Document ID: chunk:federal_register_of_legislation:F2019L00106:body:0:p49
Version: federal_register_of_legislation:F2019L00106
Segment Type: other
Provision Reference: 
Character Range: 130752–133662

Reservoir in 1994 (Whitting et al., 1996). These historical outbreaks suggest that the distribution of EHNV in redfin has extended upstream in the Murrumbidgee River system (Whittington et al., 1996). It is highly likely that the upstream Murrumbidgee River, Googong Reservoir/Queanbeyan River (now extirpated) populations of Macquarie perch were exposed to the virus (Lintermans 2006b). It has also been detected in farmed rainbow trout populations on properties in New South Wales and Victoria during late-1980s and 1990s (Whittington et al., 1994; 1999). The movement of infected trout fingerlings containing a low number of individuals with a subclinical infection was probably the most common means of spread of EHNV within the aquaculture industry (Whittington et al. 2010).
The presence of EHNV is thought to be a major impediment to recovery of populations of Macquarie perch in the Australian Capital Territory (Lintermans 1991b) and it has been suggested that EHNV may have been a cause for the decline of Macquarie perch in Lake Eildon in Victoria (Langdon 1989b). Experimental work in the 1980s demonstrated that Macquarie perch was one of several species extremely susceptible to the disease with 100 per cent mortality (Langdon 1989a; 1989b). Other native fish species found experimentally to be susceptible to EHNV include silver perch, Murray cod, golden perch and mountain galaxias (Galaxias olidus), and other introduced fish species include Atlantic salmon and eastern gambusia (Langdon et al., 1986; Langdon 1989b; Gray et al., 2000).
EHNV is characterised by sudden high mortalities of fish displaying necrosis of the renal haematopoietic tissue, liver spleen and pancreas (Langdon & Humphrey 1987). EHNV is a fast spreading and robust virus. The mechanisms of spread are uncertain in redfin but are likely to include the movement of the virus on structures such as nets, boats and gear, movement of live fish or frozen bait fish by recreational fisherman, movement with migrating fish and transmission by piscivorous birds (Whittington et al., 1996). There may be an as yet undiscovered natural host that is responsible for infection of redfin, or redfin may simply amplify the infection in an ecosystem (Whittington & Hyatt 1998). Langdon (1989b) found EHNV retained infectivity after 113 days of dry storage and Whittington et al. (1996) found similar results after freezing fish carcasses for at least a year.
Given that EHNV is known to cause direct 100 per cent mortality to Macquarie perch (Langdon 1989a; 1989b) and could be also causing indirect mortality by severely disabling feeding and predator evasive abilities and is apparently highly virulent, past impacts on populations have likely been immediate and catastrophic and may have not been detected adequately due to insufficient awareness. It appears that redfin may be developing a resistance (or reducing infection rates)