Rabbit Haemorrhagic Disease Outbreak Research Articles

Genetics of the rabbit haemorrhagic disease virus strains responsible for rabbit haemorrhagic disease outbreaks in Japan between 2000 and 2020.

Rabbit haemorrhagic disease (RHD) is a highly contagious and fatal disease in rabbits caused by the rabbit haemorrhagic disease virus (RHDV), which includes two genotypes, RHDV-GI.1 and RHDV2-GI.2. RHDVs tend to recombine among different strains, resulting in significant genetic evolution. This study evaluated the genetics of Japanese RHDV strains associated with six outbreaks between 2000 and 2020 using whole-genome sequencing, genomic recombination and phylogenetic analyses. Genomic recombination analysis using near-complete genomic sequences revealed that two Japanese strains detected in 2000 and 2002 were non-recombinant GI.1 (variant RHDVa-GI.1a) strains of different origins, most closely related to strains identified in PR China in 1997 and the USA in 2001, respectively. In contrast, four recent Japanese GI.2 strains detected between 2019 and 2020 were recombinant viruses harbouring structural protein (SP) genes from GI.2 strains and non-SP (NSP) genes from a benign rabbit calicivirus (RCV) strain of genotype RCV-E1-GI.3 (GI.3P-GI.2) or an RHDV G1-GI.1b variant (GI.1bP-GI.2). Phylogenetic analysis based on SP and NSP regions revealed that the GI.1bP-GI.2 recombinant virus detected in Ehime prefecture and the GI.3P-GI.2 recombinant viruses detected in Ibaraki, Tochigi and Chiba prefectures were most closely related to recombinant viruses identified in Australia in 2017 and Germany in 2017, respectively. These results suggested that past RHD outbreaks in Japan did not result from the evolution of domestic RHDVs but rather represented incursions of foreign RHDV strains, implying that Japan is constantly at risk of RHDV incursion from other countries.

First Rabbit Haemorrhagic Disease outbreak in Nigeria: Implications for the growing rabbit production industry

The first outbreak of rabbit haemorrhagic disease (RHD) in Nigeria was reported in 2020 after over three decades of its existence in several parts of the world. In this study, we traced the timeline of the 2020 outbreaks of RHD in Nigeria, assessed the knowledge and practices of farmers about RHD and other infectious diseases of rabbits.

Detection of a New Emerging Strain of Rabbit Haemorrhagic Disease Virus 2 (GI.2) in China.

In May 2020, an outbreak of rabbit haemorrhagic disease 2 (RHD2) caused by the rabbit haemorrhagic disease virus 2 (RHDV2, GI.2) occurred in Sichuan, China. The acute onset and short disease course resulted in rabbit mortality as high as 42.86%. Currently, basic research on the aetiology and genetic characteristics of GI.2 is lacking in China. Pathological changes in various tissues from infected rabbits were investigated and the viral genome was characterised. This study used RT-PCR, histopathology and scanning electron microscopy to identify the pathogen in samples from infected rabbits that had died. Phylogenetic trees were constructed based on whole genome sequence analysis, and recombination events were analysed. RT-PCR identified the presence of GI.2. Histopathology revealed liver cell necrosis and haemorrhaging into lung alveoli. Electron microscopy demonstrated spherical GI.2 particles that were 40 nm in size. The gene sequence length of the isolate was 7,445 bp (GenBank accession number MW178244). A phylogenetic analysis based on the genome of the isolated strain and 60 reference strains showed that the isolate was grouped together with GI.2 strain MT586027.1 in a relatively independent sub-branch. The results of the recombination analysis showed that the strain was recombined from the MT586027.1 (major parent) and MN90145.1 (minor parent) strains, and recombination breakpoints were at locations in the 2858-5137 nt range. The results of this study extend our understanding of the molecular epidemiology of GI.2.

Viral haemorrhagic disease: RHDV type 2 ten years later

Until the early 1980s, it was totally unknown that lagomorphs were the hosts of several caliciviruses, which were included in the genus Lagovirus by the International Committee on Taxonomy of Viruses (ICTV) in 2000. In those years, two new diseases appeared, with very similar clinical and pathological profiles and associated high mortality rates: rabbit haemorrhagic disease (RHD) in rabbits and European Brown Hare Syndrome (EBHS) in European brown hares. It took a few years to ascertain that both diseases, actually acute and fatal forms of hepatitis, were caused by two genetically related caliciviruses, but they were finally classified by ICTV into two distinct viral species on the basis of their molecular characterisation and epidemiological data: RHDV in rabbit and EBHSV in brown hare. RHD has had a devastating effect on rabbit farms, causing great economic damage, especially in China, where RHD was first noticed around 1982, and in Europe. RHD has also severely affected wild rabbit populations, whose drastic decline has caused serious ecological imbalances in territories such as Spain, where rabbits are a central link in the wildlife food chain. Since the early 1990s, with the increased availability on the market of RHDV vaccines effective in protecting rabbits from RHD, the impact of the disease on rabbit farms has been significantly reduced. In the following years, also considering that RHDV is an endemic virus that cannot be eradicated, farmers learned how to manage the continuous use of RHDV vaccine in relation to the epidemiological situation, the type of breeding farm and the costs of vaccination prophylaxis. Although precarious, management of the RHD risk for rabbit farmers reached an acceptable equilibrium, which was, however, completely upset starting from 2010 by the emergence of another lagovirus also causing RHD. The genome of the newly emerged virus shows limited differences from that of RHDV, but the phenotypic traits of the two viruses are distinctive in at least three main respects: 1) The antigenic profile of the virus (the “face” of the virus recognised by the antibodies) is largely different from that of RHDV. 2) Newborn rabbits only a couple of weeks old die of RHD when infected with the new virus, while RHDV infections run asymptomatic until 7-8 wk of age. 3) The new virus, which started in Europe, has spread over the years to several continents, affecting wild and/or domestic rabbit populations. During this worldwide distribution, the new virus infected several lagomorph species and was shown to cause RHD in most of them. Considering these marked differences and the fact that the new virus is not a variant of RHDV, we proposed the name RHDV type 2 (RHDV2). All these main distinctive traits that differentiate RHDV from RHDV2 have the following consequences in practice: 1) The antigenic difference between RHDV and RHDV2 (their ‘faces’) is so great that we need “new” specific vaccines to control RHDV2 (i.e. RHDV2 is a new serotype). 2) In the event of an RHDV2 infection in suckling rabbits, the presence of maternal antibodies to RHDV2 in the blood is the only way to prevent RHD. In contrast, newborns are naturally resistant to RHD if infected with RHDV and therefore, in terms of protection, the presence of maternal antibodies is useless. 3) When RHD outbreaks occur in territories where rabbits live in sympatry with populations of other lagomorphs, viral contamination in the environment reaches sufficiently high levels to facilitate the transmission of RHDV2 to other lagomorphs, including those with a lower susceptibility to infection than the rabbit. Taken together, these phenotypic traits characteristic of RHDV2 are the reason for its rapid spread across the territory and the concomitant disappearance of RHDV. Probably the most striking example of the epidemiological consequences related to the peculiar features of RHDV2 is its rapid spread in the USA and Mexico, where it is now practically endemic. There, despite repeated isolated outbreaks of RHD caused by RHDV from 2000 onwards in small rabbit farms, RHDV has never been able to become endemic.

Microbial metagenomic approach uncovers the first rabbit haemorrhagic disease virus genome in Sub-Saharan Africa

Rabbit Haemorrhagic Disease (RHD) causes high morbidity and mortality in rabbits and hares. Here, we report the first genomic characterization of lagovirus GI.2 virus in domestic rabbits from sub-Saharan Africa. We used an unbiased microbial metagenomic Next Generation Sequencing (mNGS) approach to diagnose the pathogen causing the suspected outbreak of RHD in Ibadan, Nigeria. The liver, spleen, and lung samples of five rabbits from an outbreak in 2 farms were analyzed. The mNGS revealed one full and two partial RHDV2 genomes on both farms. Phylogenetic analysis showed close clustering with RHDV2 lineages from Europe (98.6% similarity with RHDV2 in the Netherlands, and 99.1 to 100% identity with RHDV2 in Germany), suggesting potential importation. Subsequently, all the samples were confirmed by RHDV virus-specific RT-PCR targeting the VP60 gene with the expected band size of 398 bp for the five rabbits sampled. Our findings highlight the need for increased genomic surveillance of RHDV2 to track its origin, understand its diversity and to inform public health policy in Nigeria, and Sub-Saharan Africa.

Retrospective studies on rabbit haemorrhagic disease outbreaks caused by RHDV GI.2 virus on farms in France from 2013 to 2018

Rabbit haemorrhagic disease (RHD) is a critical health threat to the rabbit industry in Europe. In 2018, the French rabbit industry adopted a voluntary control plan against this disease. In this context, two epidemiological studies were conducted on RHD outbreaks that occurred between 2013 and 2018 in France. The objectives were to describe the spread of RHD due to the new genotype RHDV GI.2 (rabbit haemorrhagic disease virus GI.2) and to identify rearing factors influencing the occurrence of the disease in order to guide the prevention measures recommended in the control plan. An analysis of cases on 295 farms between 2013 and 2017 showed that 32% of farms were affected at least once; the incidence of the disease increased in 2016-2017 compared to 2013-2015. Farms already affected in 2013-2015 had a higher risk of being infected in 2016-2017 than those that remained unaffected until 2015 (Relative Risk and 95% Confident Interval 1.7 [1.1-2.7]). A case-control study carried out between 2016 and 2018 on 37 outbreaks and 32 control farms revealed variability in biosecurity and decontamination practices between farms. The risk of being infected tends to be linked to these practices, but certain structural factors (e.g. the manure disposal system, transfer of rabbits at weaning) could also influence the risk of virus introduction into farms. In the context of a limited vaccination coverage of the farms (only females are vaccinated), these hypotheses will be studied further, using information from the RHD outbreak monitoring system implemented at the same time as the control plan in 2018.

Infectivity of rabbit haemorrhagic disease virus excreted in rabbit faecal pellets

Rabbit haemorrhagic disease (RHD) is caused by a lagovirus affecting European rabbits (Oryctolagus cuniculus). Viral RNA is detected in tissues or faeces of convalescent rabbits, suggesting persistent infections; however, this RNA has not been shown to be related to infective viruses to date. In the present work, seven laboratory rabbits were challenged with the RHDV2/b virus variant. Viral RNA was individually detected by duplex qPCR in faeces collected for four weeks after infection, and the infective capacity of viral RNA excreted in the faeces of surviving rabbits was tested by challenging new rabbits with faecal inocula. As results, viral RNA was detected in faeces until the end of the assay. Viral RNA detected in the fourth week was infective only in the case of one rabbit that did not exhibit clear seroconversion, suggesting persistent infection as a result of an impaired immune response. Since the surviving rabbits were apparently healthy individuals, the importance of detecting carriers and the correct management of faeces to control RHD outbreaks in rabbitries are highlighted.

Small animal disease surveillance 2020/21: SARS-CoV-2, syndromic surveillance and an outbreak of acute vomiting in UK dogs.

Small animal disease surveillance 2020/21: SARS-CoV-2, syndromic surveillance and an outbreak of acute vomiting in UK dogs.

Emergence of rabbit haemorrhagic disease virus 2 in China in 2020.

Rabbit haemorrhagic disease (RHD) is an acute fatal disease caused by the Lagovirus rabbit haemorrhagic disease virus (RHDV), which was first reported in 1984 in China. Strains of two different genotypes (GI.1a and GI.1c) have been detected in China to date. In 2010, a new RHDV variant with a unique genetic and antigenic profile was identified in France, designated RHDV2, which rapidly spread throughout continental Europe and nearby islands. Here, we report the first outbreak of RHD induced by RHDV2 (GI.2) in rabbit farms in the Sichuan province of China. We conducted haemagglutination tests and phylogenetic analysis of the new RHDV isolate SC2020/04, which was identified as a non‐haemagglutinating strain belonging to the RHDV2 (GI.2) genogroup. Considering the serious risk of RHDV2 to the Chinese rabbit industry, the circulation of RHDV2 in the population should be carefully monitored in China.

Previous exposure to myxoma virus reduces survival of European rabbits during outbreaks of rabbit haemorrhagic disease

Abstract Exploiting synergies among diseases or parasites could increase the efficacy of biological control of invasive species. In Australia, two viruses were introduced to control European rabbits Oryctolagus cuniculus: myxoma virus in 1950 and rabbit haemorrhagic disease virus in 1995. While these biological controls caused initial declines of >95% in affected populations, and despite recurring outbreaks of both diseases, rabbits remain a problem in many areas. We used 18 years of capture–mark–recapture, dead recovery, and antibody assay data from a sentinel population in South Australia to test whether these two diseases interact to modify the survival of individual wild rabbits. We compared four joint, multistate, dead‐recovery models to test the hypotheses that rabbit haemorrhagic disease and myxoma viruses have synergistic (i.e., previous exposure to one virus affects survival during outbreaks of the other virus) or additive effects (i.e., previous exposure to one virus does not affect survival during outbreaks of the other virus). Rabbit haemorrhagic disease outbreaks reduced the survival of individuals with no immunity by more than half during the 58‐day capture‐trip intervals, i.e., from 0.86–0.90 to 0.37–0.48. Myxomatosis outbreaks had a smaller effect, reducing survival to 0.74–0.82; however, myxomatosis outbreaks were more prolonged, spanning more than twice as many trips. There was considerable information‐theoretic support (wAICc = 0.69) for the model in which exposure to myxomatosis affected survival during rabbit haemorrhagic disease outbreaks. Rabbits previously exposed to myxoma virus had lower survival during rabbit haemorrhagic disease outbreaks than rabbits never exposed to either virus. There was negligible support for the model in which previous exposure to rabbit haemorrhagic disease affected survival in myxomatosis outbreaks (wAICc < 0.01). Synthesis and applications. Our results indicate that biological control agents can have a greater impact than single‐pathogen challenge studies might suggest. Introducing additional biological control agents might therefore increase the mortality of rabbits beyond the additive effects of individual biological controls. Furthermore, our results show that by understanding and exploiting disease synergies, managers could increase the efficacy of biological controls for other invasive animals.

Rabbit haemorrhagic disease: Cross-protection and comparative pathogenicity of GI.2/RHDV2/b and GI.1b/RHDV lagoviruses in a challenge trial

European rabbits (Oryctolagus cuniculus) are severely affected by rabbit haemorrhagic disease (RHD). Caused by a lagovirus, the disease leads to losses in the rabbit industry and has implications for wildlife conservation. Past RHD outbreaks have been caused by GI.1/RHDV genotype viruses. A new virus belonging to the GI.2/RHDV2/b genotype emerged in 2010, quickly spreading and replacing the former in several countries; however, limited data are available on its pathogenicity and epidemiological factors. The present work extends these issues and evaluates cross-protection between both genotypes. Ninety-four and 88 domestic rabbits were challenged with GI.2/RHDV2/b and GI.1b/RHDV variant isolates, respectively. Cross-protection was determined by a second challenge on survivors with the corresponding strain. Mortality by GI.2/RHDV2/b was highly variable due to unknown individual factors, whereas mortality by GI.1b/RHDV was associated with age. Mortality in rabbits < 4 weeks old was 84%, higher than previously reported. Cross-protection was not identical between the two viruses because the ratio of mortality rate ratios for the first and second challenges was 3.80 ± 2.68 times higher for GI.2/RHDV2/b than it was for GI.1b/RHDV. Rabbit susceptibility to GI.2/RHDV2/b varied greatly and appeared to be modulated by the innate functionality of the immune response and/or its prompt activation by other pathogens. GI.1b/RHDV pathogenicity appeared to be associated with undetermined age-related factors. These results suggest that GI.2/RHDV2/b may interact with other pathogens at the population level but does not satisfactorily explain the GI.1b/RHDV virus’s quick replacement.

First Outbreak of Rabbit Haemorrhagic Disease in Rabbits in Finland

First Outbreak of Rabbit Haemorrhagic Disease in Rabbits in Finland

The importance of liver lesions and changes to biochemical and coagulation factors in the pathogenesis of RHD.

RHDV (rabbit haemorrhagic disease virus) is an etiologic factor of RHD (rabbit haemorrhagic disease), which is highly morbid and mortal viral infection of an adult European rabbit. Although three decades have passed since the first outbreak of rabbit haemorrhagic disease, the pathogenesis of RHD has still not been fully elucidated. It is known that RHDV replicates in the liver within the first hours following infection, causing necrotic and apoptotic cell death of hepatocytes. Anatomopathological changes are also observed in other organs of infected rabbits, i.e. lungs, spleen, kidneys, heart, as well as central nerve system. These changes leading to animals death are predominantly caused by systemic hemorrhagic diathesis with disseminated intravascular coagulation (DIC), appearing most likely as a consequence of liver cell loss through RHDV-induced apoptosis. In this paper, we presented previously described changes in biochemical and coagulation factors in RHDV infection.

Detection of the new emerging rabbit haemorrhagic disease type 2 virus (RHDV2) in Sicily from rabbit (Oryctolagus cuniculus) and Italian hare (Lepus corsicanus)

Rabbit haemorrhagic disease virus (RHDV), a member of the genus Lagovirus, causes rabbit haemorrhagic disease (RHD), a fatal hepatitis of rabbits, not previously reported in hares. Recently, a new RHDV-related virus emerged, called RHDV2. This lagovirus can cause RHD in rabbits and disease and mortality in Lepus capensis (Cape hare). Here we describe a case of RHDV2 infection in another hare species, Lepus corsicanus, during a concurrent RHD outbreak in a group of wild rabbits. The same RHDV2 strain infected rabbits and a hare, also causing a RHD-like syndrome in the latter. Our findings confirmed the capability of RHDV2 to infect hosts other than rabbits and improve the knowledge about the epidemiology and the host range of this new lagovirus.

Changes in intrapopulation resource use patterns of an endangered raptor in response to a disease-mediated crash in prey abundance

1. A long-standing question in ecology is how natural populations respond to a changing environment. Emergent optimal foraging theory-based models for individual variation go beyond the population level and predict how its individuals would respond to disturbances that produce changes in resource availability. 2. Evaluating variations in resource use patterns at the intrapopulation level in wild populations under changing environmental conditions would allow to further advance in the research on foraging ecology and evolution by gaining a better idea of the underlying mechanisms explaining trophic diversity. 3. In this study, we use a large spatio-temporal scale data set (western continental Europe, 1968-2006) on the diet of Bonelli's Eagle Aquila fasciata breeding pairs to analyse the predator trophic responses at the intrapopulation level to a prey population crash. In particular, we borrow metrics from studies on network structure and intrapopulation variation to understand how an emerging infectious disease [the rabbit haemorrhagic disease (RHD)] that caused the density of the eagle's primary prey (rabbit Oryctolagus cuniculus) to dramatically drop across Europe impacted on resource use patterns of this endangered raptor. 4. Following the major RHD outbreak, substantial changes in Bonelli's Eagle's diet diversity and organisation patterns at the intrapopulation level took place. Dietary variation among breeding pairs was larger after than before the outbreak. Before RHD, there were no clusters of pairs with similar diets, but significant clustering emerged after RHD. Moreover, diets at the pair level presented a nested pattern before RHD, but not after. 5. Here, we reveal how intrapopulation patterns of resource use can quantitatively and qualitatively vary, given drastic changes in resource availability. 6. For the first time, we show that a pathogen of a prey species can indirectly impact the intrapopulation patterns of resource use of an endangered predator.

Detection of rabbit haemorrhagic disease virus (RHDV) in nonspecific vertebrate hosts sympatric to the European wild rabbit (Oryctolagus cuniculus)

Since its detection in China in 1984, rabbit haemorrhagic disease (RHD) has been the subject of numerous studies. Yet, the evolutionary origin of rabbit haemorrhagic disease virus (RHDV) is still under debate. For example, some aspects related to the epidemiology of the disease are still unknown, such as where the virus is hosted between RHD outbreaks. To detect the presence of RHDV in rabbit-sympatric micromammals, 51 rodents (29 Mus spretus and 22 Apodemus sylvaticus) and 31 rabbits (Oryctolagus cuniculus) from the same location in central Spain were analyzed. In those samples in which the virus was detected, a fragment of the VP60 protein gene from the RHDV capsid was sequenced and the phylogenetic relationships between them and other strains of RHDV in the Iberian Peninsula were analyzed. In total, five viral strains were identified in A. sylvaticus, M. spretus and O. cuniculus. All strains were found to be well supported within the clade of RHDV found in rabbits in the Iberian Peninsula. Moreover, one of the strains was found in all three species under study, which suggests the capability of RHDV to infect other mammals apart from the rabbit which have not yet been investigated. The transmission of the virus is discussed as well as its ecoepidemiological implications.

Short-term responses of mammalian carnivores to a sudden collapse of rabbits in Mediterranean Spain

The European rabbit ( Oryctolagus cuniculus) is a key prey species for most Mediterranean predators in the Iberian Peninsula, including some endangered species such as the Iberian lynx ( Lynx pardinus). Rabbit populations in the Iberian Peninsula have collapsed since the arrival of rabbit haemorrhagic disease (RHD) in the late 1980s. We studied the dietary and numerical responses of five species of mammalian carnivores to this decline in the Doñana National Park (south-west Spain), where RHD arrived in 1990. Behavioural responses of the Iberian lynx, a rabbit specialist, were also studied through radio-tracking. All carnivores reduced rabbit intake with decreasing rabbit densities immediately after the initial RHD outbreak, though the level of reduction varied among species. Reductions in rabbit consumption were highest for the Eurasian badger ( Meles meles) and the red fox ( Vulpes vulpes), low for the genet ( Genetta genetta) and mongoose ( Herpestes ichneumon), and negligible for the Iberian lynx, thus confirming its strong dependence on rabbits for survival. The Iberian lynx social system was temporarily altered. Female lynxes increased their home range size and no subadult lynxes dispersed in the year following the rabbit crash, causing a temporal local increase of lynx density, which returned to previous values a year after the arrival of RHD. The red fox showed a negative numerical response, reducing its abundance following the rabbit decline. Despite the fact that rabbit consumption was reduced in most carnivores, the role of joint predation is discussed as a factor in the failure of rabbit recovery after this new disease.

Large‐scale spatio‐temporal shifts in the diet of a predator mediated by an emerging infectious disease of its main prey

AbstractAim To explore the influence of an emerging infectious disease (EID) affecting a prey species on the spatial patterns and temporal shifts in the diet of a predator over a large geographical scale. We reviewed studies on the diet of Bonelli’s eagles (Hieraaetus fasciatus) in order to determine the repercussions of the reduction in the density of its main prey, the rabbit (Oryctolagus cuniculus), caused by outbreaks of rabbit haemorrhagic disease (RHD) since 1988.Location Western continental Europe.Methods We compiled published and unpublished information on the diet of breeding Bonelli’s eagles from Portugal, Spain and France for a 39‐year study period (1968–2006). Nonparametric tests were used in order to analyse temporal shifts in diet composition and trophic diversity (H′) between the periods of ‘high’ (before outbreak of RHD) and ‘low’ rabbit density (after outbreak of RHD). A combination of hierarchical agglomerative clustering and non‐metric multidimensional scaling (NMDS) analyses were used to test for the existence of geographical patterns in the diet of Bonelli’s eagles in each period.Results The diet of the Bonelli’s eagle consisted of rabbit (28.5%), pigeons (24.0%), partridges (15.3%), ‘other birds’ (11.6%), ‘other mammals’ (7.1%), corvids (7.0%), and herptiles (6.4%). However, RHD had large consequences for its feeding ecology: the consumption of rabbits decreased by one‐third after the outbreak of RHD. Conversely, trophic diversity (H′) increased after outbreak of RHD. At the same time, the analyses showed clear geographical patterns in the diet of the Bonelli’s eagle before, but not after, RHD outbreak.Main conclusions Geographical patterns in the diet of the Bonelli’s eagle in western Europe seem to be driven mainly by spatio‐temporal variation in the abundance of rabbits and, to a lesser extent, by the local (territorial) environmental features conditioning the presence and density of alternative prey species. We show that an EID can disrupt predator–prey relationships at large spatial and temporal scales through a severe decline in the population of the main prey species. Hence we argue that strict guidelines should be drawn up to prevent human‐aided dissemination of ‘pathogen pollution’, which can threaten wildlife not only at the population and species level but also at the community and ecosystem scale.

European rabbit population trends and associated factors: a review of the situation in the Iberian Peninsula

ABSTRACT European rabbits are considered a keystone species in the Iberian Peninsula. Their populations have sharply declined over the past century, mainly due to habitat loss and the arrival of two viral diseases: myxomatosis in the 1950s and rabbit haemorrhagic disease (RHD) at the end of the 1980s. For the conservation of the Iberian Mediterranean ecosystem, it is important to determine whether rabbit populations are recovering two decades after the RHD outbreak, and to identify the factors associated with population recovery. Here, we review the current knowledge on recent rabbit population trends in the Iberian Peninsula and the factors associated with these trends. Although most rabbit populations are still declining in the Iberian Peninsula, a few seem to have recovered. In general, positive trends have been recorded in species‐friendly habitats characterized by non‐fragmented landscapes, interspersed patches of Mediterranean scrubland, good pastures and/or crops, soft soils that are suitable for warren construction and a Mediterranean climate with relatively high rainfall. Additionally, rabbits seem to be recovering better in areas where management practices (e.g. low hunting pressure, habitat management and predator control) are applied to increase their numbers. From these findings, it is possible to identify five broad objectives for rabbit conservation in the Iberian Peninsula. First, it is clearly necessary to establish a long‐term programme for monitoring rabbit abundance and trends on a large scale. Second, the conservation and restoration of open Mediterranean scrubland should be a priority for stabilizing and maintaining existing healthy rabbit populations. Third, despite the lack of experimental evidence, management activities aimed at increasing the quantity and quality of both refuge and food should continue to be implemented. Fourth, legislation on the timing of the hunting season should be revisited following recommendations made by scientists. Finally, experimental approaches are required to investigate whether the control of generalist predators is a successful strategy to allow rabbit populations to recover.

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

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.