1. Introduction
In late 2005, an acute disease, abalone viral ganglioneuritis
(AVG), associated with very high mortality (up to 100%) in
farmed abalone, occurred on land-based farms in Victoria, Australia
(Hooper et al., 2007). In May 2006, the disease was discovered in
wild abalone, initially in the vicinity of the affected farms, and it
subsequently spread along the Victorian coast-line. The initial mortalities
on-farm involved blacklip abalone (Haliotis rubra), greenlip
abalone (Haliotis laevigata) as well as hybrids of these two species.
The precise extent of mortality in wild populations is difficult to
determine partly due to the cryptic habitat of, in particular, young
abalone; reported mortality in wild abalone at different locations
has ranged between 10% and 90%. Following an initial investigation
by State authorities, the clinical history, clinical signs of disease,
and pathology were well-documented for this outbreak (Hooper
et al., 2007), and, based on electron microscopic examination, an
abalone herpes virus (AbHV) was identified as the putative aetiological
agent (Tan et al., 2008). Currently, the disease continues
to spread, albeit at a slow rate, along Victorian coastal waters, does
not appear to be seasonal, and threatens abalone stocks throughout
southern Australia. The disease appears to be restricted to abalone