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Article << Previous     |     Next >>   Contents Vol 31(6)

Rabbit Haemorrhagic Disease Virus: serological evidence of a non-virulent RHDV-like virus in south-western Australia

John S. Bruce A, Laurie E. Twigg B

A Protection Services, Department of Agriculture, Western Australia, 444 Albany Highway, Albany, WA 6330, Australia.
B Vertebrate Pest Research Section, Department of Agriculture, Western Australia, 100 Bougainvillea Avenue, Forrestfield, WA 6058, Australia.
 
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Abstract

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.

   
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