The following is a critique of Environment Australia’s assessment of the CSIRO proposal to use live Rabbit Calicivirus on food baits to kill rabbits. The assessment was prepared for the National Registration Authority in December 2001. This critique has been prepared by Animals Australia.

This critique is comprised of a summary of key concerns with the assessment, followed by a more detailed examination of each section of the assessment for factual inaccuracies or omissions, unsupported assertions, non-sequitur statements and illogical or circular arguments.

Key errors and concerns in relation to host species-specificity

• The Report asserts that research into the cross-infectivity of RCD has been comprehensive. In fact, the Australian research has been widely criticised by international experts as grossly inadequate.
• The Report asserts that there is no evidence that any other species have been infected with RCV. Yet it cites a study suggesting that hares have become infected with RCD (which it then refutes on the basis of an argument which appears to be irrelevant). It also fails to cite a recent study showing that pigs have become infected with RCD.
• The Report asserts that the substantial evidence of sero conversion in other species provides no evidence of cross infection. Many scientists disagree with this assumption, considering sero-conversion to be evidence of potential susceptibility to infection.
• Most of the species that have sero-converted on challenge with RCV were (a) challenged with very low doses of the virus (b) killed only 14 days after challenge and (c) not organ tested post-mortem for evidence of infection. The Report concludes that this lack of data on (a) the effects of higher doses (b) longer periods of incubation, and (c) post-mortem examination of organs, all provide positive evidence that there has been no cross-infection.
• The Report asserts that there is a growing consensus in the scientific community that RCD originated from a relatively benign form of RCV. No evidence of this consensus is provided and indeed this statement is patently false in the face of the international experts who disagree with this conclusion.
• The Report asserts repeatedly, without providing any evidence in support of the view, that pathogenic RCD most probably mutated from a benign form of RCD. It ignores the evidence from the original appearance of RCD that refutes this. Moreover, the only study mentioned which might be seen as supporting this view is not referenced in the bibliography.
• The Report admits that, if RCD were to infect another species, it might involve no visible symptoms or symptoms entirely different from those experienced by rabbits. It also repeatedly asserts that pathogenic RCD probably mutated from benign RCD. Yet it argues that the absence of obvious RCD symptoms in non-target species is evidence that the disease has not and will not cross species.
• The Report asserts that, although there has been no post release monitoring of wildlife for evidence of cross species infection, any cross species infection by RCD would come to light in the course of wildlife monitoring for other purposes. This is, in fact very unlikely because:
  • the pathology could be totally different from that of RCD in rabbits (as mentioned above);
  • infection could occur in a species or a population that is not normally monitored; and
  • RCD as a possible cause is unlikely to even enter the heads of those doing the monitoring given the continuing story being delivered by this and other reports that RCD is target specific.

• The Report admits that studies have not been conducted over a long enough period to monitor long term effects of the removal of rabbits on ecosystems. It uses this lack of data as evidence of lack of impact.
• The Report asserts that the impact of loss of rabbit prey on native prey species due to prey shifting will probably be a good thing because the exotic predators which prey on native prey will eventually decline due to lack of rabbit prey. It fails to note that this decline will not occur until all alternative sources of prey (ie native animals) have been severely reduced or exhausted.
• The Report asserts that native predators, even those that rely heavily on rabbits, will probably not be badly affected by the loss of rabbit prey because they will be able to switch to other prey. It does not consider that they will be competing for this alternative prey with other predators, both native and exotic, and there may not be enough of these for everyone.
• The Report completely ignores the impacts of rabbit decline on non-rabbit eating native predators as a consequence of competition with rabbit eating predators for alternative prey.
• The Report cites a study which it admits had collected insufficient data to report conclusive results. It ignores the study which has reported conclusive data on this matter (a study by Birds Australia, commissioned by Environment Australia, which was available to the assessors) showing that, in all areas where RCD was successful in reducing rabbit populations, not only were there substantial declines in populations of rabbit eating raptors but also in all species of non-rabbit eating raptors.
• The Birds Australia study also showed that these declines were very unlikely to be related to climatic factors because, in the past, low rainfall had not affected populations at all. The Report, however, states that, where raptors did decline it was probably caused by low rainfall.
• The Report asserts that, because rabbit crashes have occurred before, other prey and predator species are unlikely to be adversely affected. It draws this conclusion in spite of the fact that there is no data available as to the impacts of previous rabbit crashes on predator and alternative prey species.
• The Report asserts that along with improvements in vegetation where RCD has reduced rabbit populations, there has been a concomitant increases in populations of native herbivores. No evidence for this whatsoever is cited in the Report.

The background information on wild rabbits in Australia fails to note that the principal limitation on wild rabbit distribution is the presence of dense bushland.

The section goes on to make an unsupported political value judgement that rabbit control, defined as a range of types of lethal measures, "is an on-going necessity". By contrast, the benefits of wild rabbits in Australia are described as "perceived". Moreover, the "perceived benefits" do not include the fact that rabbits are now naturalised in many Australian ecosystems and provide a major food source for both native and introduced predators.

RCV Investigation and control

This section notes the monitoring and research put in place following the release of RCD by the ANZECC Task Force but fails to note that this monitoring and research did not include any monitoring of impacts and pathology in non-target species.

Origin of Rabbit Calicivirus Disease

This section asserts that "a consensus is emerging within the scientific community" that pathogenic RCV originated recently from a relatively benign form of RCV. However, no evidence is provided either here or elsewhere in the Report to support either the statement that there is a consensus on this point, or to support the view itself. The evidence cited certainly suggests that benign strains of the virus now exist, as one would expect with any virus that has been in the environment for six years and infected such a large number of individuals, but the only evidence that the benign virus pre-dates the pathogenic virus is from samples of sera collected prior to the UK and Australian outbreaks. This research (White et al 2001 and Nagesha et al 2000) which the Report cites as providing this data is omitted from the bibliography and therefore cannot be checked to see whether it is in fact evidence of a benign virus existing prior to the first appearance of RCD.

In any case, these findings would have to be repeated (a) in sera pre-dating the original appearance of RCD in China and (b) in many further tests before the conclusion ultimately reached by the Report on the basis of this evidence (ie that the benign virus was pre-existing, therefore the pathogenic virus did not come from another species, therefore there is no reason to believe that any other species will ever be infected) can be assumed. Furthermore, the statement that there is consensus on this matter in the scientific community is patently untrue if there are any scientists who do not agree with it, as there clearly are.

The report goes on to say "There is now therefore a considerable amount of data to support the view that non-pathogenic RCV was present for some time ... prior to the first outbreak of acute RHD in China". Yet the above inconclusive and unreferenced research is the only evidence actually cited.

In fact, the report completely ignores the one extremely convincing piece of evidence on which many in the international scientific community base their concern that the disease must have come from another species rather than a benign rabbit virus. Pathogenic RCV first appeared in a shipment of rabbits from Germany to China. Had a pathogenic mutation of a benign rabbit virus occurred in a rabbit with whom the rabbits in the shipment were in contact prior to shipment, other rabbits, also in contact with that one rabbit outside the shipment, would have shown signs of the disease around the same time the rabbits in the shipment became diseased. No rabbit outside the shipment did so. Therefore the mutation must have occurred within a rabbit within the shipment after they were isolated for transit. However, had the mutation occurred in a rabbit in the shipment, after isolation for transit, that one rabbit would either have got sick first or not got sick at all, and the others would have got sick later. Neither of those things happened either " they all got sick within a few hours of each other. The only way all the rabbits in the shipment could have got sick at the same time while no rabbit with whom they were in contact prior to shipment got sick would be if an identical mutation had occurred in all the rabbits in the shipment at about the same time" a virtual biological impossibility.

Clearly all the rabbits in the shipment were infected at roughly the same time, and therefore could not have been infected by any rabbit within the shipment. Since any infected rabbit outside the shipment would also have become infected and/or infected other rabbits outside the shipment, the rabbits in the shipment could not have been infected by any rabbit outside the shipment either. Therefore the only theory that makes any sense at all is that they contracted the disease from something other than another rabbit.

2. RCV release and spread in Australia

Government Regulation

This section states that prior to the original declaration of RCD as a Biological Control Agent , the BRS "comprehensively assessed scientific evidence about the issues raised in public submissions". Many international experts in the field of virology, and specifically caliciviruses, who submitted scientific evidence to this process have publicly criticised the Australian assessment as anything but comprehensive.

3. RISKS ARISING FROM THE NOVEL FORM OF EXPOSURE OF NON-TARGET ANIMALS TO RCV

3(a) Pathogenicity and infectivity

Characteristics of RCV and RCD

This section asserts that the ear rot disease which studies in NZ have shown to be associated with RCD is not related to NZ’s use of RCD baits because it has occurred in areas where the disease has spread "naturally". This is a nonsensical assertion as it would be difficult to find anywhere in NZ where the disease spread naturally. The Report goes on to say that the ear rot disease is unlikely, however, to be caused by RCD per se or it would have appeared elsewhere in the world – failing to note that NZ is the only country that has used RCD baits (albeit illegally).

Hazard description: toxicity, pathogenicity and infectivity to non-target native and introduced animals associated with the novel exposure route

The introductory paragraph to this section states that, if RCV were to manifest in other species, it might manifest with pathology similar to that in rabbits, or with different pathology, or with minor non-pathogenic effects. It fails to note one obvious conclusion that arises from this statement. If, as the Report claims (with a minimum of scientific evidence), RCD mutated from a previously benign rabbit virus, a minor non-pathogenic virus for another species might become acutely pathogenic just as suddenly and unexpectedly as the report claims RCD did for rabbits.

AAHL Studies

The report then quotes the findings of the original AAHL testing of the virus for species-specificity prior to the original release. Again, it fails to note that this testing has been widely criticised by international virology experts as grossly inadequate.

When discussing the fact that numerous other species which have been challenged by RCD have had antibody reactions (sero-conversion), the report denies that this provides any evidence of cross-infection. Some international virology experts dispute this assumption, considering that an antibody reaction indicates that the immune system has recognised a potential invader and has gone on red alert. Additionally, the report admits that, whereas the antibody reaction in most species challenged with RCD was transient, with the one species subjected to a higher dose, the reaction plateaued. It argues that, had infection occurred, the reactions would have been neither transient or plateaued but would have risen steeply. However, it fails to note that the tests did not attempt to determine what kind of reaction, in any of the species tested, would have occurred with a vastly increased dose.

This logic is bizarre. A small dose caused a transient antibody reaction. A higher dose caused a plateaued antibody reaction. Logically, it could be speculated that a much higher dose might cause a steeply rising antibody reaction, which would be indicative of infection. But no species were subjected to high enough doses to find out.

Also notably, none of the subject species tested were allowed to live longer than 14 days, so no real chance was given for infection to develop anyway. This inadequacy is noted in the next paragraph of the Report.

Does RCV infect hares

This section cites a study showing that hares may be susceptible to RCV. It then uses the fact that evidence is limited to this one study to conclude that hares are not susceptible to RCV. The studies it cites in support of the conclusion that hares are not susceptible to RCD are to do with the fact that RCD does not seem to be related in any way to Brown Hare Virus: apparently RCV challenge provides no immunity to BHV in hares or vice versa. This argument may be relevant in the absence of any actual evidence that hares can be infected with RCV, but it can scarcely be used to simply dismiss existing evidence that they can be infected with RCV.

The report repeatedly dismisses sero-conversion (antibody reaction) as indicative of the possibility of cross-infection. It argues that evidence of cross-infectivity can only be demonstrated by the presence of live virus multiplying in the challenged animal. It notes that foxes, ferrets, cats, hedgehogs, hares and harrier hawks all demonstrated sero-conversion. It does not state which of these animals were post-mortem tested for the presence of live virus in their organs, or whether all organs were tested (although the report notes elsewhere that lack of evidence of infectivity in one organ may not mean that other organs are free from infection). It then concludes that this lack of data showing that infection occurred in the other tested species is evidence that RCV is rabbit-specific.

Summary: characterisation and host range of RCV

This section makes the naive assertion that "there are many experienced and qualified persons in Australia who would, during routine work on wildlife for other purposes, notice and follow up any unexplained declines in native animal populations and recognise symptoms resembling RCD" This is total nonsense. In the first place, not all native vertebrate species (let alone invertebrates) are routinely monitored and, even of species that are routinely monitored, not all populations of are monitored. In the second place, unexplained declines in population could, frequently do, and, in fact, have occurred for a wide range of reasons, including both unknown diseases and the direct ecological impacts of RCD (ie massive reductions in a primary food source for both native and non-native predators and scavengers); wildlife workers are not necessarily in a position to research the reason for these declines. In the third place, a benign infection of other species by RCD would not manifest as a decline in populations anyway " but by the report’s own logic could become as suddenly and unexpectedly pathogenic as the report argues RCV has become for rabbits. In the fourth place, as the Report itself states, symptoms in another species may be totally unlike those manifested in rabbits.

In short, contrary to the assertions of the report:

• research into the cross-infectivity of RCD has not been comprehensive;
• there has been no post release monitoring of wildlife for evidence of cross-infection, nor any way for any such cross-infection to come to light through other wildlife monitoring programs;
• there is at least one study which shows that another species (hares) have been infected (and a recent study has now shown that RCV can infect pigs);
• there is substantial evidence of sero conversion in other species which some scientists consider to be evidence, in itself, of the possibility of cross infection;
• there has been very little post-mortem study of those who have sero-converted to show, one way or another, whether infection has occurred;
• there is little or no cited evidence that the benign form of RCV pre-dates the acute form;
• there is strong evidence, in the original appearance of RCD, that it infected the whole shipment of rabbits more or less simultaneously and therefore must have come from a non-rabbit source;
• if the pathogenic strain did come from a previously benign strain of the virus, it is completely irresponsible of the report to cite as evidence of species-specificity either:
  • the sero-conversion without infection; or
  • the vast number of occasions on which the sero-conversion could have been indicative of non-pathogenic infection where there was no actual testing done for infection.

The report concludes that evidence since 1996 "continues to support the view" that RCV is not pathogenic or infective in any other species. It does this on the basis of the following.
(1)No disease or infection from RCV has been detected in any of the 40 species tested.

• Yet the report itself has cited evidence that RCV has infected hares.
• The report also does not appear to have considered recent research showing that pigs have been infected.
• Additionally, the assumption that sero-conversion alone is not indicative of the potential for cross-infection is not widely supported by the international scientific community.

• This repeats the ludicrous assertion that such infection would not go unnoticed even in the total absence of monitoring.

• Again this is refuted by the Report’s own mention of the hare that was apparently successfully infected, and by recent evidence of infection of pigs.

• To conclude that something will not happen on the basis of tests which you admit are insufficient to find out whether or not it is going to happen is totally irresponsible.

• This seems to be a case of having their cake and eating it too. The conclusion seems to be that BHV and RCV are not related but even if they are, they only effect the rabbit family, so who cares?

• The report presents no checkable evidence that the benign virus was pre-existing.
• The report ignores the facts surrounding the first appearance of RCD and the powerful reasons for concluding the disease must have come from another species.
• Finally the report treats the conclusion that the disease came from a benign rabbit virus as evidence that it will not cross species.
  • Even if there were strong evidence for the argument that the disease came from a benign rabbit virus, this would shed no light whatsoever on the disease’ species specificity.
  • It would, in fact, make the evidence of sero-conversion in other species much more alarming. If a benign virus can suddenly become pathogenic in one species, there is no reason it cannot do so in another.

Exposure

The report admits that use of baits will expose new previously unexposed omnivores and herbivores to the virus but argues that the exposure level will still be much lower than the exposure levels of carnivores and scavengers who have already been routinely exposed to high doses of RCV without any apparent infection or pathogenicity. The report fails to note that, since the object of the baiting exercise is to get the disease into places where it has not previously taken hold, the baits will also expose carnivores and scavengers who have not previously been exposed to the disease. This will inevitably include some species or sub-species who have not been tested under laboratory conditions.

Analysis

This section states again that RCD has not been observed in any animal apart from rabbits worldwide and that there is no evidence of RCV pathogenicity or infectivity in any non-target animal before the release of RCV in Australia. Again it ignores the evidence of hare infection, appears to be unaware of the evidence of pig infection and neglects to note that there was no evidence of RCV pathogenicity or infectivity in rabbits either before the sudden emergence of the disease in 1984.

The report again asserts that the benign strain of RCV was probably already present in Australia prior to 1996 - and again fails to cite any evidence, whatsoever of this. On this basis, ie the basis of no evidence whatsoever, the report concludes that the likelihood of a mutation leading to host switching is negligible.

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