Fish health and disease

Knowledge of microbial, nutritional and environmental diseases of cultured bluefin tuna is limited. However, adult tunas appear to be relatively resistant to bacterial infections, even when subjected to trauma and other factors that predispose them to such infections (Munday et al. 2003). Table 50 shows the principal pathogens that infect bluefin tuna; more details are provided in Munday et al. (2003).

Table 50. Specific pathogens of bluefin tuna
VIRUSES
Iridoviruses
? Red seabream iridoviral (RSIV)
BACTERIA
? Aeromonas sp.
? Caligus elongatus
? Vibrio spp.
? Photobacterium damsela subsp. Piscida ? Mycobacterium marinum
PARASITES
Protozoa
? Goussia auxidis
? Uronema nigricans
Myxosporea
? Kudoa clupeidae
? Kudoa sp.
Monogenea
? Benedenia seriolae
? Caballerocotyla sp.
? Hexostoma sp.
? Metapseudaxine ventrosicula

? Nasicola sp.
? Neohexostoma sp.
? Sibitrema poonui
? Tristomella sp.
Digenea
? Anaplerurus thynnusi
? Aponurus lagunculus
? Atalostropiom sardae
? Bucephalopsis sibi
? Cardicola sp.
? Cetiotrema crassum
? Celiotrema thynni
? Colocyntotrema sp.
? Didymocylindrus filiformis
? Didymocystis sp.
? Didymocystoides semiglobularis ? Didyimoproblema fusiforme
? Didymozoon sp.
? Distomum clavatum
136 5 - TUNAS
? Hirudinella sp.
? Koellikerioides orientalis
? Kollikeria sp.
? Lescithaster gibbosus
? Lecithocladium excisum
? Lobatozoum multisacculatum
? Nematobothrium sp.
? Oesophagocystis sp.
? Prosorhynchoides sibi
? Rhipdocotyle sp.
? Sterrhurus imocavus
? Syncoelium filiferum
? Wedlia sp.
Cestoda
? Callitetrarhynchus gracilis
? Grillotia sp.
? Lacistorhyncus tenuis
? Nybelinia lingualis
? Pelichnibothrium sp.
? Tentacularia coryphaenae
? Tetraphyllidean larvae
Nematoda
? Anisakis sp.
? Contracaecum sp.
? Heptachona caudata
? Hysterothylacium sp.
? Oncophora melanocephala
? Sprirurida
Achantocephala
? Bolbosoma vasculosum
? Neorhadinorhyncus nudus
? Rhadinorhyncus pristis
Copepoda
? Brachiella thynni
? Caligus sp.
? Euryiphorus brachypterus
? Pennella filosa
? Pseudocynus appendiculatus
Young Pacific bluefin tuna are often infected with “red seabream iridovirus” but the disease never appears in those that are more than 1 year old. Sometimes mortality reaches 10% for young fish (Munday et al. 2003). Little was known about the health aspects of southern bluefin tuna when capture-based aquaculture began in 1990. Although it is probable that tuna can and do suffer from many of the commonly reported fish diseases, experience of them is limited, and treatment nearly impossible, due to the size of the cages used and the susceptibility of tuna to stress. It is known that water quality and general cleanliness are essential for tuna health. Aeromonas sp. infections have been reported in association with Caligus elongates damage to the eyes of southern bluefin tuna (Munday et al. 2003).
For several years, low levels of mortalities were recorded with an unexplained cause, subsequently identified by the late Dr Barry Munday in the University of Tasmania as the ciliate protozoan Uronema (www.sardi.sa.gov.au). The scuticociliate Uronema nigricans is an opportunistically parasitic marine ciliate known to cause disease in some aquacultural environments (Crosbie and Munday 1999). Parasitological and histological findings suggest that the parasites initially colonise the olfactory rosettes and travel along the olfactory nerves to invade the brain. Possible epidemiological factors involved in the pathogenesis of this disease include low water temperature (<18°C) and the immune status of the fish (Munday et al. 1997).
A parasitic blood fluke (Digenea: Sanguinicolidae) was identified in farmed tuna in South Australia in 1997 and was subsequently described as Cardicola forsteri (Cribb et al. 2000). Southern bluefin tuna are a new host species for blood flukes and C. forsteri is a newly described species (Colquitt et al. 2001). It was unclear if this blood fluke was causing a significant problem within the industry. Blood flukes are known to cause significant pathology in several other maricultured species (e.g. cultured seabass (Lates calcarifer) in Malaysia) and have caused mass mortality in Japanese amberjack juveniles, as reported by Ogawa and Fukudome (1994). Generally, the pathology observed in cultured southern bluefin tuna was not considered to be severe enough to lead to mortality. Histological examinations for eggs of
C. forsteri included gills, heart ventricles and other organs collected from wild and captive southern bluefin tuna. In infected farmed fish, fluke eggs impacted in the afferent filamentary blood vessels where they provoked a marked but variable inflammatory response, resulting in nodular gill lesions (Colquitt, Munday and Daintith 2001).
In April-May 1996 an extensive mortality was observed in Boston Bay (Port Lincoln, South Australia), where approximately 75% (1 700 tonnes) of the fish died. This coincided with an ocean surge and strong winds. Clinical symptoms included distress, while some of the dead fish showed large quantities of mucus flowing from their gills. Possible aetiological factors were considered to be microalgal toxicosis, hypoxia, smothering by suspended solids and hydrogen sulphide toxicity (Munday and Hallegraeff 1997). The ichthyotoxic raphidophyte flagellate Chattonella marina was successfully cultured from Boston Bay (South Australia), and could have been consistent with this mass mortality of southern bluefin tuna (Marshall and Hallegraeff 1999).
The use of oily baitfish as a source for captive tuna poses a number of problems. The presence of thiaminases [see note on thiamine on page 137] and oxidized lipids in baitfish has been, or is likely to be, responsible for nutritional problems in tuna (Munday et al. 2003). Indirect problems can occur when parasites (e.g. Kudoa) are present in trash fish (e.g. sardines); appropriate freezing procedures decrease the risk, as this kills all of the parasites (B. Jeffriess, pers. comm. 2002). Benign parasitical infestations are more common in the summer, when the warmer water temperatures that are especially important for tuna cultured in southern latitudes exist. Parasitic worms are rarely found in the flesh and though completely harmless to humans, the pin head sized white eggs they deposit are evidence of their presence and can severely affect the price of the tuna when sold to “sushi” restaurants.
The storage of the baitfish utilised for feeding tuna in captivity needs special attention. One study showed that in chilled storage the pilchards exhibited obvious deterioration within two days. Substantial peroxide values were found, and oxidised odours and flavours were clearly evident, after 4 days of chilled storage. In frozen storage, oxidation occurred after only one
month at a temperature of -20°C. Pilchards in which oxidation had commenced before freezing continued to oxidise in frozen storage (Fitz-Gerald and Bremner 1998). It was demonstrated that the oil in the pilchards readily oxidises; careful handling, chilling, freezing and storage procedures need to be adopted to provide a product that is nutritionally sound for captive tuna. Baitfish are also known to carry important viral diseases such as viral haemorrhagic septicaemia and pilchard herpes-virus (Munday et al. 2003).
In the early stages of Pacific bluefin tuna aquaculture in Japan, morbidity and mortality was reported to be caused by a shortage of thiamine [this is the most common form of vitamin deficiency in fish nutrition and is especially prevalent when raw aquatic animal products are used as feed, either solely or in combination with other ingredients (New 1987). This is particularly so when diets containing raw fish are not fed immediately after capture or manufacture, because thiaminase may partially or completely deactivate the thiamine originally present]. Some fish contain particularly high levels of thiaminase. At that time only Pacific saury (Cololabis saira) and/or Japanese anchovy (Engraulis japonicus) were fed to the tuna in Japan, resulting in a large reduction of the thiamine stores of the cultured fish. Now, several kinds of baitfish are fed to tuna in Japan and this disease no longer occurs (Munday et al. 2003).
During the processing and packing of harvested tuna in Malta, extracted organs were examined for any abnormalities or tissue changes. The organs examined (spleen, liver, stomach, intestine and kidney) were considered more as an indication of fish health status, since there was no evidence of morbidity (Peric 2003a).
Significant disease related mortality is best prevented by recognising and decreasing risk factors before they become a major problem. The Aquafin CRC, a strategic and proactive project in Australia (Aquafin CRC, 2001a,b,c,d,e,f) focuses on the development of tuna cell lines in order to have the capacity to culture viruses if these were to prove an issue in the future, either as part of grow-out activities or in the hatcheries as part of southern bluefin tuna propagation. It is a very important project because it provides, for the first time, a comprehensive review of the potential southern bluefin tuna health issues based on relevant published information and the existing tuna health database of the TBOASA (Tuna Boat Owner Association of South Australia). From this review it is intended that a qualitative assessment of the types of health risks and their potential impacts shall be tabulated, and recommendations made in regard to the likelihood/priority of the potential issue and R&D strategies appropriate to address them. The project started at the beginning of February 2002 and was expected to be completed at the beginning of May 2003. The main objectives were:
? to provide a qualitative fish health risk assessment for the tuna aquaculture industry in Australia;
? to review tuna health information and databases from the industry, research organizations and scientific literature;
? to identify areas of higher risk and propose management control measures for the industry, as well as research priorities; and
? to circulate the results of this southern bluefin tuna health risk assessment project (www.sardi.sa.gov.au).