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Rabbit haemorrhagic disease type 2 (RHDV2 or GI.21) is a highly infectious, usually fatal, disease of lagomorphs which has been present in the UK since 20102 and is now commonly diagnosed throughout the country.3 Similar to the rest of Europe, RHDV2 infection has been detected in European brown hares ( Lepus europaeus ) in England,4 although in a limited number and possibly representing a spill-over event from rabbits. …

WE read with interest the recent In Practice article ‘Diagnosis and prevention of rabbit viral haemorrhagic disease 2’.1 The article adds weight to the letter by Sarah Elliott and Richard Saunders ( VR , 11 November 2017, vol 181, p 516) urging vets to help breeders to vaccinate their rabbits, and provides information about the myxomatosis and VHD (viral haemorrhagic disease) map that is available online. Our website (www.harcourt-brown.co.uk) provides information about rabbit haemorrhagic disease (RHD), including the new variant …

Serological data on myxoma virus, rabbit haemorrhagic disease (RHD) virus and RHD-like viruses in juvenile rabbits (Oryctolagus cuniculus) trapped in 1995, 1996 and 1997 in two areas of France were analysed. For each disease, the effects of bodyweight, year, month and seropositivity for the other disease were modelled by using logistic regressions. In one area, a model including RHD seropositivity was selected to explain the myxoma virus seropositivity. Models including myxoma virus seropositivity were selected to explain the RHD seropositivity in both areas, and the odds of a rabbit being seropositive to both viruses were 5.1 and 8.4 times higher than the odds of a rabbit being seronegative to myxoma virus and seropositive to RHD. The year and bodyweight had significant effects for myxomatosis in one area and for RHD in both areas.

THE emergence of rabbit haemorrhagic disease (RHDV) virus 2 (RHDV2) in Europe (Le Gall-Recule and others 2011) has been associated with declines in wild rabbit ( Oryctolagus cuniculus ) populations (Delibes-Mateos and others 2014, Guerrero-Casado and others 2016, Monterroso and others 2016) previously exposed to RHDV. All RHDV genotypes of the G1–G6 genogroups, hereafter referred to as RHDV, belong to the same antigenic serotype (Le Gall-Recule and others 2013). The unique antigenic nature of RHDV2 (Le Gall-Recule and others 2013, Barcena and others 2015) is reflected in its capacity to kill rabbits vaccinated against RHDV (Le Gall-Recule and others 2011, Dalton and others 2014, McGowan and Choudhury 2016) and its rapid spread in Europe (Dalton and others 2012, Le Gall-Recule and others 2013, Abrantes and others 2014, Baily and others 2014, Westcott and others 2014) and Australia (Hall and others 2015) with associated peaks in RHD epizootics. The capacity of RHDV2 to overcome RHDV immunity, reported so far only in vaccinated rabbits, may partly explain the observed decline in wild rabbit populations where RHDV had already been circulating. Here the authors report the infection by RHDV2 of three Australian wild rabbits with a known RHDV antibody-positive serological history, with clinical signs of RHD visible in one fresh carcase, the first documented cases of RHDV-immune wild rabbits being infected with and/or succumbing to RHDV2 infection. This demonstrated capacity of RHDV2 to overcome immunity derived from natural infections with RHDV supports an immunogenic difference between RHDV and RHDV2 at the level of serotype. With the emergence and spread of RHDV2 …

A serological survey of 238 rabbits for antirabbit haemorrhagic disease virus (RHDV) antibodies was made in an industrial rabbitry where no signs of the disease had been reported for four years. Seroconversion was repeatedly detected and was due to a calicivirus antigenically related to RHDV but without its pathogenicity. There was a seroprevalence of 33.3 per cent among young animals at weaning at 31 days old, 27.6 per cent at five to seven days after weaning, 56.1 per cent at 13 to 14 days after weaning, 90.3 per cent at 19 to 20 days and 100 per cent at 32 to 33 days after weaning, and all the breeding rabbits were seropositive. In the last group and in the young at weaning, the anti-RHDV antibodies were mainly class IgG, but they were IgM and IgA at 13 to 14 days after weaning. In older fattening rabbits, there was a decrease of IgM and IgA and an increase of IgG confirmed seroconversion without any specific signs of rabbit haemorrhagic disease. On the basis of these results, the probable time of infection of the meat rabbits with this non-pathogenic virus was immediately after weaning.

Rabbit haemorrhagic disease was reported for the first time in the United Kingdom in 1992, and there followed four further small localised outbreaks, all in the south of England. Investigation has revealed no definitive mechanism for the introduction of the disease but it is considered that it probably originated from the near continent. The possibility of the transmission of the virus across the Channel by aerosol, birds and south coast ferry traffic is discussed, particularly with respect to the 1993 outbreaks of the disease in Kent and East Sussex. There may be implications for infection of wild rabbits, although preliminary investigation has shown no direct evidence of the disease in them.

During 1992 and 1993, outbreaks of an acute, highly fatal disease mainly affecting adult rabbits were observed in Tunisia. The clinical and pathological findings were consistent with rabbit haemorrhagic disease. A monoclonal antibody designated PG4G3 specific for surface determinants of the rabbit haemorrhagic disease virus was used to identify the aetiological agent by ELISA and by colloidal gold immunoelectron microscopy; a haemagglutination test and conventional immunoelectron microscopy were also used. The results confirmed the first recorded cases of the disease in Tunisia.

Haemagglutination and ELISA tests, and negative contrast electron microscopy, have been used to identify rabbit haemorrhagic disease virus in naturally occurring cases of the disease and in experimentally infected rabbits in the United Kingdom. Haemagglutination tests alone are not satisfactory for the diagnosis because non-haemagglutinating isolates of the virus, otherwise indistinguishable from others, have been found in some outbreaks. Haemagglutination inhibition tests have shown that a proportion of both commercial laboratory and wild rabbits in the UK are seropositive to the virus although they have not been associated with clinical disease. This observation, made previously in other parts of Europe, may indicate the longstanding circulation of a related but non-pathogenic strain of virus. Naturally occurring antibody appears to afford a high degree of protection against experimental challenge with virulent virus.

IN their short communication summarised on p 589 of this issue, Meyer and others (2011) give us a timely reminder of the changing pathologies that may be associated with feline calicivirus (FCV) infection. This highly variable pathogen is typically associated with oral ulceration and signs of upper respiratory tract disease (Gaskell and others 2006). However, some strains may be non-virulent, while others have been associated with lameness. In their article, Meyer and others (2011) point to a more recently described and sinister presentation for this virus, namely virulent systemic disease (FCV-associated VSD). This disease was first described by researchers from the University of California (Pedersen and others 2000). In this landmark paper for this virus, the authors carefully described an outbreak of disease in 1998 affecting six cats, variably associated with pyrexia, oedema, skin ulceration and jaundice, with a fatality rate (death and euthanasia) of approximately 33 per cent. The outbreak, which was initially termed haemorrhagic-like fever owing to certain similarities with rabbit haemorrhagic disease virus, seemed to start with the hospitalisation of a cat from a rescue shelter for an upper respiratory tract infection. Subsequently, the infection was probably transmitted through direct and indirect contact in the veterinary practice. Feline calicivirus was isolated from nasal swabs and, more unusually, blood from the worst affected cats. Despite the fact that FCV exists at a high prevalence in many populations of healthy cats, and as such can be an innocent bystander in cats …

WE wish to report the detection of a new variant of rabbit haemorrhagic disease virus (RHDV) (Lagovirus, Caliciviridae) which is circulating in France and has been causing high mortality in domestic and wild rabbit populations since the end of the summer of 2010. Rabbit haemorrhagic disease (RHD)

FURTHER to the recent reports of rabbit haemorrhagic disease virus variant strain 2 (RHDV-2) in Great Britain (Baily and others 2014, Westcott and others 2014) we wish to report an outbreak that occurred last year in wild rabbits on the island of Skokholm. Skokholm lies 2.5 miles off the coast of south-west Wales. It is a Site of Special Scientific Interest owned and managed by the Wildlife Trust of south and west Wales, and it is an internationally important breeding site for seabirds, in particular Manx shearwaters ( Puffinus puffinus ) and storm petrels ( Hydrobates pelagicus ). There are no …

RABBIT haemorrhagic disease virus (RHDV) causes an acute, fulminating and generally fatal disease in the European rabbit ( Oryctolagus cuniculus ). It was first discovered in China in 1984 and then confirmed in the UK in 1992, at …

A novel, recombinant myxoma virus-rabbit haemorrhagic disease virus (RHDV) vaccine has been developed for the prevention of myxomatosis and rabbit haemorrhagic disease (RHD). A number of laboratory studies are described illustrating the safety and efficacy of the vaccine following subcutaneous administration in laboratory rabbits from four weeks of age onwards. In these studies, both vaccinated and unvaccinated control rabbits were challenged using pathogenic strains of RHD and myxoma viruses, and 100 per cent of the vaccinated rabbits were protected against both myxomatosis and RHD.