A history of canine parvovirus in Australia: what can we learn?

Canine parvovirus (CPV) has been reported throughout the world since the late 1970s. Published information was reviewed to draw insights into the epidemiology, pathogenesis, diagnosis, treatment and outcomes of CPV disease in Australia and the role of scientific research on CPV occurrence, with key research discoveries and knowledge gaps identified. Australian researchers contributed substantially to early findings, including the first reported cases of parvoviral myocarditis, investigations into disease aetiopathogenesis, host and environmental risk factors and links between CPV and feline panleukopenia. Two of the world's first CPV serological surveys were conducted in Australia and a 1980 national veterinary survey of Australian and New Zealand dogs revealed 6824 suspected CPV cases and 1058 deaths. In 2010, an Australian national disease surveillance system was launched; 4940 CPV cases were reported between 2009 and 2014, although underreporting was likely. A 2017 study estimated national incidence to be 4.12 cases per 1000 dogs, and an annual case load of 20,110 based on 4219 CPV case reports in a survey of all Australian veterinary clinics, with a 23.5% response rate. CPV disease risk factors identified included socioeconomic disadvantage, geographical location (rural/remote), season (summer) and rainfall (recent rain and longer dry periods both increasing risk). Age <16 weeks was identified as a risk factor for vaccination failure. Important knowledge gaps exist regarding national canine and feline demographic and CPV case data, vaccination coverage and population immunity, CPV transmission between owned dogs and other carnivore populations in Australia and the most effective methods to control epizootics.     

Expression and Activity of Steroid Sulphatase in the Boar Testis

Oestrogens are essential for male fertility targeting the testicular-epididymal compartment. However, the underlying mechanisms are only vaguely known and species specificities must be considered. The boar has a remarkably high testicular-oestrogen output, with the biologically inactive oestrone-sulphate being the major oestrogen occurring in the testicular vein. In the boar testis and epididymis, activity of steroid sulphatase (StS) and oestrogen sulphotransferase has been demonstrated. Thus apart from their synthesis in Leydig cells, provision of biologically active free oestrone seems also to depend on the activity and localization of these enzymes. Our aim was to establish expression patterns and activity of StS in boar testis. Testes were randomly collected from healthy boars and allotted to five age groups, five animals in each, aged 50, 100, 150, 200 and 250 days. Three extra boars aged over 250 days were castrated to obtain fresh tissue for enzyme activity tests. Immunohistochemistry detected StS only in the cytoplasm of Leydig cells and – except for day-50 group in which 65.1 ± 4.9% (X ± SD) of the cells were positive – expression was constant with virtually all the cells staining positive. RT-PCR and in situ hybridization confirmed expression and localization of StS mRNA. The V _max and K _m value (X ± SD) for StS was 24.05 ± 0.3 fmol/s/μg protein and 2.15 ± 0.12 μ m . These data suggest that StS within the Leydig cells of the boar is involved in modulation of testicular oestrogen bioavailability and that the site of sulpho-conjugation is not the testis but a different compartment of the testes–epididymidis complex.