Changes in European wild rabbit population dynamics and the epidemiology of rabbit haemorrhagic disease (RHD) in response to artificially increased viral transmission

Author(s):  
Carlos Calvete ◽  
Lorenzo Capucci ◽  
Antonio Lavazza ◽  
María P. Sarto ◽  
Antonio J. Calvo ◽  
...  
2006 ◽  
Vol 33 (6) ◽  
pp. 467 ◽  
Author(s):  
Carlos Calvete ◽  
Enrique Pelayo ◽  
Javier Sampietro

The European wild rabbit (Oryctolagus cuniculus) is an introduced pest species in Australia and New Zealand. Rabbits have a devastating negative impact on agricultural production and biodiversity in these countries, and Rabbit Haemorrhagic Disease (RHD) is currently included in control strategies for rabbit populations. On the other hand, the European wild rabbit is a key native prey species in the Iberian Peninsula. Since the arrival of RHD, however, rabbit populations have undergone dramatic decreases and several predator species at risk of extinction are currently dependent on the rabbit population density. Therefore, from the point of view of biodiversity conservation, evaluating habitat correlates and trends of rabbit populations after the first RHD epizootic is of great interest to improve the long-term control or promotion of wild rabbit populations. We estimated the relationship between habitat factors and long-term population trends as well as the relationships between habitat factors and rabbit abundance 2 and 14 years after the arrival of RHD in several Iberian rabbit populations. We observed that only 26% of surveyed populations seemed to experience an increase in rabbit abundance over the last 12 years and that this increase was higher in the low-rabbit-abundance areas of l992, leading to high rabbit abundance in 2004. Our results suggested that short- and long-term impacts of RHD were related to habitat quality. The initial impact of RHD was higher in more suitable habitats, but increasing long-term population trends were positively related to good habitat quality.


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.


2005 ◽  
Vol 32 (2) ◽  
pp. 139 ◽  
Author(s):  
John S. Bruce ◽  
Laurie E. Twigg

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.


2004 ◽  
Vol 31 (6) ◽  
pp. 651
Author(s):  
G. Story ◽  
J. Scanlan ◽  
R. Palmer ◽  
D. Berman

Rabbit haemorrhagic disease virus (RHDV) escaped from quarantine facilities on Wardang Island in September 1995 and spread through South Australia to Queensland by December 1995. To determine the impact of this biological control agent on wild rabbit populations in Queensland, shot sample and spotlight count data were collected at six sites. RHDV spread across Queensland from the south-west to the east at a rate of at least 91 km month–1 between October 1995 and October 1996. The initial impact on rabbit density appeared highly variable, with an increase of 81% (255 ± 79 (s.e.) to 385 ± 73 rabbits km–2) at one site and a decrease of 83% (129 ± 27 to 22 ± 18 rabbits km–2) at another during the first outbreak. However, after 30 months of RHDV activity, counts were at least 90% below counts conducted before RHDV arrived. Using a population model to account for environmental conditions, the mean suppression of rabbit density caused by rabbit haemorrhagic disease (RHD) was estimated to be 74% (ranging from 43% to 94% between sites). No outbreaks were observed when the density of susceptible rabbits was lower than 12 km–2. Where rabbit density remains low for long periods RHDV may not persist. This is perhaps most likely to occur in the isolated populations towards the northern edge of the range of rabbits in Australia. RHDV may have to be reintroduced into these populations. Further south in areas more suitable for rabbits, RHDV is more likely to persist, resulting in a high density of immune rabbits. In such areas conventional control techniques may be more important to enhance the influence of RHD.


2002 ◽  
Vol 29 (6) ◽  
pp. 605 ◽  
Author(s):  
Glen Saunders ◽  
Barry Kay ◽  
Greg Mutze ◽  
David Choquenot

Rabbit haemorrhagic disease (RHD) may be the most important rabbit control agent to be made available to graziers in Australia since the advent of myxomatosis. Documenting the benefits of RHD to agricultural production values is an important process in determining best-practice strategies for the use of the disease in controlling rabbit populations. In this paper we review previous studies on the impact of rabbits and present recent Australian case studies that tracked the effects of RHD on agricultural production as the disease first spread across the continent. Indirect consequences of RHD, such as changes in costs of rabbit control as monitored through the use of 1080 (sodium monofluoroacetate), are reported. Potential negative impacts such as adverse effects on the wild rabbit fur and meat trade and in the spread of woody weeds are also discussed.


2002 ◽  
Vol 29 (6) ◽  
pp. 615 ◽  
Author(s):  
C. Holden ◽  
G. Mutze

The impact of rabbit haemorrhagic disease (RHD) on the population dynamics and diet of foxes and feral cats was studied in the Flinders Ranges, South Australia. Populations of both foxes and cats decreased substantially some 6–10 months after the advent of RHD, when rabbit numbers were reduced by 85%. The diet of foxes changed as a result of reduced rabbit numbers, with much less rabbit and more invertebrates and carrion being eaten. The physical condition of foxes showed little change after RHD. The diet of cats did not change markedly, but their physical condition was substantially poorer than before RHD. Total predation on native fauna is considered to have decreased after RHD.


2002 ◽  
Vol 29 (6) ◽  
pp. 627 ◽  
Author(s):  
Ben Reddiex ◽  
Graham J. Hickling ◽  
Grant L. Norbury ◽  
Chris M. Frampton

The impact of predation and rabbit haemorrhagic disease (RHD) on population dynamics of rabbits, and the survival of juvenile rabbits, was investigated between July 1999 and March 2000 in North Canterbury, New Zealand. Rabbit abundance and pre- and post-emergent rabbit mortality were monitored on four sites, two of which were subject to predator control. RHD spread naturally through all sites from late November to early December. Rabbit densities declined on all sites, but after the RHD epidemic, declines were significantly greater where populations of predators had not been controlled. Survival of rabbit nestlings was lower where predators were not controlled. All post-emergent radio-collared rabbits died at sites where predators were not controlled, whereas 18% of those collared at sites where predators were controlled survived to maturity. In contrast to the results from previous studies, rabbits born at the start of the breeding season had very high rates of post-emergent mortality, as they appeared to be susceptible to the RHD virus later in the breeding season. The age at which juvenile rabbits become susceptible to RHD, the timing of RHD epidemics, and the abundance of predators are likely to be important in determining survival of juvenile rabbits. This study demonstrates that predation can reduce rabbit populations to low levels, but only in combination with other factors, in this case RHD.


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.


2010 ◽  
Vol 37 (4) ◽  
pp. 311 ◽  
Author(s):  
Greg Mutze ◽  
Ron Sinclair ◽  
David Peacock ◽  
John Kovaliski ◽  
Lorenzo Capucci

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.


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