Journal of Fish Diseases 2003, 26, 187–206

Review 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 barry.munday@utas.edu.au)

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

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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.

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It is possible that the tuna could have eaten a fish which itself had mycobacteriosis. there were granulomas composed predominantly of epithelioid cells and fibroblasts. Williams & Bunkley-Williams (1996) reported an apparently similar condition in northern bluefin tuna in the Pacific. 26. Rough & Hawkesford (1997) reported an encephalitis in young adult southern bluefin tuna caused by Uronema nigricans. Pathology. Treatment and prevention. Peric (2002) described the spleen of the tuna as being enlarged with a rough surface. There are a number of granulomatous diseases of marine fish which can be difficult to differentiate. Sawada. He indicated that the lesions were similar to those seen in sparids with chronic pasteurellosis (P. Treatment is not practicable. Reuter (personal communication) has noted coccidial bodies in the liver of this species. damsela subsp. phosphoreum. Biavati & Manera (1991) reported a granulomatous peritonitis. Histologically. most isolates from marine species are Mycobacterium marinum (Austin & Austin 1987). The macroscopic lesions are not diagnostic as such granulomas can be caused by a variety of agents such as Mycobacterium or Nocardia spp. 187–206 B L Munday et al. Pasteurellosis is essentially a warmwater (20–25 °C) disease and as the causative organism does not survive for long outside the host. Bacilli within the granulomas were Gram positive and stained with modified Ziehl–Neelsen stain. Peric (2002) reported lesions consistent with Photobacterium damsela subsp. Diagnosis. The reported very low prevalence of pasteurellosis in northern bluefin tuna would not warrant attempts at treatment or specific prophylaxis. Diagnosis. nigricans in southern bluefin tuna. Epidemiology. albacares (Bonnaterre). it is possible that their citation actually applies to U. T. The detection of short. plump Gram-negative bacteria should enable a presumptive diagnosis but a definitive diagnosis requires isolation and identification of P. Epidemiology. from the South Pacific were infected. Treatment and prevention. Protozoan diseases Coccidiosis Aetiology. As most cultured tuna are currently fed raw baitfish.g. No clinical signs have been reported. The authors believed that the diagnosis was more likely to be mycobacteriosis than nocardiosis. Jones (1990) reported that oocysts occurred in both the liver and spleen where they produced minimal host response. 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. damsela subsp. He found no infection in 11 southern bluefin tuna although R. Otherwise it most likely became infected from the environment as aquatic mycobacteria are capable of existing as environmental organisms. infections 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. Transmission is presumed to be lateral between fish (AQIS 1999). Not required. care must be taken not to include fish with tuberculosis in the diet. Diseases of tunas Photobacterium spp. Clinical and pathological findings. Treatment and prevention. and such a report has not appeared in the mainstream scientific literature. Clinical signs. Scuticociliate infection Aetiology. histologically. Epidemiology. Ó 2003 Blackwell Publishing Ltd 189 . unpublished data). However. piscicida. piscicida in a single northern bluefin tuna. T. mycobacteriosis and nocardiosis. contained small numbers of short plump rods. pseudotuberculosis. The cut surface showed multiple granulomas which. Hamaguchi & Kusuda (1992) reported on experimental infections of Pacific bluefin tuna with P. The cause of putative tuberculosis reported in a single northern bluefin tuna (Biavati & Manera 1991) is not known. piscicida infection). Y. Munday.Journal of Fish Diseases 2003. alalunga (Bonnaterre). and an individual yellowfin tuna. Watts. As their record was not their own work. phosphoreum by isolating the organism from the kidneys of diseased fish. The method of transmission of infection is unknown. Jones (1990) found 98% (140 of 143) of albacore. Pathology. O’Donoghue. T. thynnus (Bonnaterre). Hamaguchi & Kusuda (1992) confirmed experimental infections with P. e. Only Goussia auxidis has been reported from tunas. Mycobacteriosis or piscine tuberculosis Aetiology.

1997). Adult southern bluefin tuna with Uronema encephalitis suffer from the so-called Ôswimmer syndromeÕ. Treatment. approximately half of the larvae died within 3 days (Y. such fish come to the surface. 1997). bar ¼ 50 lm). Ó 2003 Blackwell Publishing Ltd 190 . In Japan. Usually. unpublished data). Although parasites containing food vacuoles can be found in the brain (Fig. Diagnosis. Burke & Munday (1996) developed a fluorescent antibody stain for specific identification of U. Munday & K. turn light blue and swim vigorously around the cage. The reduction in prevalence of the disease in recent years appears to be associated with improved undercage environmental conditions. 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.Journal of Fish Diseases 2003. It is not known what predisposes the olfactory rosette to colonization by Uronema. Note lack of host response (PAS. Epidemiology. 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. Diseases of tunas Clinical signs. 26. larval and juvenile fish are less tolerant to copper ions than adult fish (S. unpublished data) and have decreased from about 5% in captive fish in 1993 to 1. Scuticociliate infection of larval/juvenile tuna is diagnosed by demonstrating the parasites in wet preparations or tissue sections. Pathology. 1) there is no host response except where the meninges are involved. copper ions in the range of 50–80 ppb concentration are effective. Sawada.34% in 1995 and <1% in 2001. nigricans. personal communication) and the tolerance of larval and juvenile tuna to copper is unknown.L. Rough. Morbidity and mortality rates are comparable (B. Watts. The parasites preferentially invade the epidermis and muscle of tuna larvae. of course. a higher water temperature of 28 °C has been found to be effective in reducing losses. 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. the removal of dead fish is necessary. However. The smaller larvae showed the heaviest mortality and signs of infection ceased at 18 days post-hatch. In the case of infection of 14-day post-hatch Pacific bluefin tuna larvae. Treatment is not practicable for adult tuna reared in open sea cages. Eventually. The build-up of organic matter which occurs in hatcheries is conducive to the development of high concentrations of scuticociliates and outbreaks of disease. Copper treatment has been found to be effective for scuticociliate infections of many fish which are reared in tanks in Japan. lymphocytic responses are frequent in the olfactory nerves and rosettes.M. In the case of larval Pacific bluefin tuna. Cases of Ôswimmer syndromeÕ can be diagnosed by demonstrating Uronema in wet preparations or sections of brain from affected fish. It is helpful to increase the water exchange rate in larval rearing tanks and. In adult southern bluefin tuna pathology is restricted to the olfactory system and brain. Typically. 187–206 B L Munday et al. they cease compulsive swimming and tend to alternately sink and rise to the surface until they finally sink and die (Munday et al. However. 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. Miyashita.

crumena) and 4. Epidemiology. if not all. the reader needs to be aware that. Harshbarger. type 3) infecting southern bluefin tuna. El-Matbouli. Histologically. Similar lesions because of an unidentified Kudoa sp. None reported. The parasites produce no clinical signs and. cysts in southern bluefin tuna were in peripheral nerves. Prevention. clupeidae in poorly identified Thunnus spp. it is conceivable that these prey species could be alternative hosts.C. Table 1 may still contain contentious citations. have a two-host cycle with the myxosporean in a fish and an actinosporean in an invertebrate (Kent. the myxosporean spores are found aggregated in the cystic structures and usually produce minimal host response.3–6.8–10.0 lm and have six shell valves each containing one polar capsule (Lom & Dykova 1992). Rough 2000) although Langdon (1990) produced evidence to suggest that most. Harshbarger. Hoffman.5– 9. Clinical signs. nova. However. capsalid monogenean (Rough 2000. Desser.5 · 9. T.4–5. Neither treatment nor prevention are practicable. this seems unlikely. Devlin.2 · 11. infection of northern and southern bluefin tuna producing lesions in the musculature Aetiology. Palenzeula. 1993). Lester. Neither treatment nor prevention is practicable. Prevention is by improved hygiene/ husbandry. Kent et al. possibly. Kudoa sp. but only a few are of health and/or economic importance. Hallett. 2). 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. As most juvenile tuna consume invertebrates such as squid and crustaceans (Kailola et al. Hexacapsula neothunni spores Ó 2003 Blackwell Publishing Ltd Monogenean infection of gills Aetiology. lowfin tuna and bigeye tuna. personal communication).Journal of Fish Diseases 2003. Treatment and prevention.0 lm (Kudoa sp. Hedrick. These will be discussed here. 26. 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. Treatment and prevention. The prevalence of K. 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). Histologically the cysts are found to consist of numerous Kudoa spores surrounded by a fibrous capsule (Fig. Pathology. crumena in a yellowfin tuna. but as it does not produce myoliquefaction. Hexacapsula neothunni in albacore. nigricans densities. Longshaw.9 (K. 1993). Typical myxosporean spores can be easily found in wet preparations or histological sections of affected muscles. Andree. unpublished data). Postmortem liquefaction of muscle due to myxosporean infections Aetiology. while with heavy infections cysts may be visible in the musculature.8 lm and have four shell valves each containing one polar capsule. have been reported in southern bluefin tuna and Langdon (1990) suggested that the parasite could be K.L. it may be pertinent that Crosbie (1996) found that the maximum U. An unidentified. Clinical signs and pathology. Typical Kudoa spores measuring 7. Munday. K. yel- measure 6. Siddall & Xiao 2001). Additionally. crumena in albacore was reported as 5% (J. Most myxosporeans. Kudoa nova spores measure 5. Diagnosis. Metazoan infections As given in Table 1. which were achieved during the exponential phase of cultured organisms. (Williams & Bunkley-Williams 1996).5 · 8. personal communication. while an effort has been made to identify errors in records of parasites of tunas. especially the intercostal nerves. crustaceans and salps (Kailola et al. Epidemiology. Bartholomew.6 · 7. Khattra. Kudoa nova in bigeye tuna and. obesus (Lowe). many metazoans infect Thunnus spp.C. The infection in southern bluefin tuna produces white cysts 1–10 mm in diameter which are apparently in the muscle (J. were lower at 30 °C than at 10–25 °C. (2001) reported K.) can be seen in wet preparations or histological sections. Diagnosis. 187–206 B L Munday et al. 191 . Diseases of tunas accelerate the fish’s development to the juvenile stage at which they develop higher tolerance toUronema spp. for which life cycles are known. Feist. This suggests that the effect of high water temperatures on the organisms may be the more important mechanism.

Parasite Myxosporea Hexacapsula neothunni Kudoa Kudoa Kudoa Kudoa clupeidae crumena nova sp.YFT BET YFT PBT BET. NBT NBT PBT BET BET. BET. YFT BET. Decemtestis dollfusi Dermatodidymocystis indicus Dermatodidymocystis vivipira Dermatodidymocystis viviparoides Ó 2003 Blackwell Publishing Ltd 192 . Pozdnyakov (1990) Rough (2000) Ahmad (1983) Nikolaeva & Dubina (1978) Yamaguti (1970) Yamaguti (1970) Monogenea Allopseudaxine sp. NBT NBT BET. NBT. SBT LTT BET. YFT NBT LTT.YFT LTT. Species infected Reference Alb.Journal of Fish Diseases 2003.YFT YFT Alb. YFT BET. PBT Alb. NBT. NBT YFT YFT PBT YFT PBT SBT. YFT SBT SBT Alb. YFT NBT Alb. YFT BET.YFT BET. 187–206 B L Munday et al. Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Harshbarger pers.YFT BET. NBT. NBT.YFT NBT. Kuhnia thunni Metapseudaxine ventrosicula Nasicola hogansi Nasicola klawei Neohexostoma euthynni Neohexostoma extensicaudatum Neohexostoma robustum Neohexostoma thunninae Neohexostoma sp. 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 Alb BET SBT YFT Alb. PBT. 26. SBT. YFT Arai & Matsumoto (1953). BET.YFT YFT NBT BET NBT SBT. YFT SBT YFT BET BET. Areotestis sibi Benedenia seriolae Caballerocotyla abidjani Caballerocotyla albsmithi Caballerocotyla biparasitica Caballerocotyla goueri Caballerocotyla magronum Caballerocotyla paucispinosa Caballerocotyla pseudomagronum Caballerocotyla verrucosa Caballerocotyla sp. Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Pozdnyakov (1990) Williams & Bunkley-Williams (1996) Pozdnyakov (1990).YFT PBT. BET. Rough (2000) Williams & Bunkley-Williams (1996) Nikolaeva & Parukhin (1968) Williams & Bunkley-Williams (1996) Yamaguti (1970) Cribb et al. comm. 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. 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). (2000) Manter (1970) Yamaguti (1938). 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).BFT. SBT YFT NBT BET. Capsala foliacea Capsala gotoi Capsala neothunni Capsala thynni Hexostoma acutum Hexostoma albsmithi Hexostoma dissimile Hexostoma grossum Hexostoma sibi Hexostoma thynni Hexostoma sp. NBT NBT NBT BET. Diseases of tunas Table 1 Metazoan parasites of Thunnus spp. BET. YFT BET.

Yamaguti (1934). Yamaguti (1971). YFT Alb PBT NBT Alb. YFT PBT NBT Alb YFT PBT Alb Alb BET LTT. YFT Alb BET. PBT. YFT BET NBT Alb. NBT. YFT Alb. Rough (2000) Yamaguti (1938). BET. PBT YFT Alb. 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). Williams & Bunkley-Williams (1996) Yamaguti (1970). YFT PBT PBT YFT Alb. NBT. Yamaguti (1970). PBT. Williams & Bunkley-Williams (1996) Ishii (1935) Williams & Bunkley-Williams (1996) Yamaguti (1970) Yamaguti (1970). 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. Rough (2000) Ariola (1902). NBT YFT Alb Alb Alb Ó 2003 Blackwell Publishing Ltd 193 . NBT NBT BET NBT YFT YFT NBT Alb. Williams & Bunkley-Williams (1996) Taschenberg (1879) Korotaeva & Korjakovtzeva (1983) Linton (1901) Korotaeva & Korjakovtzeva (1983) Yamaguti (1970) Yamaguti (1971) Linton (1940). 26. LTT. BET. YFT Alb.BET Alb. SBT. LTT BET. YFT Alb YFT Alb BET PBT Alb. LTT. Williams & Bunkley-Williams (1996). 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. YFT Reference Ishii (1935) Williams & Bunkley-Williams (1996) Yamaguti (1970) Yamaguti (1970). Ishii (1935). Ku & Shen (1965) Yamaguti (1970) Yamaguti (1970). BET.LTT. BET. Nikolaeva & Dubina (1985) Yamaguti (1970) Ariola (1902) Nikolaeva & Dubina (1985). NBT. Nikolaeva & Dubina (1985). Williams & Bunkley-Williams (1996) Ariola (1902). BET LTT. Murugesh & Madhavi (1995). Nikolaeva & Dubina (1985). Murugesh & Madhavi (1995) Yamaguti (1938) Yamaguti (1970) Ishii (1935). YFT Alb YFT. YFT PBT BET. 187–206 B L Munday et al. Dollfus (1952). SBT Alb.Journal of Fish Diseases 2003. BET. BET. Murugesh & Madhavi (1995) Ishii (1935) Yamaguti (1971) Dollfus (1952) Yamaguti (1970) Ishii (1935) Dollfus (1952) Dollfus (1952) Yamaguti (1970) Yamaguti (1970). Murugesh & Madhavi (1995) Dollfus (1952). PBT.

YFT NBT Alb SBT YFT YFT. NBT. Williams & Bunkley-Williams (1996) Ishii (1935). PBT Alb SBT Reference Gibson & Bray (1977). YFT YFT Alb Alb YFT PBT PBT NBT NBT. YFT NBT NBT PBT Alb Alb BET. PBT. Rough (2000) Yamaguti (1970) Yamaguti (1970) Yamaguti (1970) Yamaguti (1970) Pozdnyakov (1992) Nikolaeva (1988) Yamaguti (1970) Yamaguti (1971). YFT YFT YFT Alb. 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. PBT BET YFT PBT Alb BET 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) Williams & Bunkley-Williams (1996) Rough (2000) Ó 2003 Blackwell Publishing Ltd 194 . SBT YFT Alb. SBT YFT. BET. YFT Alb. LTT. Pelichnibothrium speciosum Pseudobothrium grimaldi Pterobothrium heteracanthum Species infected Alb. 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 YFT YFT. YFT YFT Alb. PBT Alb. YFT BET PBT BET. Williams & Bunkley-Williams (1996) Yamaguti (1971). Rough (2000) Bussieras & Aldrin (1965). Jones (1991a) Dollfus (1942) Williams & Bunkley-Williams (1996) Rough (2000) Williams & Bunkley-Williams (1996) Schmidt (1986). YFT BET Alb. Grillotia sp. NBT. Gymnorhynchus gigas Hepatoxylon trichiuri Lacistorhynchus tenuis Monorygma grimaldi Nybelinia lingualis Nybelinia sp. Baudin-Laurencin (1971) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Bussieras & Baudin-Laurencin (1973). Bussieras & Baudin-Laurencin (1973). YFT BET. YFT Alb. YFT YFT YFT. YFT NBT. NBT. Opisthorchinematobothrium nephrodomus Opisthorchinematobothrium parathunni Orbitonematobothrium perioculare Phyllodistomum thunni Platocystis alalongae Platocystis meridionalis Platocystis sp. Williams & Bunkley-Williams (1996). SBT. YFT BET BET. PBT YFT Alb. Dollfus (1952) Nikolaeva & Dubina (1985) Nikolaeva & Dubina (1985) Yamaguti (1934). NBT. NBT YFT Alb Alb. Bussieras & Baudin-Laurencin (1973) Linton (1940).Journal of Fish Diseases 2003. 187–206 B L Munday et al. NBT. BFT. 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 BET. Neonematobothrioides poonui Neophrodidymotrema ahi Oesophagocystis sp. 26. Dollfus (1952) Nikolaeva & Dubina (1985) Dollfus (1942). Rough (2000) Srivastava & Sahai (1978) Nikolaeva & Dubina (1985) Yamaguti (1970) Hafeezullah (1971) Nikolaeva & Parukhin (1968). NBT. NBT.

NBT. 195 . NBT Alb. The parasite does not cause mortality Pathology. BFT. 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). BET Alb. SBT. Ó 2003 Blackwell Publishing Ltd on the gills which appear histologically as areas of focal lamellar fusion. NBT. BET. BET. NBT. NBT. BET YFT NBT NBT Alb. YFT YFT Alb. YFT Alb. 26. PBT. Pseudocynus appendiculatus Isopoda Rocinella signata Species infected LTT BET Alb YFT. Neorhadinorhynchus nudus Neorhadinorhynchus sp. Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996). BFT. Spirurida Terranova sp. 187–206 B L Munday et al. 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. BET. YFT BET. SBT. yellowfin tuna Thunnus albacares (Bonnaterre). BFT. YFT Alb. Oncophora albacarensis Oncophora melanocephala Philometroides sp. PBT SBT Alb. YFT SBT LTT Alb. BFT. southern bluefin tuna Thunnus maccoyii (Castelnau). NBT. LTT.). Acanthocephala Bolbosoma vasculosum Bolbosoma sp. SBT. Rough (2000) described white patches but Rough (2000) stated that heavy infections lead to respiratory stress. YFT. Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Hogans (1985). YFT YFT Alb PBT YFT YFT Alb. BFT. PBT PBT Alb. Diseases of tunas Table 1 Continued Parasite Scolex pleuronectis Sphyriocephalus dollfusi Sphyriocephalus tergestinus Sphyriocephalus sp. bigeye tuna Thunnus obesus (Lowe). BET. Gorgorhynchus sp. northern bluefin tuna Thunnus thynnus (L. longtail tuna Thunnus tonngol (Bleeker). Rhadinorhynchus cadenati Rhadinorhynchus pristis Rhadinorhynchus trachuri Rhadinorhynchus sp. Pacific bluefin tuna Thunnus orientalis (Temminck & Schlegel). Clinical signs. NBT. NBT. NBT. YFT YFT YFT Alb. SBT. Tetraphyllidean larvae Nematoda Anisakis simplex Anisakis sp. (1999) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Williams & Bunkley-Williams (1996) Walters (1980). BET. Williams & Bunkley-Williams (1996) Rough et al. BFT. Capsularia marina Contracaecum sp. Caligus robustus Euryphorus brachypterus Euryphorus nordmanni Pennella filosa Pennella sp. YFT. BET. blackfin tuna Thunnus atlanticus (Lesson). YFT Alb. PBT. YFT YFT YFT YFT Alb. albacore Thunnus alalunga (Bonnaterre). NBT. YFT. BET. BFT. YFT Alb. YFT YFT Alb. Copepoda Brachiella thynni Caligus alalongae Caligus asymmetricus Caligus balistae Caligus bonito Caligus coryphaenae Caligus elongatus Caligus productus Caligus quadratus Caligus sp. LTT. Rough (2000) (1996) (1996) Jones (1991b). Heptachona caudata Hysterothylacium aduncum Hysterothylacium cornutum Metanisakis sp.Journal of Fish Diseases 2003. NBT. NBT. YFT YFT YFT YFT Alb. BFT. YFT SBT Alb. 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). Monhysterides sp. Tentacularia coryphaenae Tentacularia sp. Moravec.

Diagnosis. Note the small nerve (arrowhead) embedded in/apposed to. Cardicola forsteri (Cribb. permits a presumptive diagnosis. Ó 2003 Blackwell Publishing Ltd 196 . Note the presence of sanguinicolid eggs (arrows) and associated cellular response (H & E. bar ¼ 100 lm). The presence of white patches on the gills together with the presence of monogeneans yellowfin and bigeye tunas (Smith 1997). Note the focal. A definitive diagnosis is currently not possible in the absence of a description of the parasite. fewer cages per site and fewer fish per cage. and heavy infections to individual fishÕ. Prevention. Figure 4 Gill of southern bluefin tuna with Cardicola forsteri infection.Journal of Fish Diseases 2003. Figure 3 Gill of southern bluefin tuna with Cardicola forsteri infection. Rough (2000) stated ÔIt is more common in farmed fish but its distribution is often confined to only a few cages. Diseases of tunas Figure 2 Kudoa sp. 26. i. bar ¼ 100 lm). Cardicola ahi has been reported from Epidemiology. Blood fluke infections of tuna Aetiology. the capsule surrounding the mass of spores (H & E. Daintith & Munday 2000) occurs in southern bluefin tuna. Treatment. Therapeutic treatment would not be practicable nor warranted.e. pale lesions arranged in an arc formation (arrows). 187–206 B L Munday et al. Control would most likely be achieved by reducing stocking densities for both cages and fish in cages. nodule in muscle of southern bluefin tuna.

ahi). but definitive diagnosis depends upon flushing the adults from the heart and identifying them. 197 . alalunga (Bonnaterre). therefore. Pathology. bigeye tuna and yellowfin tuna (Williams & Bunkley-Williams 1996). unpublished data). 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.5 mm in length have been reported in albacore. 4). Clinical signs. northern bluefin tuna.. (2001). Munday & Daintith (2001) described multifocal. The lesions appeared to be the result of the fluke ova impacting in the afferent filamentary arteries where they stimulated a host response (Fig. it is only those which involve the musculature which are of commercial importance. It may not be a coincidence that bigeye tuna.L. Munday. In southern bluefin tuna the gross lesions are characteristic enough to enable a presumptive diagnosis. Prevention. There is no practicable treatment at present. Additionally. Larval cestodes (plerocercoids) do not usually cause disease in tunas and. Colquitt. 26. 5). forsteri are not known. Histopathological lesions in the gills of southern bluefin tuna have been described in detail by Colquitt et al. 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. (probably C. It is also not known if teleosts. which are known to be infected with Cardicola ahi. Larval cestode infection Aetiology. There was marked hypertrophy of the cardiac spongiosa (Fig. lethargy and slightly increased mortality (Rough 2000. Smith 1997). T.L. Munday.Journal of Fish Diseases 2003. blackfin tuna T. 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. B. Illustration from Colquitt et al. Colquitt et al. Treatment. Cardicola forsteri infections of cultured southern bluefin tuna lead to increased mucus on the gills and have been associated with signs of respiratory distress. 3). The infection is covert. atlanticus (Lesson). (2001). Epidemiology. white to yellow lesions involving the gills of infected southern bluefin tuna. unpublished data). bar ¼ 250 lm). 187–206 B L Munday et al. (2001) who noted many ova surrounded by granulomas. presumably because of increased resistance to blood passing through the partly occluded branchial vasculature. The intermediate hosts of Cardicola ahi and C. Pathology. The lesions ranged in size from 2 to 12 mm and often extended in an arc across the gills (Fig. is not possible at present. Clinical signs. therefore. Prevention of blood fluke infections depends upon an understanding of the parasitesÕ life cycle and. Tentacularia coryphaenae does produce muscle lesions in a range of tuna species and will be considered here. Histopathology is even more diagnostic. Diagnosis. Bussieras & BaudinLaurencin (1973) also reported similar lesions in yellowfin tuna infected with a Cardicola sp. act as Ó 2003 Blackwell Publishing Ltd final hosts. other than Thunnus spp. Cardiac lesions were also reported by Colquitt et al. Plerocercoids up to 9. (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.

1999). Similar. elongatus and Penella filosa have multiple hosts. sometimes. towing and harvesting should simultaneously reduce the level of infestation/damage caused by this copepod. elongatus. 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. at the present level of loss of production. was fed to the fish resulting in a large reduction of thiamin stores in the cultured fish. panopthalmitis and cataract formation. the liver. The infections are covert. retractile. (Table 1) but only C. There is no practicable treatment. In most instances tuna destined for sashimi are eviscerated soon after capture. Damage to the eye results in keratitis. (1999) have suggested that trauma may predispose to Caligus elongatus infections then reduction of damage because of capture. Many other species of fish can act as intermediate hosts. Lesions because of the above copepods are related to their grazing behaviour (C. elongatus infecting captive southern bluefin tuna. encapsulated larval nematodes in the mesenteries of tunas is suggestive of anisakid nematode infection. capture trauma and high stocking densities are believed to predispose to heavy infections (Rough et al. These baitfish contain 198 . such treatments would be uneconomical. (1999) reported that C. hook-bearing tentacles. Treatment. Prevention. A number of copepods parasitise Thunnus spp. Clinical signs. 26. Clinical signs. Euryphorus brachypterus is almost genus specific for Thunnus spp. Diseases of tunas Epidemiology. Prevention. The definitive hosts of these parasites are marine mammals. Diagnosis. 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. Rough et al. Pathology. Non-infectious diseases Nutritional diseases In the early stage of the Pacific bluefin tuna aquaculture in Japan. but definitive identification of the larvae can be difficult. It has been reported to cause the fish considerable discomfort (Williams & BunkleyWilliams 1996). Euryphros brachypterus and Penella filosa are potentially pathogenic. 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. Copepod infections Aetiology. Presumptive diagnosis can be made on the basis of the plerocercoids having a long scolex with four shallow. Pathology. These parasites are of importance because they can potentially infect humans. Treatment and prevention. In the case of C. As Rough et al. If the fish are not quickly eviscerated it is possible for the larvae to migrate to the abdominal muscles. tuna may become infected from a variety of sources. At that stage only Pacific saury. In addition. Epidemiology. However. elongatus grazes on the integument of southern bluefin tuna and may produce grazing trails including over ocular tissues. but less severe lesions may be present on the gills and skin (Williams & Bunkley-Williams 1996. The small third-stage larvae are found encapsulated in the peritoneal mesenteries and. Cololabis saira (Brevoort). and/or Japanese anchovy. Additionally. elongatus) or the damage caused by their attachment to the host (Euryphorus brachypterus and Penella filosa). Engraulis japonicus Temminck & Schlegel. Human infection can be prevented by rapid evisceration of the fish and/or cooking of the flesh. (Williams & Bunkley-Williams 1996). Diagnosis. 187–206 B L Munday et al. it would be appropriate to keep other forms of aquaculture separate from tuna farms.Journal of Fish Diseases 2003. definitive diagnosis is only possible by a scientist skilled in identifying the parasites. 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. Diagnosis. elongate bothridia and four short. Ó 2003 Blackwell Publishing Ltd The very large copepod Penella filosa (‡50 mm long) penetrates into the muscles of a number of tuna species. The presence of tightly coiled. However. Sharks are definitive hosts for this cestode which also occurs in a range of pelagic fish apart from tuna. As C. morbidity and mortality was reported caused by a shortage of thiamin (Yamaguchi 1986). Epidemiology. Treatment. Not practicable at present. Anisakid nematode infection Aetiology.

Oda. South Australia in 1996 is compelling (Munday & Hallegraeff 1998). Ishimatsu & Muramatsu 1996. 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. Clinical signs. temperature. Pickell & Trick 2000). There are no practicable treatments. several kinds of baitfish are fed to tuna in Japan and this disease no longer occurs. 6a. transfer and eventual harvest. trauma can occur during capture. Ono & Onoue 2000. 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. 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). Ishimatsu. identification and quantification are already in place when an episode occurs. Sameshima. Diagnosis. unpublished data). Clinical signs. These lesions are consistent with those produced experimentally in yellowtail exposed to Chattonella marina (Ishimatsu et al. Diseases of tunas thiaminase which is capable of producing an induced thiamin deficiency in tuna. As yellowtail have a ventilation volume of 1099. Hishida. 26. Additionally. 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. In that incident mortalities varied from 22 to 92%. Morimoto. Affected fish have skin wounds of variable size and commonly there is damage to the eyes which may lead to blindness. However. 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. At present. Severely damaged fish usually die. 187–206 B L Munday et al. 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. The toxicity of Chattonella marina and other toxic algae is governed by a range of variables including the stage of growth. Treatment. Nishio.L.Journal of Fish Diseases 2003. Prevention. Toxicoses Microalgal toxicosis Aetiology. 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). In the case of southern bluefin tuna caught by seine net when about 3 years of age. Munday. availability of iron and level of irradiation (Kawano. variable lifting of the epithelium (Fig.b) and apparent blockage of gill fenestrations by mucus. Iwashita. 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. 1996). These signs were reported in southern bluefin tuna dying in the 1996 incident. There have been no reports of nutritional diseases in cultured southern bluefin tuna. 199 . Ó 2003 Blackwell Publishing Ltd Even when such facilities are available. The most efficacious means of prevention is by towing the tuna cages away from the bloom (Rensel 2000). Khan. towing. Unequivocal diagnosis of microalgal toxicosis can often be problematic unless facilities for microalgal collection. Matsuno. Okaichi. Often this is exacerbated by unfavourable weather conditions. Epidemiology. Tamura & Oda (1996) reported that fish affected by Chattonella toxicosis had excessive production of gill mucus leading to respiratory distress. Trauma Trauma to wild-caught fish Aetiology. Haruyama. Munday & Hallegraeff (1998) reported histopathological lesions in the gills with epithelial swelling.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. Pathology. These are comparable with those (40 lg g)1) reported by McLoughlin. Ochi. Murakami & Shimada (1989) reported that 500 Chatonella marina cells mL)1 were lethal to yellowtail. Katoh. Attempts by predators to attack fish in cages can lead to substantial trauma. 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. Takano. Kennedy & Kennedy (1992) in rainbow trout with vitamin E-responsive myopathy.

2 and 1 kg and are rarely more than 48 h in transit (Miyashita. therefore. Sawada. (a) Normal southern bluefin tuna gill secondary lamellae (H & E. 200 . 2000). Note subepithelial oedema (o) (H & E. The mesh size of nets is important otherwise fish may become ÔgilledÕ and die or are damaged. In addition. Epidemiology. As would be expected damaged fish frequently have local and systemic infections with opportunistic bacteria such as Aeromonas and Vibrio spp. The end cause of the syndrome is collision of juvenile tuna with the walls of tanks or mesh of nets (Miyashita et al. Areas which require special attention are selection of mesh sizes for net pens and methods of harvesting (hook and line rather than gaffing). especially once in farm cages. 26. heavy nets. Pathology. therefore. Treatment is usually not practicable. Prevention. 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. Predators should be excluded by use of predator nets or tightly tensioned. Diseases of tunas Figure 6 Comparison of normal and abnormal southern bluefin tuna gills. it is suggested by operators that southern bluefin tuna are more robust and. However. as might be expected. Siting net cages near seal colonies can lead to increased attacks and discharge of blood during harvesting can attract sharks. Prevention is mainly by applying good husbandry principles such as not towing cages at an excessive speed. The injuries are usually self-evident but determining the cause(s) can be problematic.Journal of Fish Diseases 2003. operators suggest that a degree of netÓ 2003 Blackwell Publishing Ltd fouling makes the net more visible and. 187–206 B L Munday et al. bar ¼ 50 lm). 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. Hattori. Okada. In contrast. less likely to be impacted by the fish. Murata & Kumai 2000). Diagnosis. Treatment. (b) Abnormal southern bluefin tuna gill secondary lamellae in a fish exposed to Chattonella marina. bar ¼ 50 lm). Morbidity and mortality of Pacific bluefin tuna during hatchery and early growout culture Aetiology. do not suffer as much injury. Pacific bluefin tuna caught by Japanese operators are usually between 0. Nakatsukasa.

The syndrome is apparently the result of confining free-ranging young fish in a restricted area. but this is not possible within the confines of tanks or cages. the predatory nature of tuna is a major factor. Miyashita et al. Pathology. Prevention. Affected fish have had considerable damage to the vertebral column and the parasphenoid bones. Miyashita et al. Treatment is impracticable. Okada. 7). Prevention. Ó 2003 Blackwell Publishing Ltd Adhesion of Pacific bluefin larvae to the water surface Aetiology. Epidemiology. Kato. Clinical signs. 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. 26. respond to external stimuli by panicking and colliding with the sides of tanks or net pens (Fig. Cannibalism is related to the predatory nature of tuna and becomes a problem when there are variable sizes in a cohort of these fish. Nakatsukasa. In addition. 201 . As indicated above. Hattori. There is a continual reduction in numbers of larvae from 14 to 20 days post-hatch (Sawada. Cannibalism is often accompanied by fin and eye nipping with resultant damage to these areas. (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. Murata & Kumai (2000) reported that mortality increased from 4. Treatment. Sawada. Pathology. feed availability and other managerial factors may be involved. (2000) reported that apart from minimizing stimuli. i.Journal of Fish Diseases 2003.9% on day 33 after hatch to 8. Treatment. Miyashita. Clinical signs. Epidemiology.9% on day 52 and then stabilized at about 4% day)1 leading to very few survivors at day 60 after hatch. 187–206 B L Munday et al. Clinical signs. Diagnosis can be made by observing the fish and/or by finding the typical skeletal lesions. Illustration from Miyashita et al. 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. 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. Treatment is not possible. 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. some fish may be observed swallowing smaller fish. The fish have been observed to Management problems Cannibalism in Pacific bluefin larvae Aetiology.e. Also. Such fish usually escape danger by rapid flight. Kurata. Stocking densities may be reduced and care taken that fish do not become excessively hungry. Miyashita. Also. (2000). Okada. Diagnosis. Mukai. The condition is quite characteristic with the larvae being trapped at the surface of the water and suffering from desiccation. stocking densities. Murata & Kumai 1999). 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.

personal communication) and one each a fibroma. Cultured tuna are unlikely to be affected by this condition because they usually have adequate stores of muscle glycogen (B. Most of the corneal lesions are probably caused by contact with nets. Harshbarger. If the fish have limited glycogen reserves. such as grouper larvae. The lesions are self-evident although small cataracts can be difficult to detect. The oil film prevents the larvae being exposed to the air when they are transported to the water surface. Clinical signs. 187–206 B L Munday et al. The condition can be diagnosed by observing the typical muscle lesions. Harshbarger.). Pathology. Affected larvae can be removed to static containers but are not likely to survive. Of eight reported tumours. This preventive measure is used for other fish larvae. Diagnosis. Abnormalities vary from cataracts. Munday. The presence of larvae trapped at the surface of the water is quite obvious. Okada. Nakatsukasa. personal communication. such as the Z-discs of muscle. 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). Epidemiology. Ishibashi. 1999). Prevention.g.C. e. 26. Sawada. physical exertion. Diagnosis. two were osteomas (J. The most plausible explanation for this condition is that it is a form of calpain proteolosis (Watson 1995). Watson (1995) suggested that the stress involved in handline fishing leads to catecholamine release which promotes glycogenolysis. 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 . More efficient catching methods such as polling for wild fish should obviate the problem. Treatment. Diagnosis relies upon histological examination of the tumours. watery and soft. Prevention. Calpain is an enzyme which attacks non-contractile proteins. translucent and firm affected muscles are pale. unpublished data). although UV irradiation has been suggested as one possible cause. Harshbarger & Hetrick 1989. three were lipomas (op.cit. Pathology. The pathology has not been described in tunas. Superficial lipomas constitute the majority of reported tumours in Thunnus spp. Harshbarger.C. General discussion including future directions Other conditions ÔBurnt tunaÕ Aetiology. Diagnosis. Instead of being red. personal communication) and a melanoma (Anders 1988). providing an oil film on the water surface is very effective. Neoplasia Clinical signs. Diagnosis. Eye lesions Aetiology. Epidemiology. Until the cause of cataracts is established it is not possible to suggest means of preventing them. Additionally. Pathology. The aetiology of cataracts is not known. There are no practicable means of treating captive southern bluefin tuna for these conditions. thus inducing the condition. As larval Pacific bluefin tuna have a very high oxygen requirement (Miyashita. As indicated above. Prevention. Murata & Kumai 1999) aeration must be vigorous. The pathology has not been described. to complete loss of the orbit. an invasive schwannoma (J. Epidemiology. Improved management should reduce the prevalence of corneal lesions. The suggestion is that low intracellular ATP concentrations lead to the breakdown of calcium homeostasis with an increase in cytosolic calcium.L. Clinical signs. ATP is reduced and muscle pH elevated leading to calpain proteolysis of the Z-discs of the musculature. Diseases of tunas Pathology. Hattori. in which the same problem occurs during seedling production (Sawada et al. 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. Lester & Kelly 1983) and may constitute up to 10% of body mass. There are no clinical signs as this is a post-mortem condition. Treatment. Some are traumatic but the aetiologies of others are unknown. which activates calpain.Journal of Fish Diseases 2003. yellowfin tuna caught by handline. (Easa. to corneal ulcers.

& Richard J. Revue d’Elevage et de Me ´terinaire des Pays Tropicaux 26.G. (1977) Some ecological relationships of larval ascaridoids from south eastern Queensland marine fishes. and sp. Didymozoon parassiti del tonno. Thunnus maccoyii (Castelnau). 293–298. Canberra. the presence of thiaminases and oxidized lipids in these fish has been. Trematode parasite du ´um Thon albacore Thunnus albacares. South Australian Research and Development Institute. 11–30. First.F. Brill R. Oce Biavati S. Crane & Williams 1997). & Austin D. 233–246. 13–19. Harshbarger of the George Washington University.E. whereas most tunas used for aquaculture are southern. It is paradoxical that a great number of first class physiological studies have been undertaken on skipjack. B. International Journal for Parasitology 7. Beveridge of the University of Melbourne. Journal of Fish Diseases 24. Wise. Hexacapsula neothunni g. Arai Y.Journal of Fish Diseases 2003. Baudin-Laurencin F. Daintith & Munday.E. Experiences of Japanese workers with preliminary attempts to hatch and raise tuna have indicated that hatchery propagation is fraught with many problems and it may be some years before such fish will replace seedstock caught from the wild. & Manera M. (1988) Biologie von tumor. Munday & Burke 2002). 187–206 B L Munday et al. (1971) Crustaces et helminthes parasites de ´ l’albacore (Thunnus albacares) du Golfe de Guinee – note ´ preliminaire. 1925 from marine fishes of India. Buchanan J. yellowfin tuna Thunnus albacares and bigeye tuna T. the development of a palatable artificial feed which produces desirable carcass composition is an urgent need. 3–15. responsible for nutritional problems in the tuna (B.). (1983) Studies on digenetic trematodes of the family Opecoelidae Ozaki. & Daintith M. The authors also thank Dr Miyashiata of Kinki University and three anonymous reviewers for their helpful comments. Bushnell P. baitfish are known to carry important viral diseases such as viral haemorrhagic septicaemia (Kocan. Munday. 2002/03 Experimental Program Edition Number 1. (1991) Acid-fast bacterial granulomatous peritonitis in a tuna fish (Thunnus thynnus). this is an area requiring urgent attention. South Australia. Colquitt S. it is important that this research continues because. (1996) Selective advantage conferred by the high performance physiology of tunas. (Trematoda. 99–108.. Obviously. Ahmad J. Verlag Heino Moller. Rivista di Parassitologia 44. 137–143. Centre de Rechercher ´anographiques Abidjan 2.R. de Me ´ Bussieras J. Jones of the Western Australian Department of Fisheries and J. Yamaguchi 1986). (1990) Cardiorespiratory responses of skipjack tuna Katsuwonus pelamis. northern or Pacific bluefin tuna. (1953) On a new sporozoa. Comparative Biochemistry and Physiology 113A. 1857–1865. Neothunnus macropterus. Southern Bluefin Tuna Aquaculture Subprogram Newsletter. Munday B. n. Hine. Kearns. completing the life cycle has conservation in addition to commercial implications. (2001) Pathological findings in southern bluefin tuna. 1041–1043.L. & Aldrin J. J. ´ Bussieras J. 2000) (Digenea: Sanguinicolidae). unpublished data. & Bourke R. Ariola V. sp. ´ Baudin-Laurencin F. Bollettino. Austin B.und tumorahnlichen Kranheiten der Elbfische. (2002) Tuna research farm progress. 227–232. there is ample evidence that significant differences in physiology do occur (Bushnell. Archives de Parasitologie 6.W. The authors wish to acknowledge the valuable assistance provided by Drs I. a blood fluke. (1902) Contributo per una monografia dei Didymozoon. While it is possible to extrapolate from one species to another.A. Brill & Bourke 1990) and such extrapolation could lead to erroneous decisions being made. Ve Cannon L. 225–229.G. billfishes and dolphin fish. infected with Cardicola forsteri (Cribb. Gorgoderidae). (1973) Phyllodistomum thunni ´ n. Revue d’Elevage et ´decine Ve ´terinaire des Pays Tropicaux 18. Katsuwonas pelamis (L. (1987) Bacterial Fish Pathogens: Disease in Farmed and Wild Fish. Consequently. Also. Ausinfo. or is likely to be. from the muscle of yellowfin tuna. Adelaide.obesus to acute reductions in ambient oxygen. Dollfus 1935. Brill R. Kiel.. Ó 2003 Blackwell Publishing Ltd 203 . The reasons for this situation are probably manifold but the observation that tunasÕ immune responses may be independent of ambient temperatures would seem to be a key factor when tuna are held at relatively low temperatures (Watts. Societa Italiana di Patologie 7. In: Tuna-Brief. Elder & Winton 2001) and pilchard herpesvirus (Hyatt. & Matsumoto K. (1973) Les helminthes ´decine parasites des thons tropicaux. Diseases of tunas the occurrence of relatively few bacterial diseases. Canadian Journal of Zoology 68. 26. Jones. Bulletin du Muse National d’Histoire Naturelle 166. The use of oily baitfish as a source of food for captive tuna poses a number of problems. Anders K. Bulletin of the Japanese Society of Scientific Fisheries 18. & Baudin-Laurencin F.L. Ph.W. as in the case of the threatened southern bluefin tuna. Acknowledgements References AQIS (1999) Import Risk Analysis on Non-viable Salmonids and Non-salmonid Marine Finfish. Hershberger. and yellowfin tuna. Whittington. However. (1965) Une tetrarhynchose vasculaire ´ des thons du Golfe de Guinee due aux larves plerocercus de Dasyrhynchus talismani R. I. Documents scientifiques. 7–10 [in Italian]. Chichester. Ellis Horwood.

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