Potential use of myxoma virus and rabbit haemorrhagic disease virus to control feral rabbits in the Kerguelen Archipelago

2004 ◽  
Vol 31 (4) ◽  
pp. 415 ◽  
Author(s):  
B. D. Cooke ◽  
J.-L. Chapuis ◽  
V. Magnet ◽  
A. Lucas ◽  
J. Kovaliski

Rabbits have caused enormous damage to the vegetation on seven islands in the sub-Antarctic Kerguelen archipelago, including the main island, Grande Terre. Rabbit sera collected during 2001–02 were tested for antibodies against myxoma virus and rabbit haemorrhagic disease virus with a view to considering the wider use of these viruses to control rabbits. The results confirmed work done 15–20 years earlier that suggested that myxoma virus has not spread across all parts of Grande Terre and occurs at low prevalence among rabbits. By contrast, on Ile du Cimetière, where European rabbit fleas were introduced in 1987–88, the prevalence of myxoma antibodies is high and the rabbit population is relatively low, supporting the idea that the fleas are effective vectors of myxoma virus. Consequently, there should be benefits in releasing fleas on Grand Terre to enhance disease transmission. Reactivity of some rabbit sera in RHD-specific ELISAs suggested that a virus similar to RHDV may be present at low prevalence on Grande Terre but most rabbits are likely to be susceptible and this virus could be considered for use as a future biological control agent.

Vaccines ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 441 ◽  
Author(s):  
Sylvia Reemers ◽  
Leon Peeters ◽  
Joyce van Schijndel ◽  
Beth Bruton ◽  
David Sutton ◽  
...  

Myxoma virus (MV) and rabbit haemorrhagic disease virus (RHDV) are the major causes of lethal viral diseases in the European rabbit. In 2010, a new RHDV genotype (RHDV2) emerged in the field that had limited cross-protection with the classical RHDV (RHDV1). For optimal protection of rabbits and preventing spread of disease, a vaccine providing protection against all three key viruses would be ideal. Therefore, a novel trivalent myxoma vectored RHDV vaccine (Nobivac Myxo-RHD PLUS) was developed similar to the existing bivalent myxoma vectored RHDV vaccine Nobivac Myxo-RHD. The new vaccine contains the Myxo-RHDV1 strain already included in Nobivac Myxo-RHD and a similarly produced Myxo-RHDV2 strain. This paper describes several key safety and efficacy studies conducted for European licensing purposes. Nobivac Myxo-RHD PLUS showed to be safe for use in rabbits from five weeks of age onwards, including pregnant rabbits, and did not spread from vaccinated rabbits to in-contact controls. Furthermore, protection to RHDV1 and RHDV2 was demonstrated by challenge, while the serological response to MV was similar to that after vaccination with Nobivac Myxo-RHD. Therefore, routine vaccination with Nobivac Myxo-RHD PLUS can prevent the kept rabbit population from these major viral diseases.


2020 ◽  
Vol 8 (1) ◽  
pp. e001002 ◽  
Author(s):  
Carina Luisa Carvalho ◽  
Fábio Alexandre Abade dos Santos ◽  
Teresa Fagulha ◽  
Paulo Carvalho ◽  
Paula Mendonça ◽  
...  

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.


2006 ◽  
Vol 33 (4) ◽  
pp. 305 ◽  
Author(s):  
J. Henning ◽  
P. R. Davies ◽  
J. Meers

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.


2006 ◽  
Vol 33 (4) ◽  
pp. 293 ◽  
Author(s):  
J. Henning ◽  
D. U. Pfeiffer ◽  
P. R. Davies ◽  
J. Meers ◽  
R. S. Morris

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.


2004 ◽  
Vol 31 (6) ◽  
pp. 605 ◽  
Author(s):  
John S. Bruce ◽  
Laurie E. Twigg

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.


2002 ◽  
Vol 29 (6) ◽  
pp. 673 ◽  
Author(s):  
B. D. Cooke ◽  
S. McPhee ◽  
A. J. Robinson ◽  
L. Capucci

Serological data from wild rabbits support the hypothesis that a second RHDV-like virus was already present in Australia before rabbit haemorrhagic disease virus (RHDV) was introduced as a biological control agent. This putative virus apparently persists in most wild rabbit populations in the presence of RHDV, and antibodies raised against it appear to protect some rabbits from fatal rabbit haemorrhagic disease (RHD). High titres of these antibodies are most commonly found in rabbits from high rainfall areas; this may explain why the initial mortality from RHD declined as the disease spread from dry areas into wetter regions and why it remains less effective as a biological control in wetter regions today. The implications for further advances in rabbit control are discussed, including the need to isolate this putative RHDV-like virus and develop specific ELISA tests to facilitate its detection in the field.


Animals ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 40
Author(s):  
Fábio A. Abade dos Santos ◽  
Carolina Magro ◽  
Carina L. Carvalho ◽  
Pedro Ruivo ◽  
Margarida D. Duarte ◽  
...  

Rabbit haemorrhagic disease (RHD) is a highly contagious infectious disease of European wild and domestic rabbits. Rabbit haemorrhagic disease virus (RHDV, GI.1) emerged in 1986 in Europe, rapidly spreading all over the world. Several genotypes of RHDV have been recognised over time, but in 2010, a new virus (RHDV2/RHDVb, GI.2) emerged and progressively replaced the previous RHDV strains, due to the lack of cross-immunity conferred between RHDV and RHDV2. RHDV2 has a high mutation rate, similarly to the other calivirus and recombines with strains of RHDV and non-pathogenic calicivirus (GI.4), ensuring the continuous emergence of new field strains. Although this poses a threat to the already endangered European rabbit species, the available vaccines against RHDV2 and the compliance of biosafety measures seem to be controlling the infection in the rabbit industry Pet rabbits, especially when kept indoor, are considered at lower risk of infections, although RHDV2 and myxoma virus (MYXV) constitute a permanent threat due to transmission via insects. Vaccination against these viruses is therefore recommended every 6 months (myxomatosis) or annually (rabbit haemorrhagic disease). The combined immunization for myxomatosis and RHDV through a commercially available bivalent vaccine with RHDV antigen has been extensively used (Nobivac® Myxo-RHD, MSD, Kenilworth, NJ, USA). This vaccine however does not confer proper protection against the RHDV2, thus the need for a rabbit clinical vaccination protocol update. Here we report a clinical case of hepatitis and alteration of coagulation in a pet rabbit that had been vaccinated with the commercially available bivalent vaccine against RHDV and tested positive to RHDV2 after death. The animal developed a prolonged and atypical disease, compatible with RHD. The virus was identified to be an RHDV2 recombinant strain, with the structural backbone of RHDV2 (GI.2) and the non-structural genes of non-pathogenic-A1 strains (RCV-A1, GI.4). Although confirmation of the etiological agent was only made after death, the clinical signs and analytic data were very suggestive of RHD.


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