Table of contents

What is AVG?

Abalone Viral Ganglioneuritis (AVG) disease is caused by infection with abalone herpes virus (AbHV) also know as haliotid herpesvirus 1 (HaHV-1). AVG has caused significant mortality in wild and farmed abalone in western Victoria. This virus affects the nervous system of abalone and results in curling of the foot and swelling of the mouth, leading to weakness and ultimately death of abalone. AVG affecgs Blacklip Abalone (Haliotis rubra), Greenlip Abalone (H. laevigata), Brownlip Abalone (H. conicopora) and hybrids (H. rybra X H. laevigata). HaHV can be detected in the absence of clinical disease, allowing surveillance and monitoring during disease outbreaks, and subsequent monitoring and zoning for management purposes.

AVG has been reported in Victoria and Tasmania. In Victoria, AVG has been observed in farmed and wild abalone. In Tasmania, the disease has not been observed in wild abalone populations. However, AbHV has been detected in wild abalone, abalone held in live abalone holding facilities and abalone farms in Victoria. AVG was eradicated from Victorian abalone farms in 2006, but in 2011 it was distributed in wild abalone populations along more than 200 km of coastline in Western Victoria, from Discovery Bay to near Cape Otway (Anon, 2014).

A significant outbreak of AVG occurred in wild and farmed abalone in Victoria during December 2005/January 2006. There was no reoccurrence of AVG in wild abalone from 2010 until May 2021, when a diver working off the coast of Cape Nelson, Portland, Victoria observed dead blacklip abalone that were confirmed to be infected by AVG. A Control Area has been enforced encompassing reefs where infected abalone have been identified through a surveillance program.

What is the impact of AVG on the Australian Abalone industry?

AVG contributed to a reduced wild-catch fishery from 1614 tonnes in 2004/05 to a low of 827 tonnes in 2010/11 in Victoria. Subsequently, there has been a recovery in volume of production to 1196 tonnes in 2012/13 (Corbeil etdseyt6666 al., 2016). Natural recruitment has been observed on reefs previously infected with AVG. HaHV was successfully eradicated from farms following AVG outbreaks by completely destocking and thoroughly decontaminating the facilities. These facilities were restocked with abalone without the recurrence of AVG.

What was done in the past to solve the AVG issue?

There is no treatment for AVG. Diseased abalone and infectious wastes are the main source of HaHV in the environment and are the greatest risk for spreading the infection. The virus can spread through water from infected abalone or abalone product (offal, shells or mucus), and fishing equipment (i.e., wetsuits, anchors, rock lobster pots and ropes) that has come into contact with infected abalone or sea bottom habitat.

The spread of AVG from infected areas is minimised through establishing quarantine areas (i.e., infected, restricted, control and free areas) and implementation and enforcement of movement controls (i.e., bans and restrictions). As HaHV is transmitted through the water column and via other vectors, it is highly unlikely that the spread of HaHV can be controlled in natural systems. Consequently, spread of the disease can only be managed through containment, control and zoning, and enforcement. Eradication of HaHV has been achieved through destocking, decontamination, and fallowing procedures in semi-closed (i.e., pump ashore) abalone farms and closed live holding facilities.

The FRDC’s role

The FRDC has supported abalone fishers and farmers to better understand the epidemiology of HaHV, develop diagnostic tests, determine the recovery of abalone stocks, develop biosecurity plans, understand immune response to HaHV, and investigate the genetic response of wild abalone populations.

Related projects

2008-077 Tactical Research Fund: Developing cost-effective and reliable Industry-based surveys to advise re-opening and conservative management of abalone populations on AVG-affected reefs

2009-075 Mark St. J. Crane, Serge Corbeil, Lynette Williams and Vin Gannon. 2012. Determining the susceptibility of remnant populations of abalone previously exposed to AVG

2009-032 Corbeil, S., Williams, LM., Warner, S., Fegan, M., Moody, NJG., Mohammad, I., Ellard, K., Caraguel, C., Deveney, M., Cowley J. and Crane M. 2014. Aquatic Animal Health Subprogram: Characterisation of abalone herpeslike virus infections in abalone.

2011-033 Ierodiaconou D., Miller A.D., Rattray, A., Weeks A.R., Gorfine H.K., Peeters H., Van Rooyen A., Jalali M.A., Bell J.D., Worthington, D. 2014. Spatial patterns, landscape genetics and post virus recovery of blacklip abalone, Haliotis rubra (Leach), in the western commercial fishing zone of Victoria.

2012-236 Tactical Research Fund: Developing the decision process for setting the TAC for abalone in Victoria, particularly with reference to recovery of AVG-impacted reefs.

2013-001 Corbeil, S., Williams, L. M., Cowley, J.A., Moody, N. J. G., Crane, M. 2016. Aquatic Animal Health Subprogram: Determination of susceptibility of various abalone species and populations to the various known AbHV genotypes.

2017-117: Identification of differentially expressed innate immune genes in the New Zealand paua (Haliotis iris) and the Australian hybrid abalone (H. laevigata X H. rubra) upon immersion challenge with the abalone herpesvirus-1 (HaHV).

2018-057: Population genomic assessment of Australian blacklip abalone for abalone viral ganglioneuritis (AVG) resistance.

References

Anon. Department of Agriculture. 2014. Disease strategy: Abalone viral ganglioneuritis (Version 1.0). In: Australian Aquatic Veterinary Emergency Plan (AQUAVETPLAN), Australian Government Department of Agriculture, Canberra, ACT. 52pp.

Corbeil, S., Williams, L. M., Cowley, J.A., Moody, N. J. G., Crane, M. 2016. Aquatic Animal Health Subprogram: Determination of susceptibility of various abalone species and populations to the various known AbHV genotypes. FRDC project 2013-001. 36 pp.

Further information

Australian Aquatic Veterinary Emergency Plan