To monitor the initial releases of rabbit haemorrhagic disease virus (RHDV) into previously unexposed rabbit populations in the North Island of New Zealand.
The study programme consisted of pre-release spotlight counts of rabbits on the study farms, pre-release serological samples to check for prior exposure to RHDV, a farmer-completed questionnaire and post-release spotlight counts to measure any change in rabbit numbers following the release of RHDV. In total, 23 sites within the lower North Island where RHDV was released during the period November 1997 to June 1998, were monitored. The most common release method involved the spreading of chopped carrot bait laced with a solution of virus-infected material obtained from dead rabbits.
Eighty percent of farmers thought that the disease had spread away from the release sites to areas where virus had not been liberated, although only 27% reported finding dead rabbits more than 300 m away from release locations. Seventy-three percent of farmers were satisfied with the overall effectiveness of rabbit haemorrhagic disease (RHD) as a means of reducing rabbit numbers, but 56% indicated they would modify the way they released the virus in the future. Average pre-release night spotlight counts per property ranged from 2.2 rabbits/km to 36.9 rabbits/km, the median being 12.8 rabbits/km. The time interval from initial release to when the first dead rabbit was seen which the farmer believed to have died from RHD varied from 3 to 21 days, the mean being 7.4 days and the median 7 days. The median change in night spotlight counts per site at 3 weeks after release, expressed as a percentage relative to pre-release counts, was -15.5% (range +18.9% to -76.9%) and at 6 weeks was -49.7% (range 0% to -76.9%). The time of the estimated peak of the disease epidemic ranged from 1 to 7 weeks after release of RHDV, the mean being 3.1 and the median 3 weeks.
Rabbit haemorrhagic disease reduced rabbit numbers on the majority of farms where the virus was released, and appears to be an effective measure for controlling rabbit populations in New Zealand.
[Show abstract][Hide abstract] ABSTRACT: Rabbit haemorrhagic ,disease (RHD) was illegally released in New ,Zealand in August ,1997 and subsequently spread by farmers and naturally over all areas inhabited by rabbits. The disease has persisted, causing either annual or biennial epidemics that appear to start each spring by infecting susceptible adult rabbits and running through to the autumn infecting young rabbits of the year. Rabbit densities have been suppressed by more than 90% in many areas where numbers were initially high and epidemics returned annually, and by about 50% in areas with low initial densities and biennial epidemics, leaving between 35% and 20%, respectively, of the survivors immunised. In some areas the disease has not reduced rabbit densities and has left more than 80% (at worst) of the survivors across all age cohorts with antibodies to RHD. A possible cause of this apparent longitudinal transmission is that seropositive adult rabbits (which may retain virus) may be infectious and pass virus on to their offspring at just the right dose and age to impart immunity. A pen trial, in which we orally dosed 9-week-old rabbits born to seropositive mothers, showed that they survived and did not seroconvert, but were fully susceptible when re-dosed at about 17 weeks. Wehave evidence that the possible pre-existing calicivirus does not impart immunity,to RHD in
Wildlife Research 01/2002; 29(6). DOI:10.1071/WR00108 · 1.49 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: This review considers the history of the discovery of the rabbit haemorrhagic disease virus (RHDV) and its spread throughout the world in domestic and wild rabbits, which led eventually to its deliberate release into Australia and New Zealand for the control of a major pest, the introduced wild rabbit. The physical and genetic structure of RHDV is now well understood, and its pathogenic effects are also well known. The epidemiology of rabbit haemorrhagic disease (RHD) has been clearly documented in the field in European countries, Australia and New Zealand. Since its initial spread through largely naïve populations of wild rabbits it has established a pattern of mainly annual epizootics in most areas. The timing of epizootics is dependent on climatic variables that determine when rabbits reproduce and the appearance of new, susceptible rabbits in the population. The activity of RHDV is also influenced by climatic extremes that presumably affect its persistence and the behaviour of insect vectors, and evidence is growing that pre-existing RHDV-like viruses in some parts of Australia may interact with RHDV, reducing its effectiveness. The timing of epizootics is further modified by the resistance to RHD shown by young rabbits below 5 weeks of age and the presence of protective maternal antibodies that also protect against fatal RHD. RHD has reduced rabbit abundance, particularly in dry regions, but rabbits in cooler, high-rainfall areas have been able to maintain their populations. In Australia and New Zealand, RHD has raised the prospects for managing rabbits in low rainfall areas and brought substantial economic and environmental benefits. W R02010 RHD and t he biologi cal con tr ol of wi ld ra bbi ts B. Co o ke and F. Fe nner
Wildlife Research 01/2002; 29(6). DOI:10.1071/WR02010 · 1.49 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The natural arrival of rabbit haemorrhagic disease virus (RHDV) in south-western Australia in September 1996 resulted in a reduction in rabbit numbers of &SIM; 65% (&SIM; 90% morbidity, with &SIM; 72% mortality of infected rabbits). As no signs of the disease ( clinical or serological) were seen over the next two years, and as rabbit numbers over the last 12-month monitoring period at the site were similar to those observed before the natural 1996 RHDV epizootic (i.e. pre-RHD), RHDV was deliberately reintroduced into this rabbit population in April 1999 ( autumn). Seven RHDV-inoculated rabbits were released prior to the main breeding season when <3% of sampled rabbits (n = 118) were seropositive for RHDV antibodies. Following the deliberate release, the overall decline in rabbit numbers (68%) was comparable to that seen during the natural 1996 epizootic. However, on the basis of the observed changes in rabbit numbers, and in their serology, the impact of the deliberate RHDV release appeared to be more variable across the six trapping areas than was seen during the natural 1996 spring epizootic. The reductions in rabbit numbers on these areas 6-8 weeks after RHDV-release ranged from 55% to 90%. The serology of the surviving rabbits on the trapping areas was also variable over this period, with the proportion of seropositive rabbits ranging from 5% to 90%. Overall, only 15% of the surviving rabbit population showed evidence of recent challenge by RHDV, giving a morbidity rate of 73% 8 weeks after the release. However, over 90% of infected rabbits died. This provides further evidence that some rabbits remained un-challenged by RHDV for up to 8 weeks after its release. The variable impact of the April 1999 release may have been partially caused by the observed differences in abundance of insect vectors, and/or an apparent increase in the incidence of non-virulent RHDV in the months preceding the release.
Wildlife Research 01/2005; 32(2). DOI:10.1071/WR04025 · 1.49 Impact Factor
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