Use of ELISAs in field studies of rabbit haemorrhagic disease (RHD) in Australia

Cooke, Brian; Robinson, Anthony J.; Merchant, J. C.; Nardin, Alessandra; Capucci, Lorenzo

doi:10.1017/s0950268899003994

Cited by 105 publications

(157 citation statements)

References 22 publications

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“…Evidence of this is the emergence of the decreasingly homogenous new strains with altered antigenic and genetic features, showing different tropism and pathogenicity for the target species. The strains detected in relatively short period of time, which demonstrate new characteristics, vide phenotypic HA-negative RHDV variant, antigenic and genetic RHDVa variants, and the new American and French RHDV variants, are examples of this phenomenon (5,6,8,17,24,27,34,36). This may be due to the effect of environment, the use of vaccination, or the process of evolution.…”

Section: Discussionmentioning

confidence: 99%

“…Sporadic RHD cases have been described in North Africa (30), in Mexico (19), Cuba, the USA (10) and most recently in Canada (9). In Australia and New Zealand RHD was deliberately introduced in the mid-nineties in order to reduce the population of rabbits (8,14,15,16,36). Rabbit haemorrgahic disease virus (RHDV), a prototype of the genus Lagovirus of the Caliciviridae family, is the infectious agent responsible for RHD.…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak

Fitzner

2014

Bulletin of the Veterinary Institute in Pulawy

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The field outbreak of RHD that occurred late summer 2012 on a small-scale rabbit-rearing operation in Poland and the usefulness of techniques for RHD virus diagnosis are described. During the epizootic, the overall mortality rate of rabbits older than two months was 77%. Eight liver specimens collected from dead unvaccinated rabbits (aged 3-5 months) underwent virological examinations. RHDV specific antigen was detected in two out of eight liver homogenates by haemagglutination (HA) test and ELISA, one of the two being negative in HA assay. However the presence of genetic material of RHD virus was confirmed by RT-PCR and real-time RT-PCR in all liver samples tested. Based on antigen reactivity in ELISA and sequencing of PCR amplicons of the VP60 gene, the RHDVa subtype strain was identified as the cause of infection. The partial genome sequence of a field isolate (STR 2012), comprising the C-terminus of the polymerase gene and the full capsid protein gene, revealed 91% nucleotide homology to reference FRG89 RHDV isolate and 97% to strain Triptis representing the RHDVa variant. Serological evidence of an RHD outbreak in the STR rabbit-rearing operation was confirmed in a serum sample collected from an unvaccinated surviving rabbit. A cross-reactivity examination of RHDV positive serum revealed a decrease in HI titre against the STR 2012 field antigen, and a decrease in the RHDVa control antigen as compared to classic RHDV.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak

Fitzner

2014

Bulletin of the Veterinary Institute in Pulawy

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“…Since all dead rabbits were more than two months old, it is likely that detected antibodies were not of maternal origin [13]. Furthermore, because antibodies detected by the VP60-ELISA are known to appear 5-6 days after infection [2,16] yet RHD generally kills the rabbits 2-3 days after infection, it seems most likely that these antibodies were present before the rabbit's exposure to the virus that killed them, even though such antibodies would normally be expected to offer the rabbits some protection against the development of lethal RHD [2,16].…”

Section: Discussionmentioning

confidence: 99%

“…It is therefore important to isolate and characterise these strains, and to validate immunological tests to improve the classification of antibodies induced by these different viral strains. Some authors have already proposed criteria to differentiate antibodies due to RHDV from antibodies due to RHDV-like strains [13]. These suggested criteria, based on similarities in the profiles of antibody patterns in individual rabbits, need to take into account the differences Figure 1.…”

Section: Discussionmentioning

confidence: 99%

“…Because there was insufficient serum remaining after the first test, we tested the liver homogenate of 16 of the rabbits with ELISA tests that detect anti-RHD isotypes IgM, IgA and IgG directly in organ extracts. These ELISA use specific anti-rabbit IgM, IgA and IgG monoclonal antibodies (Mabs) and the methods employed are fully described elsewhere [5,13].…”

Section: Antibody Detectionmentioning

confidence: 99%

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Serological evidence for a non-protective RHDV-like virus

et al. 2005

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-The data were recorded during a Rabbit haemorrhagic disease outbreak that occurred in France in 2001 in a wild population of rabbits that we have been monitoring since 2000. These data suggested the existence of non-protective antibodies due to a putative RHDV-like virus. Twentyone blood and 22 liver samples were taken from the 26 corpses of recently dead rabbits that were found. RHDV was found in all liver samples. A first screening for RHD antibodies, carried out using an ELISA based on the detection of VP60-RHDV antigen, showed that 20 of the rabbits were seropositive. Moreover, we determined antibody titres for 13 of these 20 seropositive samples. All were ≥ 1/400. Such titres normally indicate antibody levels sufficient to confer protection to all known RHDV or RHDV-like strains. For 16 samples, we determined whether these rabbits had died of a chronic or an acute form of the disease, by employing monoclonal antibody (Mabs) -based differential ELISA. All had died of an acute form of RHD. Because the antibodies detected by this VP60-ELISA test are known to appear 5-6 days after infection and since acute RHD generally kills the rabbits 2-3 days after infection, we assumed that the detected antibodies must have been present before the exposure to the virus that killed these rabbits. A second detection of antibodies was made with Mabs that are specific for RHDV. The results were negative, showing that the antibodies detected with the VP60 ELISA test were not specific for RHDV. We sequenced a portion of the VP60 gene of viruses isolated in 17 rabbits. All RHDV isolates were very similar to the RHDV strains commonly isolated in France during this period, suggesting that this viral strain was not a putative variant that is not neutralised by antibodies. Therefore we conclude that the detected antibodies were probably due to a RHDV-like virus that induces the production of detectable but non-protective antibodies.

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RHDV2 outbreak reduces survival and juvenile recruitment, causing European rabbit population collapse

Letty,

Besnard,

Chatelain

et al. 2024

Ecosphere

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Infectious diseases can cause considerable mortality in vertebrate populations, especially when a new pathogen emerges. Quantifying the impact of diseases on wild populations and dissecting the underlying mechanisms requires longitudinal individual monitoring combining demographic and epidemiologic data. Such longitudinal population studies are rare. Rabbit hemorrhagic disease (RHD) is one of the main causes of the decline in European wild rabbit (Oryctolagus cuniculus) populations. A new genotype of RHD virus (RHDV), called RHDV2 or GI.2, emerged in 2010, posing a new threat to previously weakened populations, particularly as this virus can infect individuals already immune to classical RHDV strains. Taking advantage of intensive monitoring from 2009 to 2014 by physical captures and microchip detections of a semi‐captive population of rabbits, we finely assessed the demographic impact of an initial RHDV2 outbreak that occurred in the population and identified the most affected demographic parameters. A multi‐event modeling analysis revealed decreased survival in both juveniles and adults in 2011 and 2012, suggesting an RHDV2 outbreak for two consecutive years. The short‐term survival benefit of vaccination against classical RHDV strains only during these years, and the recovery of carcasses with RHDV2 detection, supported this hypothesis. Variations in population vaccination coverage also explain the difference in adult survival between the two years of the outbreak. And the transient protective effect of vaccination could explain the prolonged duration of the outbreak. A brief episode of myxomatosis in 2011 seems to have had only a limited impact on the population. During outbreak years, in individuals not recently vaccinated, monthly juvenile survival crashed (0.55), and annual adult survival was three times lower than in normal years (0.21 vs. 0.69). The combination of successive juvenile and adult survival estimates for unvaccinated rabbits during the outbreak years resulted in a very low recruitment rate in the breeding population. Finally, RHDV2 outbreaks appear to have caused mortalities comparable to those caused by older classical RHDV strains and may have a strong demographic impact on wild populations of European rabbit. This work highlights the importance of long‐term observational and experimental studies to better understand the impact of epidemics on animal populations.

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Use of ELISAs in field studies of rabbit haemorrhagic disease (RHD) in Australia

Cited by 105 publications

References 22 publications

Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak

Evaluation of the usefulness of laboratory diagnostic methods in RHD outbreak

Serological evidence for a non-protective RHDV-like virus

RHDV2 outbreak reduces survival and juvenile recruitment, causing European rabbit population collapse

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