Rabbit hemorrhagic Disease
Rabbit hemorrhagic Disease
Rabbit hemorrhagic disease (RHD) can cause high economic losses in the rabbit meat and fur industry in case of epidemic occurrence. An outbreak has significant negative ecological impacts on wild rabbit populations and indirectly on their predators. RHD has been known since the 1980s.
The causative agent of rabbit haemorrhagic disease is RHD virus (RHDV), an unsheathed, single-stranded RNA virus of the virus family Caliciviridae (genus: Lagovirus). The virus is highly resistant outside the host. In 2010, the emergence of a new variant of the RHD virus was reported in France, referred to as RHD virus 2 (RHDV-2). Rabbit hemorrhagic disease (RHD) was first described in China in 1984. A few years later, an epidemic occurrence of this disease was also detected in Europe. A similar viral infection, also caused by a calicivirus of the genus Lagovirus, had previously been detected in brown hares under the name European brown hare syndrome (EBHS). The rabbit haemorrhagic disease virus (RHDV) is distributed worldwide; it occurs in Australia, New Zealand, America, Asia and Europe. One of the ways it has spread has been through the import/export of rabbit meat. The starting point for the spread of the virus in Australia was an island off the Australian continent. There, the virus was used experimentally to decimate the wild rabbit population. The host range includes domestic and wild rabbits(Oryctolagus cuniculus). Classical RHD virus is highly host specific and is not contagious to humans or other mammals. In contrast to the "classical" RHDV, field hares are also susceptible to RHDV-2. RHDV-2 affects young animals from the age of about 1 month. In Germany, cases of RHDV-2 infection were first detected in 2014, in Austria in 2016. RHDV infections in domestic and wild rabbits are occasionally reported in Austria. Two cases of RHDV-2 infections have been diagnosed by us so far (Styria, Salzburg). The last known detection of Classical RHD was in wild rabbits from the Danube Island in Vienna at the end of 2016.
The pathogen is transmitted directly from rabbit to rabbit (via secretions and excretions) and indirectly via contaminated inanimate and animate vectors (e.g. contaminated water, food, clothing, shoes, objects, hands, blood-sucking insects). The pathogen can be ingested orally, nasally, conjunctivally, and parenterally via bloodsucking insects. The incubation period is 1-3 days. Diseased animals usually die after 12-72 hours. Young animals up to an age of approx. 2 months do not contract classical RHDV infection (juvenile resistance), whereas they can contract RHDV-2 infection from an age of 1 month.
The disease is characterized by a mostly peracute course associated with necrotizing hepatitis (liver inflammation) and generalized coagulopathy. The peracute/acute course is characterized by sudden deaths without clinical symptoms or by acute onset of lassitude, loss of appetite, high fever (> 40 °C), bloody nasal discharge, and occasionally respiratory and neurological symptoms (e.g., opisthotonos, paralyses, ataxia). The subacute/chronic course , on the other hand, is rare and characterized by milder clinical symptoms: icterus, loss of appetite, lethargy. Convalescence after the disease is rather atypical.
Control and prevention of RHD is by vaccination prophylaxis and prevention of introduction into rabbit herds. Monovalent RHDV vaccines have been reported to provide additional protection against severe clinical manifestations of RHDV-2 infection after basic immunization followed by bi-annual booster vaccinations. Since autumn 2016, a RHDV-2 vaccine has been licensed for rabbits for fattening throughout Europe.
The main findings at autopsy in deceased rabbits are a dry, brittle, scale-coloured liver, congestive organs, minor haemorrhages, splenic swelling and pulmonary oedema.
Histologically, acute hepatitis due to virus-induced death of numerous liver cells and acute congestive organs with accompanying hemorrhage due to coagulopathy and microthrombus formation predominated. On the basis of autopsy and histological findings, the diagnosis of RHD is relatively certain, but it is not possible to distinguish between RHDV and RHDV-2. The distinction is made by molecular biological methods.
In case of suspicion, it is recommended to send the carcass to the Institute of Veterinary Medicine Mödling for pathological examination. Differentiation between RHDV and RHDV-2 can then be made by further molecular biological examination (Institute of Clinical Virology, University of Veterinary Medicine Vienna).
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