Published: 10 August 2016
A Fish Health Laboratory, Department of Fisheries Western Australia, 3 Baron-Hay Court, South Perth, WA 6151, Australia
B Faculty of Science and Engineering, School of Science, Department of Environment and Agriculture, Curtin University, Bentley, WA 6102, Australia. Email: firstname.lastname@example.org
C Centre for Sustainable Tropical Fisheries and Aquaculture, College of Marine and Environmental Science, James Cook University, Cairns, Qld 4878, Australia. Email: email@example.com
Abalone species are important for recreational and commercial fisheries and aquaculture in many jurisdictions in Australia. Clinical infections with viral, bacterial and parasitic pathogens can cause significant losses of wild and cultured stock, and subclinical infections may result in decreased productivity and growth. Infections with abalone herpesviruses (AbHV), Vibrio spp. and parasites of the genus Perkinsus are of particular concern to Australian fisheries. Here we provide a brief overview of these three major pathogen groups and their diagnoses from an Australian perspective.
The protistan parasite Perkinsus olseni, was first described as a parasite of the abalone, Haliotis rubra, in the south of Australia1. P. olseni belongs to the order Perkinsida and is the causative agent of perkinsosis, a disease associated with extensive mortalities of molluscs worldwide2–5. P. olseni is included on the list of reportable disease of the World Organisation for Animal Health (OIE) because infections cause mass mortalities in oysters and clams and significant economic losses (http://www.oie.int/animal-health-in-the-world/oie-listed-diseases-2016/). P. olseni is also listed on the Network of Aquaculture Centres in Asia-Pacific (NACA). This parasite induces lesions that can impede the respiration, and other physiological processes such as growth and reproduction, sometimes leading to death, impacting fishery and aquaculture productivity6–8.
P. olseni has three main life stages. The trophozoite stage occurs in the tissues of the live host and proliferate by undergoing successive bipartitionning (schizogony) that yields up to 32 daughter cells (Figure 1)9,10. The rupture of the wall allows the liberation of immature trophozoites that will enlarge9,10. In the dying host, trophozoites gradually enlarge and become mature trophozoite or prezoosporangia. When released in the water column and under favourable environmental conditions, the prezoosporangia divide internally into hundreds of biflagellated ellipsoidal zoospores that are formed within the original cell wall and leave the zoosporangium via a discharge tube. The motile zoospores can then infect a new host. It is not yet well understood which stage is the most effective or principal stage for transmitting the disease in the natural environment11.
In the 1970s, soft white-yellow abscesses were observed in the flesh of the blacklip abalone Haliotis rubra collected in South Australia10. When clusters of Perkinsus cells are found near the surface of the abalone, they appear as a soft white nodule or microabscess10. Microabscesses develop to form brown spherical abscess or pustules up to 8 mm or more in diameter10. These abscesses are observed in the foot and muscle10. Identical lesions were observed in H. laevigata but lesions are absent in infected H. scalaris and H. cyclobates10. This parasite was associated with severe mortalities in H. laevigata wild populations in 1980s, leading to local extinction on the western shore of Gulf St Vincent, South Australia10,12. Outbreaks also occurred during the same period in H. laevigata aquaculture facilities in South Australia, when 40% of the stock died.
Mass mortalities of blacklip abalone (H. rubra) occurred from 1992 to 2002 along approximately 500 km of the NSW coastline between Port Stephens and Jervis Bay13. Histological examination of moribund abalone since 1992 and a survey of infection prevalence in abalone using Ray’s test in 2002, confirmed infections by a variant strain of P. olseni, suggesting that this parasite contributed to the mortalities observed13. Indeed, substantial tissue and organ damage occurred in abalone with high intensity of infection. Disruption of the gut epithelium and infarction in the gills suggested impairment to normal nutrient absorption and respiration14. There is some indication that stress such as that from high temperatures exacerbate the disease but the conditions under which the disease progresses are not well understood.
Perkinsus olseni was formally identified and reported in Western Australia in 2015 from wild greenlip abalone. Surveys of wild and cultured abalone stocks in WA are currently ongoing to evaluate the prevalence of this parasite and monitor any potential negative impacts.
Infections with herpes-like viruses resulting in the disease Abalone Viral Ganglioneuritis (AVG), were first identified and characterised in Australia around 2005 from Victorian land-based greenlip abalone (H. laevigata) culture facilities15. The disease is listed as reportable by the OIE and NACA and is characterised by marked inflammation and necrosis of nervous tissues (cerebral, pleuropedal and buccal ganglia, branches of the pedal nerve and peripheral nerves) in infected abalone15–17. Since their initial detection, abalone herpesvirus (AbHV) infections have been implicated in causing mass mortalities in wild abalone stocks in Victoria and in culture facilities in Tasmania, resulting in strict stock movement restrictions and enhanced biosecurity practices being enforced by jurisdictions15,16,18,19. Five genotypic variants of AbHV have now been identified from Australian Haliotis conicopora, H. laevigata and H. rubra populations, and experiments have confirmed that all five variants may cause disease and subsequent mortalities in these abalone species18,20,21.
Diagnosis of AbHV infections in abalone typically involves histopathological examination of neural tissues, electron microscopy and nucleic acid sequencing17,18,21,22. Rapid quantitative real-time PCR assays targeting the five Australian AbHV variants have been developed by the Fish Disease Laboratory at the Australian Animal Health Laboratory to aid in quickly assessing presence or absence of virus in abalone stocks for biosecurity and translocation protocols by relevant jurisdictions21,23.
Infections with Vibrio spp. have been implicated in causing severe mass mortalities in cultured abalone in numerous localities worldwide, including Australia24. These pathogens are generally considered opportunistic, causing acute infection and mortality in physically or environmentally stressed individuals25–27. The condition ‘Summer Mortality Syndrome’ observed in Australian greenlip (H. laevigata) and blacklip (H. rubra) abalone and their hybrids, refers to an increase in mortalities in association with increased water temperatures which promote infection with Vibrio species such as V. harveyi28.
Confirmative diagnosis for Vibrio spp. infection in abalone includes observing bacteria within affected tissues on histopathological examination of moribund abalone, isolation and culture of bacteria followed by matrix-assisted laser desorption ionisation time of flight mass spectrometry (MALDI-TOF) or DNA sequencing29.
Cecile Dang is a Principal Research Scientist with the Department of Fisheries Western Australia and heads the WA Fish Health Laboratory. Much of her research is focused on host/pathogen dynamics and immune response. She has worked extensively with diseases and parasites of wild and commercially important mollusc species.
Terrence L Miller is a Senior Research Scientist with the Department of Fisheries Western Australia and runs the molecular diagnostics section of the WA Fish Health Laboratory. His initial training was in the ecology and systematics of parasites of fish, but has broadened his research interests to include parasites and diseases of fish and crustaceans of commercial and recreational significance.
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