Abstract

The impact of rabbit haemorrhagic disease (RHD) on free-ranging rabbit populations, their immunological response, and the abundance of insect vectors, were monitored in detail in the southern agricultural region of Western Australia. Further, a broad-scale rabbit monitoring program was also established at nine locations across a rainfall gradient in the southern half of Western Australia to monitor the natural arrival, or controlled release, of rabbit haemorrhagic disease virus (RHDV). Changes in rabbit populations and the immune status of RHDV antibodies were monitored in these areas to enable further understanding of the epidemiology of RHD, and its impact on rabbit numbers.

RHDV had the greatest impact on rabbit populations in the arid and semi-arid areas (<360 mm per annum), where rabbit numbers were reduced to, and maintained at, 10% of pre-RHD levels. Conversely, the effects of RHD on rabbit numbers in higher-rainfall areas (360–700 mm per annum) were highly variable and patchy, and in some instances RHD had little apparent impact. In higher-rainfall areas where RHD was effective, rabbit numbers were reduced by 50–78%. RHDV was first confirmed in the southern agricultural region of Western Australia in early September 1996, ~1 year after its escape from Wardang Island, South Australia. At the detailed monitoring site (485 mm rainfall per annum), rabbit numbers declined by 65% within 2 weeks of RHDV being detected. However, ~70% of the remaining rabbits had antibodies against RHDV, indicating that they had survived the disease. There was also a demographic shift towards young rabbits (<1 year old) at this time. Further, even though there was no clinical evidence of RHD recurring in this population during the 3-year study, the presence of IgM antibodies in some rabbits well after the initial epizootic suggests that low-level transient outbreaks of RHDV had occurred at this site. Although the impact of these low-level outbreaks on population dynamics were uncertain, rabbit numbers at this site had recovered to pre-RHD levels within two breeding seasons.

The abundance of insect vectors on the detailed monitoring site was similar between years with and without RHD outbreaks. Thus, the failure of RHDV to develop clinical disease on this site after the initial epizootic was unlikely to have been caused by the lack of suitable transmission vectors. The apparent lack of disease recurrence at the detailed monitoring site may have been caused by the presence of a non-pathogenic form of RHDV, which seemed to impart at least some cross-immunity to RHDV in these rabbits. The presence of RHDV also caused a shift in the timing of natural epizootics of myxomatosis at this site.