Evidence of infection with Toxoplasma gondii and Neospora caninum in South Australia: using wild rabbits as a sentinel species.

OBJECTIVE: The aim of this study was to utilise wild rabbits (Oryctolagus cuniculus) as a sentinel species to study levels of environmental contamination with N. caninum and T. gondii in South Australia, and to examine associations with rainfall, climate and land use. DESIGN: Toxoplasma gondii (T. gondii), an apicomplexan parasite, causes the clinical disease toxoplasmosis, which can affect sheep as well as humans and many other animals. Neosporosis, the clinical disease caused by closely related Neospora caninum (N. caninum), causes abortions in cattle, with large economic impacts to cattle industries. METHODS: Aliquots of wild rabbit (Oryctolagus cuniculus) serum were obtained from twelve sites across South Australia over a period of eighteen years, with a total of 2114 samples. An in-house Modified Agglutination Test (MAT) was developed, and samples were screened for the specific antibodies against both T.gondii and N. caninum. RESULTS: Overall, 9.9% of samples screened for T. gondii tested positive and 6.1% of samples screened for N. caninum tested positive. There was no difference observed in seroprevalence of T.gondii specific antibodies between samples collected throughout summer, autumn, winter or spring. By contrast, a significantly higher (p=0.030) seroprevalence of N. caninum specific antibodies was observed in spring than any other season. T. gondii and N. caninum antibodies were discovered at sites across a broad area of South Australia, indicating these environments maybe infected with both parasites. CONCLUSION: Results provide evidence that suggests N. caninum oocysts may have different survival characteristics, such as varying tolerances to low relative humidity, than T. gondii oocysts.

Rabbit haemorrhagic disease: are Australian rabbits (Oryctolagus cuniculus) evolving resistance to infection with Czech CAPM 351 RHDV?

Rabbit haemorrhagic disease is a major tool for the management of introduced, wild rabbits in Australia. However, new evidence suggests that rabbits may be developing resistance to the disease. Rabbits sourced from wild populations in central and southeastern Australia, and domestic rabbits for comparison, were experimentally challenged with a low 60 ID50 oral dose of commercially available Czech CAPM 351 virus - the original strain released in Australia. Levels of resistance to infection were generally higher than for unselected domestic rabbits and also differed (0-73% infection rates) between wild populations. Resistance was lower in populations from cooler, wetter regions and also low in arid regions with the highest resistance seen within zones of moderate rainfall. These findings suggest the external influences of non-pathogenic calicivirus in cooler, wetter areas and poor recruitment in arid populations may influence the development rate of resistance in Australia.

The non-pathogenic Australian lagovirus RCV-A1 causes a prolonged infection and elicits partial cross-protection to rabbit haemorrhagic disease virus.

Two caliciviruses occur in Australian wild rabbits: rabbit calicivirus Australia 1 (RCV-A1) and rabbit haemorrhagic disease virus (RHDV), which is used in Australia as a biocontrol agent to reduce feral rabbit populations. There is concern that RCV-A1 acts as a natural vaccine and protects from lethal RHDV infection. To investigate this hypothesis, domestic rabbits were perorally infected with RCV-A1, monitored for 28 days and subsequently challenged with RHDV. We show that RCV-A1 causes a non-pathogenic infection and is shed in faeces for up to 7 days post-infection. RCV-A1 was detected in the bile 2 months post-inoculation, indicating a prolonged or possible persistent infection. All animals infected with RCV-A1 developed antibodies cross-reacting to RHDV. When challenged with RDHV, half of the rabbits (n=4) survived the infection. The results indicate that RCV-A1 is likely to persist in rabbit populations and can elicit partial cross-protection to lethal RHDV infection.

Monitoring the spread of rabbit hemorrhagic disease virus as a new biological agent for control of wild European rabbits in Australia.

Following the escape to the mainland of the rabbit hemorrhagic disease virus (RHDV) from Wardang Island off the coast of South Australia, a monitoring program was implemented over a 13 mo period, between October 1995 and October 1996 to determine the activity and rate of spread of the disease in the wild European rabbit (Oryctolagus cuniculus) population. All reports of dead rabbits were investigated. Whenever possible, liver and spleen tissue samples were collected from fresh carcasses and subsequently analysed for the presence of RHDV. Maximum rates of spread of rabbit hemorrhagic disease (RHD) in Australia ranged from 9 km/mo during summer to 414 km/mo in spring. New cases of RHD were moderate during late autumn and winter and peaked in spring. In summer the disease was rarely reported.