Diseases of Tunas

Journal of Fish Diseases 2003, 26, 187–206Review Diseases of tunas, Thunnus spp. B L Munday1, Y Sawada2, T Cribb3 and C J Hayward3 1 School of Human Life Sciences, University of Tasmania, Launceston, Tasmania, Australia 2 Fisheries Laboratory, Kinki University, Kushimoto, Wakayama, Japan 3 Department of Microbiology and Parasitology, University of Queensland, Brisbane, Queensland, Australia Abstract Much is known about those aspects of tuna health which can be studied in wild populations, e.g. helminth parasites. However, because aquaculture of these species is in its infancy, knowledge of microbial, nutritional and environmental diseases is limited. This review is an attempt to bring together the available information on those diseases of Thunnus spp. which cause significant morbidity, mortality or economic loss. In doing so it has become clear that much more research needs to be undertaken on the physiology of the species (southern, northern and Pacific bluefin tuna) currently used in aquaculture in order for the pathogenesis of some conditions to be properly understood. Attempts at hatchery culture of Pacific bluefin tuna has indicated that Thunnus spp. will be problematic to hatch and propagate. Keywords: diseases, parasites, pathology, pathophysiology, Thunnus spp., tuna. Introduction Tunas of the genusThunnus are very important commercial species which have, until recently, been exclusively wild-caught (Kailola, Williams, Stewart, Reichelt, McNee & Grieve 1993). However, the drastic reduction in stocks resulting from uncontrolled harvesting has led to the imposition of stringent quotas for certain species and concurrent Correspondence B L Munday, School of Human Life Sciences, University of Tasmania, Locked Bag 1320, Launceston, Tasmania 7250, Australia (e-mail [email protected]) establishment of aquaculture of some of these species (Lee 1998). There is little information on diseases of these fish and this review is an attempt to assemble this information in one place for the use of interested parties. Both pathological and pathophysiological conditions will be addressed. Tunas are superb athletes and a number of species maintain stable body temperatures by having relatively high metabolic rates complemented by the use of heat-exchange mechanisms. Some species have been extensively studied at the physiological level, despite the practical problems involved in working with such fish (reviewed by Brill 1996; Farrell 1996; Korsmeyer, Dewar, Lai & Graham 1996). These studies have provided a sound basis for understanding pathophysiological conditions encountered in these species but more work is required, especially in southern bluefin tuna, Thunnus maccoyii Castlenau, which is the basis for the Australian tuna aquaculture industry. With regard to pathology, there is little published information available with the exception of parasitological studies which have mainly been undertaken for parasite taxonomical studies or identification of discrete stocks of Thunnus spp. (Yamaguti 1970; Jones 1991a; Williams & Bunkley-Williams 1996). It is notable that adult tunas appear to be relatively resistant to bacterial infections even when subjected to trauma and other factors likely to predispose to such infections. This review is based on the published literature supplemented with unpublished data from the authors and colleagues. The diseases are divided into those of infectious and non-infectious origins with appropriate sub-divisions. Ó 2003 Blackwell Publishing Ltd 187 Journal of Fish Diseases 2003, 26, 187–206 B L Munday et al. Diseases of tunas Infectious diseases Virus diseases Red sea bream iridoviral infection Aetiology. The disease is caused by red sea bream iridovirus (RSIV) which is a member of a recently recognized group of very pathogenic viruses affecting marine species in the Asian region (Miyata, Matsuno, Jung, Danayadol & Miyazaki 1997). Whereas many fish iridoviruses belong to the genus Ranavirus (Hyatt, Gould, Zupanovic, Cunningham, Hengstberger, Whittington, Kattenbelt & Coupar 2000), RSIV does not. Young Pacific bluefin tuna, Thunnus orientalis (Temminck & Schegel), are often infected with this virus, but the disease never appears in bluefin tuna more than 1 year of age. Occurrence of the disease is restricted to periods of higher water temperature (>24 °C). Sometimes the mortality reaches some tens of percent for young fish. Clinical signs. Infected fish have dark body colour and anorexia. If the fish do not die during the acute phase of the disease they become emaciated and die later. Pathology. As in other fish species, basophilic, hypertrophied cells (probably leucocytes) are observed in sections of spleen from diseased Pacific bluefin tuna. Epidemiology. Among tunas, this infection has only been reported in Pacific bluefin tuna (Kawakami & Nakajima 2002). Net cages for young wild-caught tuna are often sited near cages containing other fish which are susceptible to this virus. Therefore, it is likely that wild-caught young tuna for aquaculture, which are not infected at the time of capture, become infected by being caged alongside other cultured fish. Diagnosis. The histopathological picture of enlarged cells in the spleen, liver, kidney and gills which stain strongly with Giemsa is very characteristic of RSIV infection. Further confirmation can be obtained by demonstrating iridovirus virions by electron microscopy, culture of the virus in RTG-2, CHSE-214, FHM, BF-2 or KRE-3 cells at 20–25 °C, detection of specific antibody by immunofluorescence using monoclonal antibodies and detection of specific genomic sequences by PCR (Inouye, Yamano, Maeno, Nakajima, Matsuoka, Wada & Sorimachi 1992;Nakajima, Maeno, Yokoyama, Kaji & Manabe 1998; OshiÓ 2003 Blackwell Publishing Ltd ma, Hata, Hirasawa, Ohtaka, Hirono, Aoki & Yamashita 1998). Treatment. There is no available treatment. Prevention. Apart from normal hygienic precautions, especially siting tuna cages well away from other aquaculture species such as red sea bream, Chrysophrys major (Temminck & Schlegel), and yellowtail, Seriola quinqueradiata Temminck & Schlegel, there are no current specific control measures for the disease. However, promising vaccination trials have been reported (Nakajima, Maeno, Honda, Yokoyama, Tooriyama & Manabe 1999; Nakai & Nakajima 2002). Bacterial diseases Opportunistic bacterial infections Aetiology. Aeromonas sp. infections have been reported in association with Caligus elongatus damage to the eyes of southern bluefin tuna (Rough, Lester & Reuter 1999). Buchanan (2002) and R. Reuter (personal communication) have reported a variety of Aeromonas and Vibrio spp. in the kidney and other internal organs of southern bluefin tuna, especially those which have suffered trauma. Clinical signs. Rough et al. (1999) reported dissolution of the lens and consequent loss of the eye in Caligus elongatus infections. In instances of external trauma there may be large wounds which do not heal and the fish eventually die, presumably from a combination of bacteraemia and osmoregulatory failure. Epidemiology. The organisms concerned are normal environmental inhabitants which are able to colonize wounds resulting from mechanical or parasitic trauma. Diagnosis. Isolation of the organisms from the orbit or kidney is regarded as diagnostic. However, isolation of such bacteria from superficial wounds may only indicate contamination from the water column. Treatment. It is difficult to treat captive tuna and it is doubtful if severely affected animals would respond to therapy. Prevention. The prevalence and severity of superficial wounds can be reduced by careful handling of the fish. At present, C. elongatus infections are not a sufficient problem to warrant treatment but this may be necessary in the future to reduce morbidity. 188 The method of transmission of infection is unknown. It is possible that the tuna could have eaten a fish which itself had mycobacteriosis. Sawada. Reuter (personal communication) has noted coccidial bodies in the liver of this species. Treatment and prevention. There are a number of granulomatous diseases of marine fish which can be difficult to differentiate. damsela subsp. Rough & Hawkesford (1997) reported an encephalitis in young adult southern bluefin tuna caused by Uronema nigricans. care must be taken not to include fish with tuberculosis in the diet. Mycobacteriosis or piscine tuberculosis Aetiology. Unidentified scuticociliates have caused significant mortalities of larval Pacific bluefin tuna at 14–18 days post-hatch in hatcheries in Japan (Miyashita & Kumai 2002.Journal of Fish Diseases 2003. from the South Pacific were infected. Jones (1990) found 98% (140 of 143) of albacore. Protozoan diseases Coccidiosis Aetiology. Bacilli within the granulomas were Gram positive and stained with modified Ziehl–Neelsen stain. Epidemiology. phosphoreum by isolating the organism from the kidneys of diseased fish. and an individual yellowfin tuna. Only Goussia auxidis has been reported from tunas. As their record was not their own work. Scuticociliate infection Aetiology. alalunga (Bonnaterre). damsela subsp. Diagnosis. 26. piscicida in a single northern bluefin tuna. and such a report has not appeared in the mainstream scientific literature. Peric (2002) described the spleen of the tuna as being enlarged with a rough surface. Hamaguchi & Kusuda (1992) confirmed experimental infections with P. Diagnosis. Epidemiology. unpublished data). Clinical and pathological findings. He found no infection in 11 southern bluefin tuna although R. The reported very low prevalence of pasteurellosis in northern bluefin tuna would not warrant attempts at treatment or specific prophylaxis. T. Biavati & Manera (1991) reported a granulomatous peritonitis. there were granulomas composed predominantly of epithelioid cells and fibroblasts. nigricans in southern bluefin tuna. Jones (1990) reported that oocysts occurred in both the liver and spleen where they produced minimal host response. Epidemiology. pseudotuberculosis. histologically. The detection of short. The latter can be differentiated from the first two on the basis that the organisms are Gram negative but the other two require isolation and identification of the causal bacteria. As most cultured tuna are currently fed raw baitfish. infections Aetiology. The macroscopic lesions are not diagnostic as such granulomas can be caused by a variety of agents such as Mycobacterium or Nocardia spp. Hamaguchi & Kusuda (1992) reported on experimental infections of Pacific bluefin tuna with P. Pathology. The cause of putative tuberculosis reported in a single northern bluefin tuna (Biavati & Manera 1991) is not known. e. T. The authors believed that the diagnosis was more likely to be mycobacteriosis than nocardiosis. thynnus (Bonnaterre). Otherwise it most likely became infected from the environment as aquatic mycobacteria are capable of existing as environmental organisms. Treatment and prevention. Pasteurellosis is essentially a warmwater (20–25 °C) disease and as the causative organism does not survive for long outside the host. T. Watts. plump Gram-negative bacteria should enable a presumptive diagnosis but a definitive diagnosis requires isolation and identification of P. 187–206 B L Munday et al. However. piscicida infection). The cut surface showed multiple granulomas which. Clinical signs. mycobacteriosis and nocardiosis. it is possible that their citation actually applies to U. Treatment and prevention. Transmission is presumed to be lateral between fish (AQIS 1999). Ó 2003 Blackwell Publishing Ltd 189 . Y. Peric (2002) reported lesions consistent with Photobacterium damsela subsp. Williams & Bunkley-Williams (1996) reported an apparently similar condition in northern bluefin tuna in the Pacific. Diseases of tunas Photobacterium spp.g. No clinical signs have been reported. Munday. albacares (Bonnaterre). O’Donoghue. He indicated that the lesions were similar to those seen in sparids with chronic pasteurellosis (P. Histologically. Not required. most isolates from marine species are Mycobacterium marinum (Austin & Austin 1987). piscicida. phosphoreum. contained small numbers of short plump rods. Treatment is not practicable. Pathology. Typically. Epidemiology. In the case of infection of 14-day post-hatch Pacific bluefin tuna larvae. It is not clear whether the higher temperature prevents proliferation of the parasite or if higher temperatures Figure 1 Brain of southern bluefin tuna showing presence of Uronema nigricans (arrows) containing food vacuoles. It is helpful to increase the water exchange rate in larval rearing tanks and. unpublished data) and have decreased from about 5% in captive fish in 1993 to 1. personal communication) and the tolerance of larval and juvenile tuna to copper is unknown.L. Treatment. It is not known what predisposes the olfactory rosette to colonization by Uronema. approximately half of the larvae died within 3 days (Y. 187–206 B L Munday et al. Copper treatment has been found to be effective for scuticociliate infections of many fish which are reared in tanks in Japan. The parasites preferentially invade the epidermis and muscle of tuna larvae. The reduction in prevalence of the disease in recent years appears to be associated with improved undercage environmental conditions. Cases of Ôswimmer syndromeÕ can be diagnosed by demonstrating Uronema in wet preparations or sections of brain from affected fish. Burke & Munday (1996) developed a fluorescent antibody stain for specific identification of U. but water temperature appears to be an important variable because the disease does not occur when the water temperature is above 18 °C (Munday et al.34% in 1995 and <1% in 2001. turn light blue and swim vigorously around the cage. the removal of dead fish is necessary. unpublished data). 1) there is no host response except where the meninges are involved. Rough. Ó 2003 Blackwell Publishing Ltd 190 . Morbidity and mortality rates are comparable (B. Usually. Diseases of tunas Clinical signs.M. such fish come to the surface. Treatment is not practicable for adult tuna reared in open sea cages. Note lack of host response (PAS. nigricans. In Japan. 1997). Eventually. Watts. lymphocytic responses are frequent in the olfactory nerves and rosettes. Adult southern bluefin tuna with Uronema encephalitis suffer from the so-called Ôswimmer syndromeÕ. Diagnosis. bar ¼ 50 lm). Miyashita. However. The smaller larvae showed the heaviest mortality and signs of infection ceased at 18 days post-hatch. However. Pathology. Scuticociliate infection of larval/juvenile tuna is diagnosed by demonstrating the parasites in wet preparations or tissue sections. In adult southern bluefin tuna pathology is restricted to the olfactory system and brain. Munday & K. The build-up of organic matter which occurs in hatcheries is conducive to the development of high concentrations of scuticociliates and outbreaks of disease.Journal of Fish Diseases 2003. In the case of the Ôswimmer syndromeÕ it is believed that the scuticociliates proliferate in the undercage sediment and invade the olfactory rosette of the fish when water passes through the nares during olfaction. 1997). this concentration of copper ions is achieved by the use of a simple electrolytic apparatus which consists of copper electrodes installed in the pipework carrying the influent water. they cease compulsive swimming and tend to alternately sink and rise to the surface until they finally sink and die (Munday et al. copper ions in the range of 50–80 ppb concentration are effective. In the case of larval Pacific bluefin tuna. larval and juvenile fish are less tolerant to copper ions than adult fish (S. a higher water temperature of 28 °C has been found to be effective in reducing losses. of course. Although parasites containing food vacuoles can be found in the brain (Fig. Sawada. 26. 9 (K. Pathology. Khattra. Siddall & Xiao 2001). clupeidae in poorly identified Thunnus spp. Similar lesions because of an unidentified Kudoa sp. (Williams & Bunkley-Williams 1996). unpublished data). Lester. it is conceivable that these prey species could be alternative hosts. Prevention is by improved hygiene/ husbandry. 187–206 B L Munday et al. These will be discussed here. Metazoan infections As given in Table 1. Bartholomew. K. infection of northern and southern bluefin tuna producing lesions in the musculature Aetiology.8–10.Journal of Fish Diseases 2003. Hedrick. crumena in albacore was reported as 5% (J.6 · 7. Histologically. especially the intercostal nerves. yel- measure 6. Munday. obesus (Lowe). 2). Neither treatment nor prevention are practicable. Clinical signs. Harshbarger. crumena) and 4. Clinical signs and pathology. Feist.0 lm and have six shell valves each containing one polar capsule (Lom & Dykova 1992).3–6. the myxosporean spores are found aggregated in the cystic structures and usually produce minimal host response. Epidemiology. 26. El-Matbouli. it is the postmortem liquefaction of the muscle caused by the release of proteases from the parasites that is the most dramatic result of the infection (Ogawa 1996). Treatment and prevention. Andree. Histologically the cysts are found to consist of numerous Kudoa spores surrounded by a fibrous capsule (Fig. nigricans densities. many metazoans infect Thunnus spp. Harshbarger. Infections have also been reported in southern bluefin tuna in South Australia (Rough 2000) and wild fish caught off the New South Wales coast where the prevalence of about 1% affected fish was a cause of commercial loss (B. 191 . crustaceans and salps (Kailola et al. Treatment and prevention. Typical myxosporean spores can be easily found in wet preparations or histological sections of affected muscles. it may be pertinent that Crosbie (1996) found that the maximum U.4–5.5 · 8. Kudoa nova spores measure 5. which were achieved during the exponential phase of cultured organisms. 1993). possibly. An unidentified. The infection in southern bluefin tuna produces white cysts 1–10 mm in diameter which are apparently in the muscle (J. T.) can be seen in wet preparations or histological sections. for which life cycles are known. Kudoa sp.8 lm and have four shell valves each containing one polar capsule. This suggests that the effect of high water temperatures on the organisms may be the more important mechanism. Hoffman. As most juvenile tuna consume invertebrates such as squid and crustaceans (Kailola et al. type 3) infecting southern bluefin tuna. Neither treatment nor prevention is practicable. Prevention. while with heavy infections cysts may be visible in the musculature. However. have been reported in southern bluefin tuna and Langdon (1990) suggested that the parasite could be K. Postmortem liquefaction of muscle due to myxosporean infections Aetiology. the reader needs to be aware that. this seems unlikely. Most myxosporeans. capsalid monogenean (Rough 2000. Diseases of tunas accelerate the fish’s development to the juvenile stage at which they develop higher tolerance toUronema spp. personal communication). but only a few are of health and/or economic importance.5– 9. personal communication. Typical Kudoa spores measuring 7. The infections described by Langdon (1990) were in southern bluefin tuna caught off southwestern Western Australia when the fish would have been 1–3 years of age and feeding on cephalopods. nova. Hallett. Kent et al. Diagnosis. Desser. Epidemiology. Hexacapsula neothunni spores Ó 2003 Blackwell Publishing Ltd Monogenean infection of gills Aetiology. Hexacapsula neothunni in albacore.0 lm (Kudoa sp. lowfin tuna and bigeye tuna.5 · 9.C.2 · 11. Kudoa nova in bigeye tuna and. 1993). Palenzeula. Rough 2000) although Langdon (1990) produced evidence to suggest that most. Diagnosis. but as it does not produce myoliquefaction. Longshaw. have a two-host cycle with the myxosporean in a fish and an actinosporean in an invertebrate (Kent. The prevalence of K.L. Table 1 may still contain contentious citations. cysts in southern bluefin tuna were in peripheral nerves. while an effort has been made to identify errors in records of parasites of tunas. Additionally. crumena in a yellowfin tuna. if not all. Devlin. None reported. were lower at 30 °C than at 10–25 °C. The parasites produce no clinical signs and. (2001) reported K.C. PBT. YFT SBT YFT BET BET. Sibitrema poonui Tristomella interrupta Tristomella nozawae Tristomella onchidiocotyle Udonella caligorum Zeuxapta taylori Digenea Anaplerurus thynnusi Angionematoborium cephalodomus Aponurus lagunculus Atalostroppion sardae Botulus microporus Brachyphallus parvus Bucephalopsis sibi Cardicola ahi Cardicola forsteri Cetiotrema crassum Coeliotrema thynni Colocyntotrema sp. 187–206 B L Munday et al. Decemtestis dollfusi Dermatodidymocystis indicus Dermatodidymocystis vivipira Dermatodidymocystis viviparoides Ó 2003 Blackwell Publishing Ltd 192 . Rough (2000) Williams & Bunkley-Williams (1996) Nikolaeva & Parukhin (1968) Williams & Bunkley-Williams (1996) Yamaguti (1970) Cribb et al. NBT NBT NBT BET. Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Harshbarger pers. Kuhnia thunni Metapseudaxine ventrosicula Nasicola hogansi Nasicola klawei Neohexostoma euthynni Neohexostoma extensicaudatum Neohexostoma robustum Neohexostoma thunninae Neohexostoma sp. Areotestis sibi Benedenia seriolae Caballerocotyla abidjani Caballerocotyla albsmithi Caballerocotyla biparasitica Caballerocotyla goueri Caballerocotyla magronum Caballerocotyla paucispinosa Caballerocotyla pseudomagronum Caballerocotyla verrucosa Caballerocotyla sp. Williams & Bunkley-Williams (1996) Langdon (1990) Pozdnyakov (1990) Pozdnyakov (1990) Kohn & Cohen (1998) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Murugesh (1995) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990). SBT YFT NBT BET. (2000) Manter (1970) Yamaguti (1938). Capsala foliacea Capsala gotoi Capsala neothunni Capsala thynni Hexostoma acutum Hexostoma albsmithi Hexostoma dissimile Hexostoma grossum Hexostoma sibi Hexostoma thynni Hexostoma sp. Rough (2000) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Williams & Bunkley-Williams (1996) Payne (1990) Srivastava & Sahai (1978) Nikolaeva & Parukhin (1968) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996).YFT BET. BET. PBT Alb. Diseases of tunas Table 1 Metazoan parasites of Thunnus spp. YFT NBT Alb BET SBT YFT Alb. YFT NBT Alb. YFT NBT LTT. BET. YFT BET. Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Williams & Bunkley-Williams (1996) Pozdnyakov (1990). NBT NBT BET.YFT PBT. SBT. YFT SBT SBT Alb. Species infected Reference Alb. BET. Rough (2000) Young (1970) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Williams & Bunkley-Williams (1996) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Murugesh (1995) Wheeler & Beverley-Burton (1987) Walters (1980).YFT NBT. Parasite Myxosporea Hexacapsula neothunni Kudoa Kudoa Kudoa Kudoa clupeidae crumena nova sp. Pozdnyakov (1990) Rough (2000) Ahmad (1983) Nikolaeva & Dubina (1978) Yamaguti (1970) Yamaguti (1970) Monogenea Allopseudaxine sp.YFT YFT NBT BET NBT SBT. NBT NBT PBT BET BET. NBT. YFT BET. comm.YFT YFT Alb.YFT BET YFT PBT BET. 26.BFT. YFT BET.Journal of Fish Diseases 2003. SBT LTT BET. NBT YFT YFT PBT YFT PBT SBT. YFT BET. NBT.YFT LTT. YFT Arai & Matsumoto (1953). BET.YFT BET. NBT. NBT. NBT NBT BET NBT YFT YFT NBT Alb. PBT. BET. Nikolaeva & Dubina (1985). Dollfus (1952) Yamaguti (1971) Dollfus (1952) Dollfus (1952) Yamaguti (1938) Didymocystis thynni Didymocystis wedli Didymocystoides alalongae Didymocystoides bifasciatus Didymocystoides buccalis Didymocystoides oesophagicola Didymocystoides opercularis Didymocystoides pectoralis Didymocystoides semiglobularis Didymocystoides superpalati Didymonaja branchialis Didymoproblema fusiforme Didymostoma bipartitum Didymosulcus aahi Didymosulcus dimidiatus Didymosulcus katsuwonicola Didymozoon filicolle Didymozoon longicolle Didymozoon pretiosus Didymozoon thynni Dinurus breviductus Distomum clavatum Ectenurus lepidocybii Hirudinella ahi Hirudinella clavata Hirudinella fusca Hirudinella marina Hirudinella oxysoma Hirudinella poirieri Hirudinella spinulosa Alb. Dollfus (1952). SBT. YFT Alb PBT NBT Alb. Nikolaeva & Dubina (1985) Yamaguti (1970) Ariola (1902) Nikolaeva & Dubina (1985). Nikolaeva & Dubina (1985). YFT Alb. Williams & Bunkley-Williams (1996) Ariola (1902). NBT YFT Alb Alb Alb Ó 2003 Blackwell Publishing Ltd 193 . YFT PBT PBT YFT Alb. Yamaguti (1970). Ishii (1935). BET. YFT Alb BET. YFT PBT. Diseases of tunas Table 1 Continued Parasite Didymocylindrus filiformis Didymocystis acanthocybii Didymocystis alalongae Didymocystis bifurcata Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis Didymocystis crassa dissimilis guernei irregularis katsuwonicola lanceolata macrorchis nasalis oesophagicola opercularis orbitalis ovata palati philobranchia philobranchiarca poonui reniformis rotunditestis semiglobularis soleiformis spirocauda superpalati Species infected PBT YFT Alb. LTT BET. Murugesh & Madhavi (1995) Ishii (1935) Yamaguti (1971) Dollfus (1952) Yamaguti (1970) Ishii (1935) Dollfus (1952) Dollfus (1952) Yamaguti (1970) Yamaguti (1970). NBT. BET. YFT Alb YFT Alb BET PBT Alb. 187–206 B L Munday et al. Yamaguti (1971). BET LTT. Williams & Bunkley-Williams (1996). YFT PBT NBT Alb YFT PBT Alb Alb BET LTT. 26. Yamaguti (1934). YFT Alb YFT. YFT Alb. LTT.BET Alb. LTT. Rough (2000) Yamaguti (1938). Murugesh & Madhavi (1995) Dollfus (1952). YFT PBT BET. Williams & Bunkley-Williams (1996) Ishii (1935) Williams & Bunkley-Williams (1996) Yamaguti (1970) Yamaguti (1970).Journal of Fish Diseases 2003. SBT Alb. BET. Murugesh & Madhavi (1995) Williams & Bunkley-Williams (1996) Yamaguti (1970) Williams & Bunkley-Williams (1996) Yamaguti (1971) Yamaguti (1970) Yamaguti (1971) Williams & Bunkley-Williams (1996) Pozdnyakov (1987a) Ishii (1935) Ariola (1902) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Ishii (1935) Ishii (1935). NBT. NBT. Murugesh & Madhavi (1995). PBT. Williams & Bunkley-Williams (1996) Yamaguti (1970). BET. BET. PBT YFT Alb. YFT Reference Ishii (1935) Williams & Bunkley-Williams (1996) Yamaguti (1970) Yamaguti (1970). YFT BET NBT Alb. Ku & Shen (1965) Yamaguti (1970) Yamaguti (1970).LTT. PBT. Murugesh & Madhavi (1995) Yamaguti (1938) Yamaguti (1970) Ishii (1935). Rough (2000) Ariola (1902). Williams & Bunkley-Williams (1996) Taschenberg (1879) Korotaeva & Korjakovtzeva (1983) Linton (1901) Korotaeva & Korjakovtzeva (1983) Yamaguti (1970) Yamaguti (1971) Linton (1940). YFT YFT Alb. SBT YFT. Dollfus (1952) Nikolaeva & Dubina (1985) Dollfus (1942). Rough (2000) Srivastava & Sahai (1978) Nikolaeva & Dubina (1985) Yamaguti (1970) Hafeezullah (1971) Nikolaeva & Parukhin (1968). NBT. Dollfus (1952) Nikolaeva & Dubina (1985) Nikolaeva & Dubina (1985) Yamaguti (1934). Jones (1991a) Dollfus (1942) Williams & Bunkley-Williams (1996) Rough (2000) Williams & Bunkley-Williams (1996) Schmidt (1986). YFT BET. YFT Alb.Journal of Fish Diseases 2003. BFT. SBT. NBT. YFT YFT Alb Alb YFT PBT PBT NBT NBT. YFT BET Alb. PBT. Opisthorchinematobothrium nephrodomus Opisthorchinematobothrium parathunni Orbitonematobothrium perioculare Phyllodistomum thunni Platocystis alalongae Platocystis meridionalis Platocystis sp. NBT YFT Alb Alb. YFT NBT. Bussieras & Baudin-Laurencin (1973). 187–206 B L Munday et al. LTT. YFT BET. YFT BET. Diseases of tunas Table 1 Continued Parasite Hirudinella ventricosa Koellikerioides apicalis Koellikerioides externogastricus Koellikerioides internogastricus Koellikerioides intestinalis Koellikerioides orientalis Koellikerioides splenalis ¨llikeria abdominalis Ko ¨llikeria bipartita Ko ¨llikeria globosa Ko ¨llikeria orientalis Ko ¨llikeria pylorica Ko ¨llikeria reniformis Ko ¨llikeria retrorbitalis Ko ¨llikeria submaxillaris Ko Lecithaster gibbosus Lecithocladium excisum Lobatozoum multisacculatum Metanematobothrium guernei Nematobothrium latum Nematobothrium sp. Williams & Bunkley-Williams (1996) Yamaguti (1970) Yamaguti (1970) Williams & Bunkley-Williams (1996) Nikolaeva & Dubina (1978) Yamaguti (1970) Yamaguti (1970) Baudin-Laurencin & Richard (1973) Yamaguti (1938) Pozdnyakov (1987b) Nikolaeva & Parukhin (1968) Yamaguti (1940) Eckmann (1932) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996). YFT YFT YFT Alb. Williams & Bunkley-Williams (1996) Yamaguti (1971). BET YFT YFT. Prosorhynchoides sibi Rhipidocotyle pentagonum Rhipidocotyle septpapillata Sterrhurus imocavus Syncoelium filiferum Umatrema indica Univietellodidymocystis lingualis Univietellodidymocystis neothunni Uroproctinella attenuata Uroproctinella spinulosa Wedlia bipartita Wedlia lingualis Wedlia musseliusae Wedlia orientalis Yamaguticystis ariellii Cestoda Callitetrarhynchus gracilis Dasyrhynchus talismani Echeneibothrium sp. Bussieras & Baudin-Laurencin (1973) Linton (1940). YFT YFT YFT. Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Rough (2000) Ó 2003 Blackwell Publishing Ltd 194 . Baudin-Laurencin (1971) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Bussieras & Baudin-Laurencin (1973). NBT. YFT NBT NBT PBT Alb Alb BET. Williams & Bunkley-Williams (1996) Ishii (1935). NBT. PBT Alb. Williams & Bunkley-Williams (1996). YFT NBT Alb SBT YFT YFT. NBT. PBT Alb SBT Reference Gibson & Bray (1977). 26. NBT. Pelichnibothrium speciosum Pseudobothrium grimaldi Pterobothrium heteracanthum Species infected Alb. YFT BET PBT BET. Grillotia sp. YFT Alb. BET. Neonematobothrioides poonui Neophrodidymotrema ahi Oesophagocystis sp. Rough (2000) Yamaguti (1970) Yamaguti (1970) Yamaguti (1970) Yamaguti (1970) Pozdnyakov (1992) Nikolaeva (1988) Yamaguti (1970) Yamaguti (1971). Shen (1990) Yamaguti (1970) Ishii (1935) Yamaguti (1970) Yamaguti (1970) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Ishii (1935) Yamaguti (1938) Dollfus (1952) Nikolaeva & Dubina (1985). YFT BET BET. PBT BET YFT PBT Alb BET BET. NBT. Gymnorhynchus gigas Hepatoxylon trichiuri Lacistorhynchus tenuis Monorygma grimaldi Nybelinia lingualis Nybelinia sp. PBT YFT Alb. Rough (2000) Bussieras & Aldrin (1965). SBT YFT Alb. Rough (2000) described white patches but Rough (2000) stated that heavy infections lead to respiratory stress. (1999) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Walters (1980). BET. BET. Neorhadinorhynchus nudus Neorhadinorhynchus sp. longtail tuna Thunnus tonngol (Bleeker). NBT. SBT. BET. Monhysterides sp. LTT. Tentacularia coryphaenae Tentacularia sp. NBT. PBT SBT Alb. NBT. Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996). NBT. BET Alb. NBT. BFT. PBT PBT Alb. YFT Alb. Oncophora albacarensis Oncophora melanocephala Philometroides sp. SBT. Gorgorhynchus sp. YFT BET. YFT Alb. YFT YFT YFT Alb. Clinical signs. BET. YFT. BET. Spirurida Terranova sp. BFT. NBT. YFT. YFT Alb Reference Murugesh (1995) Bussieras & Aldrin (1965) Williams & Bunkley-Williams Williams & Bunkley-Williams Williams & Bunkley-Williams Williams & Bunkley-Williams Williams & Bunkley-Williams (1996) (1996) (1996) (1996) (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Humphrey (1995) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Humphrey (1995). LTT. Rough (2000) (1996) (1996) Jones (1991b). YFT YFT Alb. Acanthocephala Bolbosoma vasculosum Bolbosoma sp. Kohn & Santos (1999) Williams & Bunkley-Williams (1996) Rough (2000) Cannon (1977) Williams Williams Williams Williams Williams Williams Williams Williams Williams & & & & & & & & & Bunkley-Williams Bunkley-Williams Bunkley-Williams Bunkley-Williams Bunkley-Williams Bunkley-Williams Bunkley-Williams Bunkley-Williams Bunkley-Williams (1996) (1996) (1996) (1996) (1996) (1996) (1996). Pacific bluefin tuna Thunnus orientalis (Temminck & Schlegel). SBT. YFT YFT YFT YFT Alb. Ó 2003 Blackwell Publishing Ltd on the gills which appear histologically as areas of focal lamellar fusion. bigeye tuna Thunnus obesus (Lowe). NBT. Capsularia marina Contracaecum sp. YFT SBT Alb. southern bluefin tuna Thunnus maccoyii (Castelnau). Copepoda Brachiella thynni Caligus alalongae Caligus asymmetricus Caligus balistae Caligus bonito Caligus coryphaenae Caligus elongatus Caligus productus Caligus quadratus Caligus sp. Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Hogans (1985). NBT. NBT Alb. 195 . PBT. YFT. BET. BET. The parasite does not cause mortality Pathology.Journal of Fish Diseases 2003. Diseases of tunas Table 1 Continued Parasite Scolex pleuronectis Sphyriocephalus dollfusi Sphyriocephalus tergestinus Sphyriocephalus sp. northern bluefin tuna Thunnus thynnus (L. YFT YFT Alb PBT YFT YFT Alb. YFT Alb. Pseudocynus appendiculatus Isopoda Rocinella signata Species infected LTT BET Alb YFT. BFT. blackfin tuna Thunnus atlanticus (Lesson). BFT. NBT. YFT SBT LTT Alb. 26. YFT YFT YFT YFT Alb. yellowfin tuna Thunnus albacares (Bonnaterre). NBT. albacore Thunnus alalunga (Bonnaterre).). YFT YFT Alb. Moravec. BFT. BFT. Rhadinorhynchus cadenati Rhadinorhynchus pristis Rhadinorhynchus trachuri Rhadinorhynchus sp. Williams & Bunkley-Williams (1996) Rough et al. BET YFT NBT NBT Alb. YFT Alb. Heptachona caudata Hysterothylacium aduncum Hysterothylacium cornutum Metanisakis sp. NBT. PBT. Tetraphyllidean larvae Nematoda Anisakis simplex Anisakis sp. Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Alb. 187–206 B L Munday et al. Caligus robustus Euryphorus brachypterus Euryphorus nordmanni Pennella filosa Pennella sp. BFT. BFT. SBT. i. nodule in muscle of southern bluefin tuna. Diseases of tunas Figure 2 Kudoa sp. Treatment. permits a presumptive diagnosis. Ó 2003 Blackwell Publishing Ltd 196 . The presence of white patches on the gills together with the presence of monogeneans yellowfin and bigeye tunas (Smith 1997). Blood fluke infections of tuna Aetiology. Therapeutic treatment would not be practicable nor warranted. bar ¼ 100 lm). Note the presence of sanguinicolid eggs (arrows) and associated cellular response (H & E. the capsule surrounding the mass of spores (H & E. Daintith & Munday 2000) occurs in southern bluefin tuna. Diagnosis.e. Note the focal. 26. and heavy infections to individual fishÕ. Rough (2000) stated ÔIt is more common in farmed fish but its distribution is often confined to only a few cages. Figure 4 Gill of southern bluefin tuna with Cardicola forsteri infection. Cardicola forsteri (Cribb. Prevention. bar ¼ 100 lm).Journal of Fish Diseases 2003. A definitive diagnosis is currently not possible in the absence of a description of the parasite. Control would most likely be achieved by reducing stocking densities for both cages and fish in cages. Figure 3 Gill of southern bluefin tuna with Cardicola forsteri infection. Note the small nerve (arrowhead) embedded in/apposed to. pale lesions arranged in an arc formation (arrows). fewer cages per site and fewer fish per cage. Cardicola ahi has been reported from Epidemiology. 187–206 B L Munday et al. There is no practicable treatment at present. 26. Cardicola forsteri infections of cultured southern bluefin tuna lead to increased mucus on the gills and have been associated with signs of respiratory distress.L. It may not be a coincidence that bigeye tuna. (2001) who noted many ova surrounded by granulomas. unpublished data). ahi). tuna farmers have reported that infections tend to be more severe at new cage sites suggesting that the parasite may also have a deleterious effect on the intermediate host (B. The intermediate hosts of Cardicola ahi and C. Bussieras & BaudinLaurencin (1973) also reported similar lesions in yellowfin tuna infected with a Cardicola sp. The infection is covert. alalunga (Bonnaterre).Journal of Fish Diseases 2003. Munday. 5). Munday & Daintith (2001) described multifocal. have a much more compact ventricular myocardium (74%) compared with northern bluefin tuna (30–50%) which have not been reported to be to be infected with blood flukes (Santer & Greer-Walker 1980. Histopathology is even more diagnostic. other than Thunnus spp. Smith 1997).5 mm in length have been reported in albacore. The lesions ranged in size from 2 to 12 mm and often extended in an arc across the gills (Fig. 197 . 3). presumably because of increased resistance to blood passing through the partly occluded branchial vasculature. bigeye tuna and yellowfin tuna (Williams & Bunkley-Williams 1996). 4). The lesions appeared to be the result of the fluke ova impacting in the afferent filamentary arteries where they stimulated a host response (Fig. B. Pathology. (2001) reported that the prevalence and severity of the infection increased with the time that southern bluefin tuna were held in captivity suggesting that the life cycle was maintained in the vicinity of the cages. Larval cestodes (plerocercoids) do not usually cause disease in tunas and. (probably C. 187–206 B L Munday et al. In southern bluefin tuna the gross lesions are characteristic enough to enable a presumptive diagnosis. (2001). is not possible at present. Colquitt. T.. Cardiac lesions were also reported by Colquitt et al. Munday. (2001). Diagnosis. unpublished data).L. Additionally. Larval cestode infection Aetiology. Epidemiology. atlanticus (Lesson). Clinical signs. Clinical signs. It is also not known if teleosts. white to yellow lesions involving the gills of infected southern bluefin tuna. Pathology. There was marked hypertrophy of the cardiac spongiosa (Fig. lethargy and slightly increased mortality (Rough 2000. therefore. Tentacularia coryphaenae does produce muscle lesions in a range of tuna species and will be considered here. but definitive diagnosis depends upon flushing the adults from the heart and identifying them. bar ¼ 250 lm). Diseases of tunas Figure 5 Spongiosa of southern bluefin tuna heart with Cardicola forsteri infection showing myocardial hypertrophy and presence of granulomas surrounding parasite eggs (arrows) (H & E. therefore. Prevention of blood fluke infections depends upon an understanding of the parasitesÕ life cycle and. northern bluefin tuna. it is only those which involve the musculature which are of commercial importance. Plerocercoids up to 9. Histopathological lesions in the gills of southern bluefin tuna have been described in detail by Colquitt et al. forsteri are not known. Treatment. which are known to be infected with Cardicola ahi. Colquitt et al. act as Ó 2003 Blackwell Publishing Ltd final hosts. Illustration from Colquitt et al. Prevention. blackfin tuna T. Euryphros brachypterus and Penella filosa are potentially pathogenic. 1999). Pathology. hook-bearing tentacles. There is no practicable treatment. but definitive identification of the larvae can be difficult. encapsulated larval nematodes in the mesenteries of tunas is suggestive of anisakid nematode infection. Prevention. tuna may become infected from a variety of sources. Similar. Epidemiology. Treatment. 26. Sharks are definitive hosts for this cestode which also occurs in a range of pelagic fish apart from tuna. was fed to the fish resulting in a large reduction of thiamin stores in the cultured fish. elongatus grazes on the integument of southern bluefin tuna and may produce grazing trails including over ocular tissues. Experienced diagnosticians can make a presumptive diagnosis of these copepod infections based on the morphology of the parasites and the types of lesions induced by their activities. elongatus and Penella filosa have multiple hosts. In the case of C. definitive diagnosis is only possible by a scientist skilled in identifying the parasites. As C. Cololabis saira (Brevoort). Human infection can be prevented by rapid evisceration of the fish and/or cooking of the flesh. In most instances tuna destined for sashimi are eviscerated soon after capture. (Williams & Bunkley-Williams 1996). Anisakid nematode infection Aetiology. Clinical signs. Very heavy infections of Euryphorus brachypterus have been reported in northern bluefin tuna in which the pseudobranch has been carpeted with the parasite leading to ulceration and bleeding. the liver. Diagnosis. (1999) reported that C. Engraulis japonicus Temminck & Schlegel. These parasites are of importance because they can potentially infect humans. it would be appropriate to keep other forms of aquaculture separate from tuna farms. The definitive hosts of these parasites are marine mammals. Presumptive diagnosis can be made on the basis of the plerocercoids having a long scolex with four shallow. Lesions because of the above copepods are related to their grazing behaviour (C. such treatments would be uneconomical. capture trauma and high stocking densities are believed to predispose to heavy infections (Rough et al. The presence of tightly coiled. elongate bothridia and four short. However. panopthalmitis and cataract formation. elongatus infecting captive southern bluefin tuna. Clinical signs. Damage to the eye results in keratitis. Treatment. towing and harvesting should simultaneously reduce the level of infestation/damage caused by this copepod. The small third-stage larvae are found encapsulated in the peritoneal mesenteries and. Parasites of interest are Anisakis simplex and Hysterothylacium cornutum (Williams & Bunkley-Williams 1996). as this parasite and Penella filosa are carried by other species of fish. Ó 2003 Blackwell Publishing Ltd The very large copepod Penella filosa (‡50 mm long) penetrates into the muscles of a number of tuna species. and/or Japanese anchovy. (Table 1) but only C. sometimes. However. The infections are covert. In addition. Copepod infections Aetiology.Journal of Fish Diseases 2003. Diagnosis. Treatment and prevention. elongatus. Rough et al. Prevention. (1999) have suggested that trauma may predispose to Caligus elongatus infections then reduction of damage because of capture. Pathology. At that stage only Pacific saury. 187–206 B L Munday et al. Although a number of therapeutants are capable of killing copepod parasites (Lester & Roubal 1999) it is impracticable to use these agents under current tuna aquaculture conditions. Not practicable at present. at the present level of loss of production. Epidemiology. Non-infectious diseases Nutritional diseases In the early stage of the Pacific bluefin tuna aquaculture in Japan. Diseases of tunas Epidemiology. It has been reported to cause the fish considerable discomfort (Williams & BunkleyWilliams 1996). Additionally. If the fish are not quickly eviscerated it is possible for the larvae to migrate to the abdominal muscles. Diagnosis. retractile. Many other species of fish can act as intermediate hosts. These baitfish contain 198 . but less severe lesions may be present on the gills and skin (Williams & Bunkley-Williams 1996. Euryphorus brachypterus is almost genus specific for Thunnus spp. A number of copepods parasitise Thunnus spp. morbidity and mortality was reported caused by a shortage of thiamin (Yamaguchi 1986). elongatus) or the damage caused by their attachment to the host (Euryphorus brachypterus and Penella filosa). As Rough et al. South Australia in 1996 is compelling (Munday & Hallegraeff 1998). diagnosis depends upon observing typical clinical signs and pathology in association with appropriate levels of microalgal cells in the water column at the time of the mortality. Brill & Bourke 1990) then it is to be expected that a much lower concentration of Chattonella marina (170 mL)1) would be toxic for Thunnus spp.L. Ishimatsu. 199 . Trauma Trauma to wild-caught fish Aetiology. identification and quantification are already in place when an episode occurs. Epidemiology.6 mL/kg/min and yellowfin tuna (no data are available for southern bluefin tuna) have a ventilation volume of 3900 mL kg)1 min)1 (Bushnell. Additionally.b) and apparent blockage of gill fenestrations by mucus. Oda & Ishimatsu (1998) found that yellowtail were much more suceptible to this toxicosis than red sea bream or Japanese flounder and the relative susceptibilities were directly related to the ventilation volumes of these fish. Diseases of tunas thiaminase which is capable of producing an induced thiamin deficiency in tuna. several kinds of baitfish are fed to tuna in Japan and this disease no longer occurs. unpublished data). These lesions are consistent with those produced experimentally in yellowtail exposed to Chattonella marina (Ishimatsu et al. There are no unequivocal reports of mortalities in tuna because of toxic microalgae but the evidence for Chattonella marina causing the mass mortality episode in southern bluefin tuna at Port Lincoln. Other strategies are the use of perimeter skirts in association with airlifts and spreading certain types of clays to remove toxic microalgae from net-pens by flocculation (Rensel 2000). Okaichi. Iwashita. Katoh. In that incident mortalities varied from 22 to 92%. Munday & Hallegraeff (1998) reported histopathological lesions in the gills with epithelial swelling. Ochi. Sameshima. The toxicity of Chattonella marina and other toxic algae is governed by a range of variables including the stage of growth. Morimoto. Severely damaged fish usually die. Nishio. variable lifting of the epithelium (Fig. However. Toxicoses Microalgal toxicosis Aetiology. Clinical signs. Seedlings (20–40 cm total length) for Pacific bluefin tuna aquaculture in Japan are caught by trolling and these fish are sometimes injured in their jaws or other parts of the body.Journal of Fish Diseases 2003. 187–206 B L Munday et al. Ono & Onoue 2000. Munday. Haruyama. In relation to the latter it is important to note that the Australian Chattonella marina isolates are adapted to much higher irradiances than Japanese isolates (Marshall & Hallegraeff 1999). These are comparable with those (40 lg g)1) reported by McLoughlin. Pathology. towing. Clinical signs. Murakami & Shimada (1989) reported that 500 Chatonella marina cells mL)1 were lethal to yellowtail. Oda. Other host-associated factors to be considered are the additive effects of low dissolved oxygen in the water and cardiopathy because of blood fluke infection. relatively low levels of vitamin E have been found in the livers (mean 33 lg g)1) of southern bluefin tuna fed on baitfish (B. Unequivocal diagnosis of microalgal toxicosis can often be problematic unless facilities for microalgal collection. There have been no reports of nutritional diseases in cultured southern bluefin tuna. Attempts by predators to attack fish in cages can lead to substantial trauma. As yellowtail have a ventilation volume of 1099. In the case of southern bluefin tuna caught by seine net when about 3 years of age. Affected fish have skin wounds of variable size and commonly there is damage to the eyes which may lead to blindness. There are no practicable treatments. Kennedy & Kennedy (1992) in rainbow trout with vitamin E-responsive myopathy. 26. Matsuno. 6a. availability of iron and level of irradiation (Kawano. temperature. transfer and eventual harvest. At present. Diagnosis. Ishimatsu & Muramatsu 1996. Treatment. The most efficacious means of prevention is by towing the tuna cages away from the bloom (Rensel 2000). Tamura & Oda (1996) reported that fish affected by Chattonella toxicosis had excessive production of gill mucus leading to respiratory distress. Pickell & Trick 2000). Hishida. 1996). Ó 2003 Blackwell Publishing Ltd Even when such facilities are available. Often this is exacerbated by unfavourable weather conditions. Prevention. Takano. These signs were reported in southern bluefin tuna dying in the 1996 incident. trauma can occur during capture. Khan. Although most tuna harvesters and/or farmers use basically the same techniques there are differences based on the species and age of the tuna and the distance between the capture site and the farms. Okada. The end cause of the syndrome is collision of juvenile tuna with the walls of tanks or mesh of nets (Miyashita et al. Siting net cages near seal colonies can lead to increased attacks and discharge of blood during harvesting can attract sharks.Journal of Fish Diseases 2003. Treatment. Areas which require special attention are selection of mesh sizes for net pens and methods of harvesting (hook and line rather than gaffing). Predators should be excluded by use of predator nets or tightly tensioned. heavy nets. operators suggest that a degree of netÓ 2003 Blackwell Publishing Ltd fouling makes the net more visible and. Murata & Kumai 2000). (a) Normal southern bluefin tuna gill secondary lamellae (H & E.2 and 1 kg and are rarely more than 48 h in transit (Miyashita. Pacific bluefin tuna caught by Japanese operators are usually between 0. it is suggested by operators that southern bluefin tuna are more robust and. Hattori. Diseases of tunas Figure 6 Comparison of normal and abnormal southern bluefin tuna gills. However. 187–206 B L Munday et al. do not suffer as much injury. Note subepithelial oedema (o) (H & E. bar ¼ 50 lm). especially once in farm cages. Pathology. Morbidity and mortality of Pacific bluefin tuna during hatchery and early growout culture Aetiology. In contrast. southern bluefin tuna sourced by Australian operators are usually 12–20 kg and may be towed for up to 2 weeks before reaching the farming sites. Prevention is mainly by applying good husbandry principles such as not towing cages at an excessive speed. Treatment is usually not practicable. as might be expected. therefore. Prevention. Nakatsukasa. As would be expected damaged fish frequently have local and systemic infections with opportunistic bacteria such as Aeromonas and Vibrio spp. 2000). less likely to be impacted by the fish. bar ¼ 50 lm). Epidemiology. therefore. (b) Abnormal southern bluefin tuna gill secondary lamellae in a fish exposed to Chattonella marina. Diagnosis. The injuries are usually self-evident but determining the cause(s) can be problematic. 26. 200 . In addition. The mesh size of nets is important otherwise fish may become ÔgilledÕ and die or are damaged. Sawada. The thick skin mucus layer which is present from hatching and develops with age causes the larvae to adhere to the surface of the water when carried there by aeration currents. Okada. Hattori. Miyashita. Stocking densities may be reduced and care taken that fish do not become excessively hungry. There is a continual reduction in numbers of larvae from 14 to 20 days post-hatch (Sawada. In addition. Diagnosis. (2000) reported that apart from minimizing stimuli. As the fish become older and more competent swimmers they are able to extricate themselves (Sawada 1999). swimming ability develops in advance of steering ability. Murata & Kumai (2000) reported that mortality increased from 4.e. Treatment. Epidemiology. Murata & Kumai 1999). Illustration from Miyashita et al. Such fish usually escape danger by rapid flight. Sawada. (2000). Prevention. Pathology. Treatment. (2000) make the point that in Pacific tuna juveniles development of muscle and caudal fin shape occurs earlier than development of pectoral fins and caudal keels. Epidemiology. 7). but this is not possible within the confines of tanks or cages. Kurata. Mukai. 187–206 B L Munday et al. Treatment is not possible. respond to external stimuli by panicking and colliding with the sides of tanks or net pens (Fig. Clinical signs. Nakatsukasa. Clinical signs. Affected fish have had considerable damage to the vertebral column and the parasphenoid bones. Pathology. feed availability and other managerial factors may be involved. The condition is quite characteristic with the larvae being trapped at the surface of the water and suffering from desiccation. Prevention. Diagnosis can be made by observing the fish and/or by finding the typical skeletal lesions.9% on day 52 and then stabilized at about 4% day)1 leading to very few survivors at day 60 after hatch. Clinical signs. some fish may be observed swallowing smaller fish. 26. Miyashita. Miyashita et al. Also. Cannibalism is related to the predatory nature of tuna and becomes a problem when there are variable sizes in a cohort of these fish. The fish have been observed to Management problems Cannibalism in Pacific bluefin larvae Aetiology. As indicated above. Ó 2003 Blackwell Publishing Ltd Adhesion of Pacific bluefin larvae to the water surface Aetiology. Okada. Also. 201 . Miyashita et al.9% on day 33 after hatch to 8. i. stocking densities. Even weak stimuli such as flashes of light or vibrations were reported to lead to panic responses in the juvenile tuna resulting in collisions with the sides of the culture vessels/nets. Treatment is impracticable. The syndrome is apparently the result of confining free-ranging young fish in a restricted area.Journal of Fish Diseases 2003. Cannibalism is often accompanied by fin and eye nipping with resultant damage to these areas. the most useful preventive measure was to institute a 24-h light regime so that the sides of the tanks/nets were visible to the fish at all times. Diseases of tunas Figure 7 Juvenile Pacific bluefin tuna embedded in PVC sheeting used to prevent the fish impacting directly on the walls of the tank. Kato. the predatory nature of tuna is a major factor. g. Sawada. If the fish have limited glycogen reserves. Prevention. Neoplasia Clinical signs. Eye lesions Aetiology. Superficial lipomas constitute the majority of reported tumours in Thunnus spp. Diagnosis. Clinical signs.C. As larval Pacific bluefin tuna have a very high oxygen requirement (Miyashita. to corneal ulcers. Improved management should reduce the prevalence of corneal lesions. Pathology. The condition can be diagnosed by observing the typical muscle lesions. Hattori. ÔBurnt tunaÕ are mainly associated with the yellowfin tuna handline fishery (Watson 1995) and the condition has been reported occasionally in southern bluefin tuna (Williams 1986). Watson (1995) suggested that the stress involved in handline fishing leads to catecholamine release which promotes glycogenolysis.cit. thus inducing the condition. More efficient catching methods such as polling for wild fish should obviate the problem. There are no practicable means of treating captive southern bluefin tuna for these conditions. Treatment. General discussion including future directions Other conditions ÔBurnt tunaÕ Aetiology. This preventive measure is used for other fish larvae. Instead of being red. Prevention. Epidemiology. Diseases of tunas Pathology. Okada. Abnormalities vary from cataracts. 187–206 B L Munday et al. As indicated above. Most of the corneal lesions are probably caused by contact with nets. Lester & Kelly 1983) and may constitute up to 10% of body mass. The pathology has not been described. The aetiology of cataracts is not known.L. There are no clinical signs as this is a post-mortem condition. an invasive schwannoma (J.C. two were osteomas (J. although UV irradiation has been suggested as one possible cause. yellowfin tuna caught by handline. physical exertion.). such as grouper larvae. Pathology. Epidemiology. ATP is reduced and muscle pH elevated leading to calpain proteolysis of the Z-discs of the musculature. Epidemiology. Prevention. The presence of larvae trapped at the surface of the water is quite obvious. watery and soft. The suggestion is that low intracellular ATP concentrations lead to the breakdown of calcium homeostasis with an increase in cytosolic calcium. Harshbarger. Nakatsukasa. Diagnosis. Munday. Clinical signs. 1999). personal communication) and a melanoma (Anders 1988). The pathology has not been described in tunas. Use of oxygen rather than air as a source of water oxygenation over the first 7 days after hatch may allow less vigorous ÔaerationÕ and thus reduce losses. to complete loss of the orbit. e. unpublished data). translucent and firm affected muscles are pale. Diagnosis relies upon histological examination of the tumours. three were lipomas (op. Some are traumatic but the aetiologies of others are unknown. Of eight reported tumours. Harshbarger & Hetrick 1989. The lesions are self-evident although small cataracts can be difficult to detect. Calpain is an enzyme which attacks non-contractile proteins. The most plausible explanation for this condition is that it is a form of calpain proteolosis (Watson 1995). providing an oil film on the water surface is very effective. Diagnosis. Additionally. Murata & Kumai 1999) aeration must be vigorous. Diagnosis. such as the Z-discs of muscle. which activates calpain. Low intracellular ATP concentrations are likely to occur in fish which have low glycogen reserves and are subjected to intense Ó 2003 Blackwell Publishing Ltd The present system of using wild-caught seedstock for aquaculture purposes has been characterized by 202 . (Easa. Harshbarger.Journal of Fish Diseases 2003. Harshbarger. Cultured tuna are unlikely to be affected by this condition because they usually have adequate stores of muscle glycogen (B. Pathology. Until the cause of cataracts is established it is not possible to suggest means of preventing them. Treatment. in which the same problem occurs during seedling production (Sawada et al. Affected larvae can be removed to static containers but are not likely to survive. 26. The oil film prevents the larvae being exposed to the air when they are transported to the water surface. personal communication) and one each a fibroma. personal communication. Ishibashi. Jones of the Western Australian Department of Fisheries and J. (1965) Une tetrarhynchose vasculaire ´ des thons du Golfe de Guinee due aux larves plerocercus de Dasyrhynchus talismani R. (1973) Les helminthes ´decine parasites des thons tropicaux. (1991) Acid-fast bacterial granulomatous peritonitis in a tuna fish (Thunnus thynnus). 293–298. The use of oily baitfish as a source of food for captive tuna poses a number of problems. Yamaguchi 1986). from the muscle of yellowfin tuna.W. Harshbarger of the George Washington University.G. & Baudin-Laurencin F. Oce Biavati S. Southern Bluefin Tuna Aquaculture Subprogram Newsletter. Brill R. (1988) Biologie von tumor. Comparative Biochemistry and Physiology 113A. and yellowfin tuna. Hershberger. billfishes and dolphin fish. Jones. and sp.L. Arai Y. 26. Bushnell P. & Austin D. Ariola V. Canberra. Obviously.Journal of Fish Diseases 2003. completing the life cycle has conservation in addition to commercial implications. 13–19. 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