scholarly journals Rabbit haemorrhagic disease and the biological control of wild rabbits, Oryctolagus cuniculus, in Australia and New Zealand

2002 ◽  
Vol 29 (6) ◽  
pp. 689 ◽  
Author(s):  
B. D. Cooke ◽  
F. Fenner
Keyword(s):  
New Zealand ◽  
Environmental Benefits ◽  
Wild Rabbit ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Climatic Extremes ◽  
Rabbit Haemorrhagic Disease ◽  
Deliberate Release ◽  
History Of ◽  
Major Pest ◽  
Haemorrhagic Disease

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.

Seropositivity to rabbit haemorrhagic disease virus in non-target mammals during periods of viral activity in a population of wild rabbits in New Zealand

2006 ◽  
Vol 33 (4) ◽  
pp. 305 ◽  
Author(s):  
J. Henning ◽  
P. R. Davies ◽  
J. Meers
Keyword(s):  
New Zealand ◽  
Disease Virus ◽  
Small Sample ◽  
European Rabbit ◽  
Wild Rabbit ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Target Species ◽  
Rabbit Population ◽  
Rabbit Haemorrhagic Disease ◽  
Haemorrhagic Disease

As part of a longitudinal study of the epidemiology of rabbit haemorrhagic disease virus (RHDV) in New Zealand, serum samples were obtained from trapped feral animals that may have consumed European rabbit (Oryctolagus cuniculus) carcasses (non-target species). During a 21-month period when RHDV infection was monitored in a defined wild rabbit population, 16 feral house cats (Felis catus), 11 stoats (Mustela erminea), four ferrets (Mustela furo) and 126 hedgehogs (Erinaceus europaeus) were incidentally captured in the rabbit traps. The proportions of samples that were seropositive to RHDV were 38% for cats, 18% for stoats, 25% for ferrets and 4% for hedgehogs. Seropositive non-target species were trapped in April 2000, in the absence of an overt epidemic of rabbit haemorrhagic disease (RHD) in the rabbit population, but evidence of recent infection in rabbits was shown. Seropositive non-target species were found up to 2.5 months before and 1 month after this RHDV activity in wild rabbits was detected. Seropositive predators were also trapped on the site between 1 and 4.5 months after a dramatic RHD epidemic in February 2001. This study has shown that high antibody titres can be found in non-target species when there is no overt evidence of RHDV infection in the rabbit population, although a temporal relationship could not be assessed statistically owning to the small sample sizes. Predators and scavengers might be able to contribute to localised spread of RHDV through their movements.

The reintroduction, and subsequent impact, of rabbit haemorrhagic disease virus in a population of wild rabbits in south-western Australia

2005 ◽  
Vol 32 (2) ◽  
pp. 139 ◽  
Author(s):  
John S. Bruce ◽  
Laurie E. Twigg
Keyword(s):  
Disease Virus ◽  
Western Australia ◽  
Morbidity Rate ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Rabbit Population ◽  
Rabbit Haemorrhagic Disease ◽  
Deliberate Release ◽  
Haemorrhagic Disease ◽  
The Impact ◽  
Variable Impact

The natural arrival of rabbit haemorrhagic disease virus (RHDV) in south-western Australia in September 1996 resulted in a reduction in rabbit numbers of ~65% (~90% morbidity, with ~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.

Temporal dynamics of rabbit haemorrhagic disease virus infection in a low-density population of wild rabbits (Oryctolagus cuniculus) in New Zealand

2006 ◽  
Vol 33 (4) ◽  
pp. 293 ◽  
Author(s):  
J. Henning ◽  
D. U. Pfeiffer ◽  
P. R. Davies ◽  
J. Meers ◽  
R. S. Morris
Keyword(s):  
New Zealand ◽  
Disease Virus ◽  
Oryctolagus Cuniculus ◽  
Temporal Dynamics ◽  
Population Decline ◽  
Adult Survivors ◽  
European Rabbit ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Rabbit Haemorrhagic Disease ◽  
Haemorrhagic Disease

A longitudinal capture–mark–recapture study was conducted to determine the temporal dynamics of rabbit haemorrhagic disease (RHD) in a European rabbit (Oryctolagus cuniculus) population of low to moderate density on sand-hill country in the lower North Island of New Zealand. A combination of sampling (trapping and radio-tracking) and diagnostic (cELISA, PCR and isotype ELISA) methods was employed to obtain data weekly from May 1998 until June 2001. Although rabbit haemorrhagic disease virus (RHDV) infection was detected in the study population in all 3 years, disease epidemics were evident only in the late summer or autumn months in 1999 and 2001. Overall, 20% of 385 samples obtained from adult animals older than 11 weeks were seropositive. An RHD outbreak in 1999 contributed to an estimated population decline of 26%. A second RHD epidemic in February 2001 was associated with a population decline of 52% over the subsequent month. Following the outbreaks, the seroprevalence in adult survivors was between 40% and 50%. During 2000, no deaths from RHDV were confirmed and mortalities were predominantly attributed to predation. Influx of seronegative immigrants was greatest in the 1999 and 2001 breeding seasons, and preceded the RHD epidemics in those years. Our data suggest that RHD epidemics require the population immunity level to fall below a threshold where propagation of infection can be maintained through the population.

Rabbit Haemorrhagic Disease Virus: serological evidence of a non-virulent RHDV-like virus in south-western Australia

2004 ◽  
Vol 31 (6) ◽  
pp. 605 ◽  
Author(s):  
John S. Bruce ◽  
Laurie E. Twigg
Keyword(s):  
Disease Virus ◽  
Western Australia ◽  
Biological Control Agent ◽  
Clinical Signs ◽  
Wild Rabbit ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Serological Evidence ◽  
Rabbit Haemorrhagic Disease ◽  
European Rabbits ◽  
Haemorrhagic Disease

Although several different cELISAs have been used to assess the exposure of European rabbits to rabbit haemorrhagic disease (RHD), the interpretation of the results of such assays is not always straight-forward. Here we report on such difficulties, and on the likely presence of a non-virulent rabbit haemorrhagic disease virus–like virus (nvRHDV-LV) in south-western Australia. Analysis of sera collected from European rabbits at Kojaneerup (near Albany) in Western Australia provided the first serological evidence of the likely presence of a nvRHDV-LV in wild rabbit populations outside the east coast of Australia and New Zealand, before the deliberate introduction of RHDV as biological control agent in both countries. Six out of 30 rabbits (20%) sampled 1–2 months before the known arrival of RHDV at Kojaneerup were seropositive to RHD on the basis of their IgG isoELISAs. However, none of these positive samples were positive for the RHDV antibody cELISA (1 : 10), indicating likely exposure to nvRHDV-LV. Subsequent serological analysis of 986 rabbits sampled between September 1996 and August 1999 at Kojaneerup indicated that nvRHDV-LV persisted in these rabbits following the natural arrival of RHDV in September 1996. At least 10–34% of rabbits appeared to have been exposed to nvRHDV-LV during the 3-year study. The presence of nvRHDV-LV seemed to offer only limited protection to rabbits from RHDV during the initial epizootic; however, persistence of nvRHDV-LV may have mitigated further RHDV activity after this epizootic. Fewer than 1% of rabbits (9 of 986) showed evidence of RHDV-challenge during the 30 months following the initial RHDV epizootic. Furthermore, except for the epizootic in September 1996, no clinical signs of the disease were apparent in the population until RHDV was deliberately reintroduced in April 1999. Mortality of rabbits exposed to RHDV at this time appeared to be correlated with their IgG isoELISA titre.

Does a benign calicivirus reduce the effectiveness of rabbit haemorrhagic disease virus (RHDV) in Australia? Experimental evidence from field releases of RHDV on bait

2010 ◽  
Vol 37 (4) ◽  
pp. 311 ◽  
Author(s):  
Greg Mutze ◽  
Ron Sinclair ◽  
David Peacock ◽  
John Kovaliski ◽  
Lorenzo Capucci
Keyword(s):  
Disease Virus ◽  
Disease Outbreaks ◽  
Wild Rabbit ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Agricultural Pests ◽  
Genetic Sequencing ◽  
Rabbit Haemorrhagic Disease ◽  
Almost All ◽  
Haemorrhagic Disease ◽  
The Impact

Context. European rabbits are serious environmental and agricultural pests throughout their range in Australia. Rabbit haemorrhagic disease virus (RHDV) greatly reduced rabbit numbers in arid central Australia but had less impact in cooler, higher-rainfall areas. RHDV-like benign caliciviruses (bCVs) have been implicated in limiting the impact of RHDV in the higher-rainfall regions of Australia and also in Europe. Aims. Experimental releases of RHDV on bait were tested as a means of initiating disease outbreaks. Serological evidence of antibodies to bCVs was examined to determine whether they reduce mortality rates and/or spread of the released RHDV, and how that might influence the effectiveness of future RHDV releases for rabbit management. Methods. Four experimental releases were conducted in high-rainfall and coastal regions of southern Australia. Virus activity was implied from recapture rates and serological changes in marked rabbits, and genetic sequencing of virus recovered from dead rabbits. Changes in rabbit abundance were estimated from spotlight transect counts. Key results. Release of RHDV on bait produced disease outbreaks that challenged almost all animals within the general release area and spread up to 4 km beyond the release sites. Recapture rates were high in marked rabbits that possessed antibodies from previous exposure to RHDV and extremely low amongst rabbits that lacked any detectable antibodies. Rabbits carrying antibodies classified as being due to previous infection with bCVs had recapture rates that were dependent on circulating antibody titre and were ~55% of recapture rates in rabbits with clear antibodies to RHDV. Conclusions. This is the first quantified evidence that antibodies produced against bCVs provide significant protection against RHD outbreaks in field populations of rabbits. Implications. bCVs can greatly reduce the impact of RHDV on wild-rabbit populations in Australia and presumably elsewhere. RHDV can be effectively released on bait although further releases are likely to be of minor or inconsistent benefit for controlling rabbit numbers where bCVs are common.

Myxoma virus and rabbit haemorrhagic disease virus 2 coinfection in a European wild rabbit (Oryctolagus cuniculus algirus), Portugal

2020 ◽  
Vol 8 (1) ◽  
pp. e001002 ◽  
Author(s):  
Carina Luisa Carvalho ◽  
Fábio Alexandre Abade dos Santos ◽  
Teresa Fagulha ◽  
Paulo Carvalho ◽  
Paula Mendonça ◽  
...  
Keyword(s):  
Disease Virus ◽  
Oryctolagus Cuniculus ◽  
Rare Event ◽  
Myxoma Virus ◽  
European Rabbit ◽  
Wild Rabbit ◽  
Rabbit Haemorrhagic Disease Virus ◽  
Sample Collection ◽  
Rabbit Haemorrhagic Disease ◽  
Haemorrhagic Disease

Myxoma virus (MYXV) and rabbit haemorrhagic disease virus 2 (RHDV2) are two major pathogens that affect the European rabbit (Oryctolagus cuniculus). Between August 2017 and August 2019, 1166 wild rabbits (971 legally hunted and 195 found dead) were tested by PCR-based methods for MYXV and RHDV2 within the scope of an ongoing surveillance programme on wild leporids in Portugal. Despite never having been reported before and being considered a rare event, coinfection by RHDV2 and MYXV was detected in one juvenile wild rabbit found dead in the Évora district located in Alentejo. The relative frequency of coinfection in the group of diseased rabbits (found dead in the field) was 0.52 per cent (1/195). The positivity percentage of each single virus was much higher, namely, 14.36 per cent (28/195) for MYXV and 55.38 per cent (108/195) for RHDV2, within the 2 years of sample collection considered.

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