodies, and
the structure of their genome.

What are caliciviruses?

Caliciviruses are spherical in shape, lack a lipid coat, and use RNA as their genetic material. They belong to the Caliciviridae family C the name calici deriving from the cup-shaped depressions on the surface of the virions of many members.

There are many different caliciviruses. Individual members of the family have been found in a wide range of species, including humans, a pygmy chimpanzee, calves, pigs, cats, dogs, mink, skunks, rabbits, hares, sea lions, walruses and dolphins.

Viruses biologically similar to caliciviruses have been found in reptiles, amphibians and insects. It is likely that there are many caliciviruses as yet undiscovered in other species.

Some of the human caliciviruses differ from other caliciviruses. They cause intestinal problems and, probably, hepatitis (hepatitis E virus). They can be divided into two distinct groups:one has the classic cup-shaped depressions on their surface, the other has small round virus particles.

All other caliciviruses found so far have the classic calicivirus characteristics, including the virus causing rabbit calicivirus disease (RCD), and are distinct from the human groups.

What is mutation?

Every living organism has a genome, or set of genes. In all organisms, except for the RNA- containing viruses, this genome is made up of DNA. The DNA, and the RNA in the case of RNA viruses, is in turn made up of building blocks that are called nucleotides.

Any genome is made up of the strings of some of the four types of nucleotides in a fixed combination, ranging from thousands in viruses to many millions in animals. The particular combination of these four types of nucleotide is a code that instructs the organism in how to make exact copies of itself. That is why each organism is unique.

However, in the process of making copies of itself, errors are made in this unique combination of nucleotides. One nucleotide is substituted for another, duplicated or lost completely in a process called mutation. These mutations accumulate in all organisms and over time have resulted in the myriad of organisms that exist today.

Some mutations are lethal, and therefore not passed on. However, others provide benefits by giving the host an advantage in a particular environment. Others, called silent, cause no change in the host.

Do mutations occur in caliciviruses?

Mutations occur in caliciviruses as in any other organism. An example is feline calicivirus, one of the causes of a disease complex including conjunctivitis, nasal and oral ulcers and occasionally pneumonia called "snuffles" in kittens. The coat of this calicivirus contains variable regions that are targets for antibodies.

After infection by only one virus particle, an animal rapidly becomes colonised by billions of virions, and the animal’s immune system mounts a defense. Part of the defense is an antibody on the surface of the virus. It is speculated that the mutations of the coat of the feline calicivirus are caused by a selection of virions that do not bind to an antibody during infection. As the virus multiplies, the enzyme that makes copies of the RNA genome makes mistakes, and these variants or mutant’s chance of survival depends on whether the mistakes were made in an essential part of the set of genes, or in an area that can tolerate the error. The regions tolerating error are often those that encode protein on the surface of the virion, which is exposed to body fluids and antibodies in those fluids. The mutants that do not bind to the antibody are not neutralised, so it is an advantage to the virus to mutate in this way.

Although feline calicivirus and probably other caliciviruses mutate in this way, there is no evidence that mutation has lead to host-switching.

What is host-switching?

Host-switching is where the normal host range of the virus suddenly changes to infect a new species that was previously not susceptible. Documented examples of this are few and far between, considering the tens of thousands of viruses that must exist in nature.

In recent history, only one virus has been proven to have done this; the feline panleukopaenia virus, which is not a calicivirus. It is accepted that this virus mutated to cause a new disease of dogs; canine parvovirus disease. Studies shown that the two viruses have only a few nucleotides different. Although this change led to the ability to cause disease to a new host, many scientists believe that this new parvovirus arose, and was initially spread, as a contaminant of a canine vaccine.

However, there is no reason to believe that caliciviruses, and rabbit calicivirus in particular, will switch hosts. Host-switching must be distinguished from host range; the range of hosts the virus infects, either naturally, or that have been shown to be susceptible by deliberate inoculation. Host range with most viruses is a feature of the virus over a considerable period of time: for example, rabies virus has a broad host range, while the myxoma virus has a narrow host range.

Generally, caliciviruses are host-specific, but there are exceptions. The virus of sea lions, San Miguel sea lion virus, can cause disease in pigs and infect a range of other species, including fish. As previously outlined, feline calicivirus can infect dogs. However, after extensive testing, the rabbit calicivirus has so far proven to be highly host-specific. Species tested in Australia and elsewhere include:

animals: horses, cattle, sheep, deer, goats, pigs, dogs, cats and fowls.
animals: foxes, hares C including New Zealand examples, ferrets, rats and mice.
mammals: bush rats, spinifex hopping mice, plains rats, fat-tailed dunnarts, northern brown bandicoots, brush-tailed bettongs, tammar wallabies, brushtailed possums and the short-tail bat, New Zealand’s only native land mammal.
long-billed corellas, feral pigeons, silver gulls, brown falcons, kiwis and emus
common blue-tongue lizards.

In New Zealand the kiwi and native bat were tested, and other species have been tested elsewhere in the world.

European brown hare syndrome virus (EBHS) has been shown to be the most closely related, genetically, to the RCD virus and distinct from all other known caliciviruses. Inoculation of hares with RCD does not cause disease and neither does EBHS virus cause disease in rabbits. Antibodies to EBHS do not protect rabbits against the development of RCD.

How often does host-switching occur?

This is extremely uncommon. Only one example has been recorded, feline panleukopaenia virus, and it was probably due to just a few nucleotide changes.

Is there any evidence that caliciviruses have switched hosts?

There is no evidence of host-switching in caliciviruses. It is likely that each calicivirus has evolved with its host and during this evolution has become adapted, such that it would take multiple mutations in most, if not all of the virus proteins, to lead to a host switch.

The observation that RCD appears to have arisen suddenly in rabbit populations in Europe and China about ten years ago has led to speculation that the virus arose from another host. At first it was thought that it may be derived from the hare virus, but studies have shown this is unlikely. It has also been shown that RCD virus is not closely related to any other calicivirus. It is now thought that an ancestor virus, which probably causes a benign infection, may have been present in European rabbits prior to the appearance of RCD. If this is the case, then it may be the case that a mutation has occurred in that virus that has enabled it to cause the severe disease we now call RCD.

Will the rabbit calicivirus disease switch hosts?

Studies of the rabbit calicivirus have demonstrated that changes do occur in the genome, which is to be expected. This type of mutation is common, particularly in RNA viruses. Each mammal species supports a set of viruses, many of which are RNA viruses.

The RCD virus in rabbits must be placed in the context of the many thousands of species of mammals that exist and the many RNA viruses that they support. The chances of the RCD virus switching hosts are no greater than those many thousand that already exist.

There is also no evidence in the 41 countries where the RCD virus has been reported that the virus has shown any potential to switch hosts. While changes may be expected in the coat protein, host switching is not seen as a consequence of those changes.

In rabbits older than eight weeks, there is a high mortality rate (around 99%), with survival times of two to three days. This is before the animal has a chance to produce antibodies, which means that the opportunity for antibody pressure to select variants is minimal. In older animals antibody pressure to alter the coat protein will not occur.

The action of RCD in rabbits older than eight weeks is unique; producing a rapid clotting known as DIC (disseminating intravascular coagulation). It has been speculated that an enzyme encoded by the virus might be activating the clotting system. In young animals DIC does not occur, and the consequences of infection are minimal. This suggests that DIC is the only consequence of infection.

Whatever it is in young rabbits that prevents DIC, any retention of it in older rabbits would be likely to lead to a reduction in the virulence of the disease. If DIC is important for transmission, it is likely that evolutionary pressure will select against attenuation and the virulence be maintained.

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