6 infectious diseases of warmwater fish in marine …marine and freshwater fish (wolf, 1988)....

6 Infectious Diseases of Warmwater Fish inMarine and Brackish Waters

Leong Tak Seng1 and Angelo Colorni21School of Biological Sciences, Universiti Sains Malaysia, Penang, Malaysia;

2Israel Oceanographic and Limnological Research, National Center for Mariculture,PO Box 1212, Eilat 88112, Israel

Introduction

The culture of marine finfish in cages thathang from floating rafts was successfullyinitiated in Japan in the 1950s and in South-east Asia in the 1970s. In those early years,fish for culture were obtained from thewild. While in many regions this is still theway culture is started, some species of fishare today successfully hatchery-produced.The cage culture system is basically similarthroughout the world wherever intensivemariculture is practised. However, diseasetypes and severity are greatly influenced bythe species of fish, the conditions in whichthe animals are cultured and the husbandrymanagement.

Fish cultured in floating cages becomeparticularly susceptible to disease whenvarious environmental parameters such astemperature, salinity, dissolved oxygen andsuspended particles fluctuate suddenly orwidely, or following rough, although oftenunavoidable, handling operations. Onceconditions suitable for pathological changesdevelop, progress to disease in the warm-water environment is rapid. Early detectionof behavioural changes and clinical signs inthe cultured animals are critical for properdiagnosis of the disease.

The warmwater culture of marinefinfish in floating cages is concentrated in

two main geographic regions, namely WestAsia and Southeast Asia. The West Asiaregions present wider fluctuations of envi-ronmental conditions, particularly watertemperature, whereas in Southeast Asiathey are generally more stable. The speciesof fish cultured in the various regionsreflect these environmental differences.Other warmwater areas where cage cultureis practised on a commercial scale are thetropical islands of the Pacific Ocean.

The most common species of marinefish cultured in floating cages are summa-rized in Table 6.1.

Diseases Caused by Viruses

Viral diseases in cage-cultured fish havebeen on the increase since the 1980s in EastAsia and the 1990s in Southeast Asia (Nakaiet al., 1995; Arthur and Ogawa, 1996;Muroga, 1997; Bondad-Reantaso, 2001;Roongkamnertwongse et al., 2001; Zhang,2001). Virological research received a newimpetus following the high mortality inhatchery-bred juvenile fish soon after beingplaced in sea cages (Fukuda et al., 1996;Park and Sohn, 2001). With the increasingawareness of virus-related diseases andwith new species of fish being selected forculture, more reports of known and new

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viral diseases are to be expected. Theviruses reported in cultured marine fishare summarized in Table 6.2.

Lymphocystis

Lymphocystis is a highly contagiousinfection caused by a cytoplasmic DNAiridovirus. The disease follows a chroniccourse and, in general, mortalities arelimited. The infected fish recover within afew weeks of the onset of the outbreak,

displaying little or no scar tissue (Papernaet al., 1982). Although the unsightlyappearance of the typical lesions rendersthe infected fish unmarketable, juvenilesare considerably more susceptible to theinfection than larger, market-sized stages.

Host range. Although known to infect 30families of marine fish (Wolf, 1988),lymphocystis is a host-specific disease(Overstreet and Howse, 1977; Chao, 1984),therefore the disease is most probablycaused by a group of different viral strains.

194 T.S. Leong and A. Colorni

Species East Asia Southeast Asia West Asia

Serranidae (seabass and groupers)Dicentrarchus labrax (European seabass)Epinephelus aeneus (white grouper)E. coioides (greasy grouper)E. malabaricus (black dot grouper)E. bleekeri (brown grouper)E. fuscoguttatus (tiger grouper)

Lutjanidae (snappers)Lutjanus argentimaculatus (mangrove snapper)L. johni (golden snapper)L. russellii (Russell’s snapper)

Chanidae (milkfish)Chanos chanos (milkfish)

Centropomidae (snooks)Lates calcarifer (Asian seabass)

Mugilidae (mullets)Mugil cephalus (mullet)

Scorpaenidae (scorpion fishes)Sebastes schlegeli (black rockfish)

Carangidae (jacks)Seriola quinqueradiata (yellowtail)S. dumerili (yellowtail)Caranx (Pseudocaranx) dentex (striped jack)Trachurus japonicus (horse mackerel)

Tetraodontidae (puffers)Takifugu rubripes (tiger puffer)

Sparidae (seabream)Sparus aurata (silver seabream)Rhabdosargus sarba (goldlined seabream)Pagrus major (red seabream)P. schlegeli (black seabream)Acanthopagrus bifasciatusi (black seabream)

Sciaenidae (drumfish)Sciaenops ocellatus (red drum)

Pleuronectidae (flounders)Paralichthys olivaceus (Japanese flounder)

−−++++

+−+

+

−

−

−

++++

+

−++−−

−

+

−−++++

++−

+

+

−

−

−−−−

−

−−−−−

−

−

+++−−−

−−−

−

−

+

+

−−−−

-

+−−++

+

-

Table 6.1. Species (common name) of marine fish cultured in cages in Asia.



In Southeast Asia, only seabass (Latescalcarifer) has been reported to be affectedby this disease (Limsuwan et al., 1983; Chao,1984). In Israel, it was reported in seabream(Sparus aurata), a species reared in the RedSea but originally imported from theMediterranean Sea (Paperna et al., 1982),and in the red drum (Sciaenops ocellatus),originally imported from the USA (Colorniand Diamant, 1995). Lymphocystis hasbeen listed as a major viral diseaseof maricultured fish in Japan (Muroga,1995). In East Asia, outbreaks of thisdisease have been reported for seabass(Lateolabrax japonicus) (Miyazaki andEgusa, 1972; Chen, 1996; Park and Sohn,1996), yellowtail (Seriola quinqueradiata)(Matsusato, 1975), Japanese flounder(Paralichthys olivaceus) (Tanaka et al.,1984; Park and Sohn, 1996), red seabream(Pagrus major) (Chen, 1996; Park and Sohn,1996; Muroga, 1997) and rockfish (Sebastesschlegeli) (Chun, 1998). Matsuoka (1995)reported that the incidence of this diseasehas increased since the early 1990s, particu-larly in Japanese flounder.

Geographic distribution. Lymphocystisdisease is not restricted to warm seas, but iswidespread throughout the world in bothmarine and freshwater fish (Wolf, 1988).

Infectious Diseases of Warmwater Fish in Salt Water 195

Disease Causative agent Species affected

Lymphocystis (LCDV)

Red seabream iridoviraldisease

Viral nervous necrosis(SJNNV and VNN)

DNA virusIridovirus

RSIV

RNA virusNodavirus

Japanese flounder (Paralichthys olivaceus)Japanese seabass (Lateolabrax japonicus)Seabream (Sparus aurata)Red drum (Sciaenops ocellatus)Red seabream (Pagrus major)Grouper (Epinephelus malabaricus)

Striped jack (Pseudocaranx dentex)Black spotted grouper (Epinephelus bleekeri )Greasy grouper (Epinephelus coioides)Black spotted grouper (Epinephelus malabaricus)Grouper (Epinephelus tauvina)Marbled leopard grouper (Plectropomus maculates)European seabass (Dicentrarchus labrax)Asian seabass (Lates calcarifer)

Table 6.2. Viral diseases of warmwater maricultured finfish.

Diagnosis. The disease is characterized bytumour-like masses of tissue on the bodysurface (Fig. 6.1). These growths are clustersof extremely hypertrophic fibroblasticdermal cells (Fig. 6.2). In yellowtail, theinfected cells are dispersed, covered by alayer of epithelium and surrounded by blackpigment cells, thus appearing as small blackdots (Matsusato, 1975). Occasionally inter-nal organs can become infected (Colorni andDiamant, 1995).

Lymphocystis-infected cells are mainlyspherical in shape with a thick elastic mem-brane, but may be distorted when in clusters,due to pressure from adjacent cells. Theinfected cells apparently stimulate prolifera-tion of the adjacent healthy tissue. After 2weeks of infection, the cells enlarge signifi-cantly. Both nucleus and nucleolus presentlarge basophilic cytoplasmic inclusionbodies that react positively for DNA.

Diagnosis of lymphocystis disease isconfirmed through histological sections andappropriate staining of the tissue lesions. Infact, this is one of the few viral diseases thatcan be identified histologically. The obser-vation of the typical icosahedral virions byelectron microscopy offers further confirma-tion. Horizontal transmission is the mostprobable route, facilitated by high stockingdensity and unfavourable environmentalconditions. In Southeast Asia, trash fish



used as feed may be another source of infec-tion (T.S. Leong, personal observation).

Prevention and control. There is presentlyno effective therapy for this disease. Adecrease in stocking density and culling ofvisibly infected individuals are the onlyknown measures that can be adopted toreduce the impact of the disease.

Red seabream and brown-spottedgrouper iridovirus

The virus belongs to the family Iridoviridae.In electron microscopy, the particles appear

hexagonal in shape, with a diameter of200–240 nm (in red seabream) and140–160 nm (in brown-spotted grouper)(Danayadol et al., 1997; Kasornchandra andKhongpradit, 1997).

Host range. Red seabream iridovirus(RSIV) was first diagnosed in Japan where itcaused a systemic infection in farmed redseabream (Inouye et al., 1992). This seriousdisease, however, affects other culturedmarine fish species (Nakajima et al., 1995).In 1993/94, an iridovirus disease similarto RSIV was reported in cultured grouper(Epinephelus malabaricus) in Thailand(Danayadol et al., 1997). So far, RSIV has


Fig. 6.1. Lymphocystis in Asian seabass, Lates calcarifer.

Fig. 6.2. Hypertropic fibroblastic cells in caudal fin of Asian seabass, Lates calcarifer.



been found in more than 20 marine species(Matsuoka et al., 1996; Nakajima, 1997).Juvenile and young red seabream cultured incages are highly susceptible to the disease.

Geographic distribution. Red seabreamiridovirus disease and similar iridoviraldiseases have been reported in Southeastand East Asia.

Diagnosis. Affected fish become lethargicand severely anaemic. The gills are haemor-rhagic. The spleen is hypertrophic and theiridovirus appears in a crystalline arrayin the enlarged, basophilic splenic cells(Inouye et al., 1992). Presumptive diagnosisbased on Giemsa staining of histologicalsections can be confirmed by immuno-fluorescence with a monoclonal antibody ora PCR assay (Inouye et al., 1992; Nakajimaand Sorimachi, 1994; Nakajima et al., 1995,1997). RSIV can be isolated in several celllines including RTG-2, CHSE-214 and FHM(Inouye et al., 1992). Sensitivity was particu-larly high in KRE-3 and BF-2 (Nakajima andSorimachi, 1994). However, viral infectivitydecreased progressively with cell subcul-tures. The grouper iridovirus grew well inepithelioma papulosum cyprini (EPC) andgrouper fin (GF) cell lines (Kasornchandraand Khongpradit, 1997).

Prevention and control. An experimentalvaccine prepared by Nakajima et al. (1997)produced a higher survival in treated redseabream than in the control group, suggest-ing the possibility of controlling the diseasethrough vaccination.

Viral nervous necrosis (VNN)

The terms fish viral encephalitis andencephalopathy have been used to describea number of infections with a similar syn-drome. VNN was first reported in Japaneseparrotfish (Oplegnathus fasciatus) in a1985–1987 disease outbreak (Yoshikoshiand Inoue, 1990) and the causative agenthas since been identified as a member ofthe Nodaviridae and named striped jack

nervous necrosis virus (SJNNV) (Mori et al.,1992).

Electron microscopy demonstrates thatthe virus particles are packed in the cyto-plasm of affected retinal and brain cells andare non-enveloped, icosahedral in shape,about 20 nm in grouper and 25–34 nm instriped jack (Danayadol et al., 1993; Nguyen,1996).

Host range. Since it was first reported inJapanese parrotfish, VNN has been diag-nosed in more than ten fish species in Japan(Mori et al., 1991; Arimoto et al., 1993;Muroga, 1995; Nakai et al., 1995). Similarviral diseases have been reported in Asianseabass (see Glazebrook et al., 1990; Mundayet al., 1992; Comps et al., 1994), grouper(Epinephelus spp.) (Chong and Chao, 1986;Danayadol et al., 1993, 1995; Chua et al.,1995; Boonyaratpalin et al., 1996; Tanakaet al., 1998; Bondad-Reantaso et al., 2001),European seabass (Dicentrarchus labrax)(Breuil et al., 1991; Comps et al., 1994),turbot (Scophtalmus maximus) (see Blochet al., 1991) and halibut (Hippoglossushippoglossus) (see Grotmol et al., 1995). Asimilar syndrome was reported in the Euro-pean seabass cultured in Martinique, FrenchCaribbean Islands (Bellance and Gallet deSaint Aurin, 1988; Gallet de Saint Aurinet al., 1990).

Geographic distribution. VNN disease hasbeen found in all warmwater marineenvironments where marine fish have beencultured in cage environments, particularlyin juvenile stages.

Diagnosis. Infected fish exhibit whirlingmovements, lethargy, dark body coloration,loss of balance and hyper-excitability inresponse to noise and light. Mortalities areusually high and occur within a week of theonset of first signs. Extensive spongiosis istypically observed in the retina, brain andcentral nervous system (Glazebrook et al.,1990; Yoshikoshi and Inoue, 1990; Arimotoet al., 1992, 1993; Munday et al., 1992;Danayadol et al., 1995; Boonyaratpalin et al.,1996; Nguyen, 1996). SJNNV can be detected




by ELISA and PCR (Arimoto et al., 1992;Mushiake et al., 1992, 1994). A PCR methodbased on the sequence of the virus coatprotein gene (RNA2) was used to diagnosethe virus in spawners, suggesting verticaltransmission of the infection (Arimoto et al.,1992; Mushiake et al., 1992; Nishizawaet al., 1994, 1995).

Prevention and control. At present there isno known method of therapy, but vaccina-tion using recombinant coat protein of livepiscine nodavirus in sevenband grouper,Epinephelus septemfasciatus, resulted insignificantly lower mortality in the viruschallenge tests, indicating great potential forprotection against the virus.

Diseases Caused by Bacteria

Many clinical signs of bacterial diseases ofcultured marine fish are similar. Definitivediagnosis requires the isolation and in vitroculture of the organisms involved. A greatnumber of aquatic bacteria are oppor-tunistic and under normal environmentalconditions do not cause disease, becomingpathogenic only when the balance of thehost/environment is changed by elevatedstocking densities, inadequate nutrition,deteriorating water quality, rough handling(e.g. net changing, grading) and other stressfactors. The bacteria reported in culturedmarine fish are summarized in Table 6.3.

Epitheliocystis

The epitheliocystis organism is a chlamydia-like, obligate, intracellular prokaryote thathas not been cultured in vitro. Infection pri-marily involves epithelial cells of the gillsthat become packed with a large mass of theminute coccoid organisms. Transmission isapparently horizontal and direct. Extensiveinfections occur in juveniles and are oftenlethal. Epitheliocystis is highly infectiveand host-specific, indicating that thedisease in different species of fish is mostprobably caused by different strains of

epitheliocystis organisms (Lannan et al.,1999). Two distinct developmental lifecycles have been recently hypothesized fora highly pleomorphic chlamydia-like organ-ism that causes epitheliocystis infection inseabream (S. aurata) (Crespo et al., 1999).

Host range. Epitheliocystis infections havebeen reported from over 25 species offish, including Carangidae, Centrarchidae,Centropomidae, Mugilidae, Pleuronectidae,Serranidae and Sparidae (see Crespo et al.,1999).

Geographic distribution. Epitheliocystis isnot limited to a warm marine environmentand has been reported worldwide (see Noga,1996; Crespo et al., 1999; Lannan et al.,1999).

Diagnosis. Affected fish typically displayflared opercula and fast, shallow respiration.In histological sections, epithelial hyperpla-sia and fusion of adjacent gill lamellae areapparent. Infected cells (up to 220 × 100 µmin size, depending on developmental stage)are basophilic and appear either amorphousor uniformly granular.

Prevention and control. At present, noeffective therapy for epitheliocystis isknown.

Gram-negative bacteria

Vibriosis

Vibriosis is the disease caused by a groupof bacteria belonging to the family Vibrion-aceae. The infectious disease they cause isone of the most significant in mariculture.Age and sex of fish are not relevant factorsin the disease (Sano and Fukuda, 1987;Arthur and Ogawa, 1996; Leong, 1996;Sako, 1996; Shariff and Arulampalam,1996). In Southeast Asia, 4–6-week-oldcaged grouper weighing approximately200 g often die overnight without anyapparent signs of disease except that thebody darkens. This condition is referred to




as ‘sleepy-grouper syndrome’, but its aetiol-ogy is still controversial. In Singapore andIndonesia, cases of sleepy-grouper syn-drome were originally attributed to a virus(Chua et al., 1994; Arthur and Ogawa,1996), with vibrios considered as secondaryinvaders. In Malaysia, groupers withsleepy-grouper syndrome were found withhigh numbers of monogeneans as well aswith gastroenteritis vibriosis (however, fishwere not examined for virus) (Leong andWong, 1993).


Causative agent Disease Species affected

Gram-negative pathogensVibrionaceae

Listonella anguillarum

Vibrio alginolyticus

Vibrio parahaemolyticus

Photobacterium damsela

EnterobacteriaceaeEdwardsiella tarda

CytophagaceaeFlexibacter maritimus

Gram-positive pathogensStreptococcus spp.

Acid-fast pathogensNocardiaceaeNocardia seriolaeMycobacteriaceaeMycobacterium marinum

Vibriosis

Vibriosis

Vibriosis

‘Pasteurellosis’

Edwardsiellosis

Saltwatermyxobacteriosis

Streptococcosis

Nocardiosis

Mycobacteriosis

Yellowtail (Seriola quinqueradiata)Amberjack (Seriola dumerili )Horse mackerel (Trachurus japonicus)Red seabream (Pagrus major)Greasy grouper (Epinephelus coioides)European seabass (Dicentrarchus labrax)Seabream (Sparus aurata)Golden snapper (Lutjanus johni)Seabream (S. aurata)Yellowtail (S. quinqueradiata)Amberjack (S. dumerili )European seabass (D. labrax)Seabream (S. aurata)Red drum (Sciaenops ocellatus)

Japanese flounder (Paralichthys olivaceus)

Red seabream (P. major)Greasy grouper (E. coioides)Asian seabass (Lates calcarifer)Mangrove snapper (Lutjanus argentimaculatus)Japanese flounder (P. olivaceus)

Greasy grouper (E. coioides)Yellowtail (S. quinqueradiata)Amberjack (S. dumerili )European seabass (D. labrax)Red drum (S. ocellatus)Tilapia (O. mossambicus) (adapted to seawater)

Yellowtail (S. quinqueradiata)Amberjack (S. dumerili )Seabream (S. aurata)European seabass (D. labrax)

Table 6.3. Bacterial diseases of warmwater maricultured finfish.

Host range. The majority of marine fishcultured in cages are susceptible to vibriosis,with some fish species more sensitive tothe infection than others. In East Asia,yellowtail, red seabream, horse mackereland flounder are particularly susceptible.In Southeast Asia, grouper, seabass andsnapper have been frequently reported asaffected by vibriosis. The greasy grouper(Epinephelus coioides) (Fig. 6.3) is moresusceptible than black-spotted grouper (E.malabaricus) and brown-spotted grouper



(Epinephelus bleekeri), even when all threespecies are cultured in the same cage. Itoccurs frequently during periods of fluctua-tions in salinity, increased organic load,or stress brought on by net changing andgrading of fish. The period following initialstocking is particularly critical. Horizontaltransmission is the most probable route,with bacteria being shed from open lesions.

In Israel, mortalities of seabream cul-tured in the Red Sea were associated withisolation from the blood stream of Vibrioalginolyticus, Vibrio parahaemolyticus andVibrio anguillarum or anguillarum-like.Infection by these microorganisms, how-ever, was low (Colorni et al., 1981).

Geographical distribution. Vibrios are ubiq-uitous in all marine environments and mostare facultative pathogens. The species ofvibrios involved in diseases reflect regionaldifferences. In East and West Asia, the mostcommonly isolated species are Vibrio ord-alii, Vibrio ichithyoenteri, Vibrio trachuri,Vibrio damsela and Listonella (Vibrio)anguillarum (Kusuda and Kawai, 1997). InSoutheast Asia, V. parahaemolyticus and V.alginolyticus are the main species involved(Wong and Leong, 1986, 1990).

Diagnosis. Vibriosis is characterized byhaemorrhagic septicaemia. The clinicalsigns are capillary congestion and ‘red boils’

appearing on the body surface and gradualdarkening of the body. Initially, the haemor-rhage usually enlarges into irregular anddeep lesions, which disintegrate the skin,exposing the underlying muscle, whichbecomes necrotic. Vibrios produce a widevariety of proteases and extracellularenzymes that are responsible for theextensive tissue damage (Thune et al., 1993).

Two forms of vibriosis are recognized.The first form produces external haemor-rhage and is referred to as the dermatitisform of vibriosis. The second form is lesscommon and is referred to as gastroenteritisvibriosis. The latter does not have externalsigns (Muroga et al., 1990; Egusa, 1992). Inthe dermatitis form of vibriosis, internalpathology occurs as the disease progresses,with congestion and haemorrhage of theliver and enlargement and liquefaction ofspleen, liver and kidney. The histopatho-logical changes are associated with intesti-nal haemorrhage and destruction of thetunica mucosa. Groupers with sleepy-grouper syndrome tend to give out a charac-teristic strong, foul smell from the abdomenwhen examined. Biochemical and immuno-logical methods are used for identification,but most require culture and isolation ofthese pathogens. The organisms are Gram-negative rods with motile polar flagella,non-capsulated and non-spore producing.They are positive for oxidase and catalase,


Fig. 6.3. Vibriosis in greasy grouper, Epinephelus coioides.



and generally ferment a large number ofcarbohydrates.

Prevention and control. Leong et al. (1997)reported that groupers vaccinated againstvibriosis do not show any sign of sleepy-grouper syndrome. The vaccinated grouperswere healthier and grew faster, suggestingthat the sleepy-grouper syndrome in groupercould in fact be gastroenteric vibriosis. Goodhusbandry practice and adequate nutritionare essential to prevent the development ofvibriosis. The initial stage of the disease canbe treated with a number of sulphur drugs infeed with good results. The dosage variesbetween 50 and 200 mg kg−1 fish weightday−1 for 10–20 days (Sano and Fukuda,1987). Intraperitoneal injection has beenmost effective for the treatment of vibriosisin adult grouper.

‘Pasteurellosis’

‘Pasteurellosis’ is the second most impor-tant infectious disease in cultured yellow-tail in Japan. It causes the loss of thousandsof tonnes of cultured yellowtail (Sanoand Fukuda 1987; Sako, 1996). The routeof infection is probably oral. Stress is animportant predisposing factor to infection.

Although the aetiological agent was firstdescribed by Janssen and Surgalla (1968)as a member of the Pasteurella genus, itstaxonomic position was later questionedby Gauthier et al. (1995) who placed it inthe genus Photobacterium and renamed itPhotobacterium damsela subsp. piscicida.However, while confirming that thepathogen should be included in the genusPhotobacterium, Thyssen et al. (1998) foundno evidence, morphological or biochemical,to justify its classification as a subspecies ofPhotobacterium damselae.

Host range. The seabream in Israel(Colorni, 1998) and yellowtail, blackseabream, horse mackerel and Japaneseflounder in Japan and Korea have beenreported to be seriously affected by thebacterium (Sano and Fukuda, 1987; Kusuda

and Salati, 1993; Park and Sohn, 1996; Sako,1996).

Geographical distribution. The majority ofdisease outbreaks involving this bacteriumhave been reported in both Mediterraneanand Red Sea Israeli fish farms (Colorni, 1998),as well as in Japan, America and Mediter-ranean countries. This bacterium is affectedby water temperature and the disease tendsto occur in the summer months with watertemperature between 20 and 25°C.

Diagnosis. Pasteurellosis is a septicaemicdisease with no external signs exceptoccasional darkened spots on the bodysurface in yellowtail (Kubota et al., 1970a;Fukuda and Kusuda, 1981). A large numberof white spots of 0.5–3.5 mm correspondingto foci of bacterial colonization engulfedby phagocytes is found in the spleen andkidney, and to a lesser extent in the liver(Kubota et al., 1970a,b, 1972; Egusa, 1992).The numbers of macrophages increase in thespleen, kidney, gill and liver, which oftenappear necrotic and enlarged (Figs 6.4 and6.5). Many bacteria are able to survive in themacrophage (Nelson et al., 1989). The dis-eased fish rapidly lose their vigour, sink tothe bottom of the cage and die.

P. damsela is Gram-negative, non-motile, usually short (0.5–0.7 × 0.7–2.6 µm),bipolar and pleomorphic (from coccoidal torod-like, depending on the culture and envi-ronmental conditions). A variety of media,including yeast peptone agar, brain andheart infusion agar and blood agar contain-ing 1.5–2.0% NaCl can be used to isolate thebacterium. Colonies are small (1–2 mm indiameter) and translucent.

Prevention and control. Ampicillin (Aokiand Kitao, 1985) and florfenicol (Yasunagaand Yasumoto, 1988) have been reportedto be effective when administered in feed.This bacterium is known, however, readilyto become resistant to antibiotics. Vaccinepreparations also gave satisfactory results(Fukuda and Kusuda, 1985; Kusuda andHamaguchi, 1988; Kusuda et al., 1988).




Edwardsiellosis

Edwardsiellosis, caused by bacteria ofthe genus Edwardsiella (family Enterobac-teriaceae), is a systemic bacterial disease,reported in warm freshwater and marinefish. The pathogenesis in cultured marinefish has not been well documented. Twospecies are involved, Edwardsiella tarda(infecting a variety of both freshwater andmarine fish) and Edwardsiella ictaluri(infecting mainly cultured catfish of thegenus Ictalurus) (see Chapter 7).

Host range. This bacterial disease has beenreported from a large variety of culturedmarine fish including mullet (Mugil

cephalus) (Kusuda et al., 1976a), crimsonseabream (Evynnis japonica) (Kusuda et al.,1977), yellowtail (S. quinqueradiata), redseabream (Chrysophrys major) (Yasunagaet al., 1982) and Japanese flounder (P.olivaceus) (Nakatsugawa, 1983).

Geographic distribution. E. tarda has aworldwide distribution, occurring in bothfreshwater and marine environments. Itcauses severe disease problems in a varietyof cultured marine fish, mainly in SoutheastAsia (see Plumb, 1999).

Diagnosis. Edwardsiellosis is characterizedby cutaneous haemorrhagic ulcers, which


Fig. 6.4. Enlarged spleen with white spots in seabream, Sparus aurata, typical of ‘pasteurellosis’ byPhotobacterium damsela.

Fig. 6.5. Splenic foci of Photobacterium damsela, typical of ‘pasteurellosis’ in seabream, Sparus aurata.



gradually deepen into the muscle forminglarge necrotic abscesses. Internally, greyish-white spots develop in the spleen andkidney (Kusuda et al., 1977). E. tarda isan enteric, Gram-negative motile rod withperitrichous flagella. It grows on mediawith 0.5–4% NaCl, a temperature rangeof 15–41°C and a pH level of 5.5–9.0,with small circular transparent colonies(Wakabayashi and Egusa, 1973; Kusudaet al., 1976a, 1977; Amandi et al., 1982;Yasunaga et al., 1982; Nakatsugawa, 1983;Farmer and McWhorter, 1984; Waltmanet al., 1986). Little variation in the biochemi-cal and biophysical characteristics existedin 116 isolates from Taiwan and the USA(Waltman et al., 1986). Traditional diagnosisof edwardsiellosis involves isolation of thebacterium and identification by biochemicaltests. A fluorescent antibody (FA) methodand an ELISA have been developed (Kusudaand Salati, 1993).

Prevention and control. Infection of E. tardacan be treated by application of antibioticmedicated feed. Salati (1988) reported thatthe most effective drug is oxolinic acid,followed by trimethoprim, oxytetracycline,furazolidone and piromidic acid. Althoughthe bacterium is sensitive to a wide varietyof antibiotics, strains resistant to chloram-phenicol, furazolidone and sodium nifur-styrenate have been detected (Aoki et al.,1977, 1989; Waltman and Shotts, 1986).

Most studies on vaccination against E.tarda have been carried out on eel in Taiwanand Japan (Song and Kou, 1979; Song et al.,1982; Salati et al., 1983; Salati, 1985; Salatiand Kusuda, 1985a,b), but overall littleresearch has been carried out on the vac-cination of cultured marine fish. Salati et al.(1987) showed that vaccination of redseabream with formalin-killed cells andcrude lipopolysaccharide (LPS) preparationof E. tarda enhanced phagocytosis andincreased antibody titres.

Gliding bacterial disease/tail rot disease

A columnaris disease in Asian seabass wasreported in Thailand in 1983 (Danayadolet al., 1984) and the bacterium involved was

identified as a Flexibacter sp. (Ruangpan,1985; Ruangpan et al., 1987). Since 1988,disease epizootics have been observedwhenever the seabass fingerlings have beenintroduced for culture in netcages through-out Southeast Asia (Chong and Chao, 1986;Perngmark, 1992; Leong, 1994).

A disease associated with glidingbacteria was described in red seabream andblack seabream in Japan by Masumura andWakabayashi (1977). This disease is similarin appearance to columnaris disease offreshwater fish and the aetiological agentalso belongs to the genus Flexibacter.Wakabayashi et al. (1986) proposed thename Flexibacter maritimus for the organ-ism, which has an obligate requirement forseawater irreplaceable by NaCl alone forgrowth (Hikida et al., 1979). In SoutheastAsia, gliding bacteria were reported asFlexibacter sp. (Danayadol et al., 1984;Ruangpan, 1985; Baxa et al., 1986; Chongand Chao, 1986: Wakabayashi et al., 1986;Ruangpan et al., 1987; Leong, 1994).

Two species of Flexibacter have beendescribed, F. maritimus from seabream (P.major) (see Wakabayashi et al., 1986) andFlexibacter ovolyticus from Atlantic halibut(H. hippoglossus L.) (see Hansen et al.,1992). The flexibacter-like bacteria thatcause tail rot syndrome in cultured marinefish, particularly Asian seabass, have notbeen characterized.

Host range. A variety of marine fishcultured in cages has been reported to beaffected by gliding bacteria. In East Asia,yellowtail, red seabream, black seabream,Japanese flounder, tiger puffer, grouperand grey mullet are susceptible to thisgliding bacterial disease (Masumura andWakabayashi, 1977; Baxa et al., 1986,1987a,b; Arthur and Ogawa, 1996;Lavilla-Pitogo et al., 1996; Liao et al., 1996;Park and Sohn, 1996; Sako, 1996; Kusudaand Kawai, 1997).

In Southeast Asia, caged Asian seabass(Fig. 6.6) are most susceptible to tail rot,followed by the mangrove snapper, goldensnapper and grouper, though to a lesserextent (Danayadol et al., 1984; Ruangpan,1985; Chong and Chao, 1986; Ruangpan




et al., 1987; Leong et al., 1992; Perngmark,1992). Histopathological study of the tail rotsyndrome in Asian seabass has indicatedthat the onset of the disease is through thepathogen infection in the tail region andproliferation in the epidermis and dermis(Perngmark, 1992).

Geographic distribution. Gliding bacteria ofthe genus Flexibacter appear to have aworldwide distribution. Only F. maritimushas been reported in East Asia.

Diagnosis. In seabream and yellowtail inEast Asia, the gliding bacteria first gain entrythrough the damaged caudal fin, wherethe tissues are gradually eroded away bythe action of the bacteria. The bacteria theninvade the muscular region, the musclesdisintegrate and typical tail rot occurs.No pathological changes are normallyobserved in the internal organs. The diseaseusually affects seabream and Asian seabassfry, 2–3 weeks after their introduction intosea cages.

F. maritimus is a long slenderGram-negative rod, which exhibits glidingmovements on a wet surface. Culture (oncytophaga medium) requires at least 30%seawater, which cannot be replaced by NaCl.Colonies are pale yellow.

Prevention and control. It is difficult toprevent and control the disease in the cageenvironment. The standard treatment is feedmedicated with oxytetracycline or a bath insodium nifurstyrenate. However, the resultsare usually unsatisfactory. A combination offreshwater treatment and reduction ofstocking density helps to reduce mortality inaffected seabass (T.S. Leong, unpublisheddata).

Gram-positive bacteria

Two Gram-positive bacteria are ofmajor importance in maricultured fish:Enterococcus seriolicida and Streptococcusiniae (Kusuda and Salati, 1999).

Streptococcosis

The taxonomy of fish streptococci is stillcontroversial, but more than one speciescausing a similar syndrome is involved.The disease is most severe when farmedfish are stressed and water temperature ishigh. The onset of the disease is related tothe rapid growth of the bacterium in theintestine where both extracellular and intra-cellular toxins are produced (Kusuda et al.,1978; Kimura and Kusuda, 1979, 1982).


Fig. 6.6. Trail rot syndrome in juveniles of Asian seabass, Lates calcarifer.



Kusuda and Hamaguchi (1989) showed thatthe former have haemolytic activity andthe latter leucocidal activity. The diseaseis transmitted by contact (Robinson andMeyer, 1966), but feed may also be a sourceof infection (Taniguchi, 1983).

Host range. A large variety of freshwaterand marine fish species has been reported tobe susceptible to Streptococcus spp. Thefarmed species affected by streptococci aregrouper and rabbitfish in Southeast Asia(Chong and Chao, 1986; Leong, 1994), andyellowtail, red seabream, Japanese flounder,Japanese seaperch, rockfish and horsemackerel in East Asia.

In Israel, Streptococcus spp. have beenisolated from European seabass, tilapia(Oreochromis mossambicus) adapted to sea-water and red drum. This last isolate wasidentified as S. iniae (Eldar et al., 1999).

Geographic distribution. Streptococcosis isnot confined to warm water, and both fresh-water and marine species can be affected.Heavy losses have been reported inyellowtail, horse mackerel and Japaneseflounder in Japan (Kusuda et al., 1976b;Kitao et al., 1979; Sako, 1996) but thisdisease has been known to occur in avariety of fish in Australia, Italy, Israel,South Africa and the USA (see Austin andAustin, 1993). In Israel, severe mortalitieswere recorded among the red drum culturedin cages on the Mediterranean coast (Eldaret al., 1999).

Diagnosis. The clinical signs vary depend-ing on the fish species affected. In tilapia,S. iniae infection produces panophthalmitisand meningitis with only minor pathologi-cal changes in other organs (Eldar et al.,1995). In red drum, clinical signs includelethargy, loss of orientation, protrusion ofthe eye with clouding of the cornea anderosion of the skin (Eldar et al., 1999). Othercommon signs are darkening of the body,erratic swimming, haemorrhage in the intes-tine, liver, spleen and kidney, and abdomi-nal distention. Necrosis in the heart, gill,skin, spleen and eye have also been reported(Egusa, 1992).

Confirmation of the diagnosis requiresculturing the pathogen, preferably on ablood-enriched medium. Pathogen presencecan also be confirmed through direct or indi-rect fluorescent antibody methods (Kusudaand Kawahara, 1987; Kawahara et al., 1989).Recent studies have placed some isolates inthe genus Enterococcus (Kusuda et al., 1991;Kusuda and Salati, 1999). Streptococcus spp.(Fig. 6.7) are non-motile, Gram-positive,spherical to ovoid-shape cells, less than2 µm in diameter. When grown in liquidmedia, they occur in pairs or form shortchains (Kusuda and Kawai, 1982; Kusudaet al., 1991). Most are facultative anaerobes,without endospores, while some form cap-sules. Streptococci can be isolated fromdiseased fish using brain heart infusionagar with or without 1.5–2% NaCl.

Prevention and control. Control is mainlyby chemotherapy. Antibiotic treatment with


Fig. 6.7. Streptococcus iniae from seabass, Dicentrarchus labrax.



erythromycin, spiramycin and josamycinhas proved effective (Kashiwagi et al.,1977a,b; Shiomitsu et al., 1980; Kusuda andOnizaki, 1985; Kusuda and Takemaru, 1987;Takemaru and Kusuda, 1988a,b,c, 1990).

Acid-fast bacteria

Mycobacteriosis

The aetiological agents of mycobacteriosis,Mycobacterium marinum and other Myco-bacterium spp., cause systemic, chronicinfections in fish and other aquatic animals,and can occasionally cause skin ulcers inhumans.

Host range. Since its first isolation fromthe European seabass in 1990 in Eilat (RedSea, Israel) (Colorni, 1992), M. marinum hasbeen detected in at least 18 other species oflocal fish and may have spread from seacages to other farmed and native speciesin the Gulf of Eilat (Diamant and Colorni,1995). The commercial species found to beinfected are seabream (S. aurata), stripedbass (Morone saxatilis), sheepshead (sharp-snout) (Puntazzo puntazzo), red drum(S. ocellatus), rabbitfish (Siganus rivulatus),mullet (M. cephalus), red seabream (P.major), hybrid red seabream (P. major ×

S. aurata), grouper (Epinephelus aeneus)and tilapia (O. mossambicus). Of these, onlyS. rivulatus and M. cephalus are native to theRed Sea.

Geographic distribution. Fish mycobacter-iosis is not restricted to warm seas, but iswidespread throughout the world in bothmarine and freshwater environments. Differ-ent endemic strains of M. marinum exist,specific to geographic regions (Colorni et al.,1996).

Diagnosis. The disease follows a chroniccourse and remains asymptomatic for a longtime. Superficial ulcers and exophthalmiaare often the only external signs. Spleen andkidney, however, are severely affected andare enlarged with granulomatous lesionsthat appear macroscopically as whitishnodules (Fig. 6.8). In advanced cases theselesions spread to liver, heart, mesentery, etc.Special media (such as Löwenstein–Jensenor Middlebrook) are required for the cultureof these mycobacteria, whose growth is usu-ally slow (2–3 weeks for the first colonies tobecome visible). A Ziehl–Nielsen stainreveals the typical slender acid-fast rods(Fig. 6.9).

Prevention and control. There is no effec-tive control.


Fig. 6.8. Extremely enlarged granulomatous spleen of seabass, Dicentrachus labrax, infected withMycrobacterium maritimus.



Nocardiosis

Nocardiosis is a chronic bacterial diseasethat affects both freshwater and marine fish.In Japanese yellowtail, amberjack andstriped jack it is caused by Nocardiakampachi (Kariya et al., 1968; Kawatsuet al., 1976; Sako, 1996).

Host range. N. kampachi appears to berestricted to yellowtail, amberjack andstriped jack (Kariya et al., 1968; Kubotaet al., 1968).

Geographic distribution. N o r c a d i o s i scaused by N. kampachi is restricted toEast Asia, primarily where yellowtails arecultured.

Diagnosis. Many clinical characteristics ofnocardiosis are similar to mycobacteriosis.The disease occurs sporadically duringautumn but outbreaks can extend from Julyto February. Early signs of infection includeanorexia, inactivity, skin discoloration andemaciation. In the late stages, nodular skinlesions may ulcerate or extend to skeletalmuscle and visceral organs, causing abdomi-nal distension.

The morphology of Nocardia varies, butcells are generally filamentous, branched orbeaded. The bacterium is acid-fast and cangrow on a variety of media containing carbonand nitrogen sources. It can be isolated onbrain heart infusion agar (BHIA), tryptonesoya agar (TSA) and nutrient agar (NA), withoptimum growth temperature at 20–30°C

(Kusuda and Taki, 1973; Kusuda et al.,1974). It produces flat, wrinkled coloniesafter 10 days at 25°C. N. kampachi does notgrow at 37°C.

Prevention and control. There is no effectivetherapy for this disease. The route of infec-tion in fish is not known, but is probablythrough direct contact or contaminated food.A clean environment is an important factorin preventing the occurrence of the disease.Kusuda and Nakagawa (1978) showed thatN. kampachi can survive for more than90 days in the presence of 100 mg l−1 fishextracts, but only 2 days in open seawater.

Diseases Caused by Protistans

A large, heterogeneous group of pathogenicone-cell organisms are associated with fish.Some are ectoparasites while others areendoparasites. Many of these organisms arenot selective in their host preferences andcan cause severe damage to any marine fishin intensive culture. Others may coexistwith their host as epicommensals or asfacultative parasites. The obligate parasiticspecies are host-specific, thus better adaptedto coexist with their host causing limitedharm (Lom, 1984). The endoparasites mayconsiderably alter the appearance, taste andodour in the affected fish.

Myxosporean infections

Myxosporeans are endoparasites that canreside either in visceral cavities such asthe gallbladder, swimbladder and urinarytract (coelozoic species), or settle as inter-or intracellular parasites in blood, muscleor connective tissue (histozoic species).Spores with four polar bodies in the stellatearrangement typical of the genus Kudoa(6.4–13.6 µm in length) have been foundin the viscera of seabream cultured in theRed Sea (Paperna, 1982). This histozoicmyxosporean may have originated in theMediterranean Sea and been introducedinto the Red Sea with infected seabream.


Fig. 6.9. Mycobacterium marinum in seabass,Dicentrachus labrax (Ziehl–Neelsen stain).



The parasite causes relatively benign infec-tions, usually limited to a few individuals.

A debilitating myxosporean disease wasdescribed in S. aurata by Diamant (1992)and Diamant et al. (1994). The aetiologicalagent, Myxidium leei, is a histozoic speciesthat settles in the intestinal mucosa. In heavyinfections, fish present an enlarged abdo-men, with the intestinal tract filled withpurulent, foul-smelling liquid. Histologi-cally, small plasmodia (22 µm average size),which each give rise to two spores, aredetected between the epithelial cells of themucosa along the entire intestinal tract.As the same parasite was later discoveredin other Mediterranean sparids and greymullets (Lom and Bouix, 1995), M. leei toowas probably imported with its host into theRed Sea. Recently, Diamant (1997) demon-strated that transmission of this organismdoes not require an intermediate host.

Another histozoic myxosporean, S.epinepheli, was described in the urinarysystem of adult groupers (E. malabaricus)from Southeast Asia (Supamattaya et al.,1990, 1993). Presporogonic stages, roundto oval in shape (1.98–10.75 µm), carriedin the blood stream, settle in the kidneytubules where sporogenesis occurs. Maturespores, subspherical to spherical in shape(7.8–10 µm in length, 12.3–14.5 µm inthickness, 7–9.5 µm in width) present tworound polar capsules. The epithelium ofthe renal tubules harbouring the parasitesappears highly vacuolated. The life cycleof myxosporean parasites from marinehosts is unknown, but as Diamant (1997)demonstrated for M. leei, the notion that anintermediate host is indispensable for thecompletion of the myxosporeans’ life cycleneeds to be revised.

A Sphaerospora-like myxosporideanwas reported to have caused a high cumu-lative mortality (90%) in cultured cobia,Rachycentron canadian (L.), in Taiwan(Chen et al., 2001). The extrasporogonicand/or sporogonic stages appeared in theblood, glomerulus, renal tubules and renalinterstitium. Matured spores with polarfilaments were elongated or spherical,with numerous refractile granules in thecytoplasm.

Infections by ciliates

Brooklynellosis

Brooklynella hostilis is a ciliate protozoanthat was first described in aquarium fish byLom and Nigrelli (1970) as a gill pathogen.However, B. hostilis can also cause seriousskin lesions (Noga, 1996). In heavy infec-tions the ciliates destroy the host’s surfacetissue with their cytopharyngeal armature,feeding on tissue debris, ingesting bloodcells and causing haemorrhage in the gills(Lom and Dyková, 1992).

Host and geographic distribution. Europeanseabass (D. labrax) and lutjanids culturedin Martinique suffered heavy infestationsof this parasite (Gallet de Saint Aurinet al., 1990). B. hostilis has been detectedrepeatedly in mariculture facilities inKuwait and Singapore (Lom and Dyková,1992). Recently, it was diagnosed in cage-cultured seabream (S. aurata) in the Red Sea(Diamant, 1998).

Diagnosis. B. hostilis is recognizable byits oval, dorsoventrally flattened shape,notched oral area and size, measuring36–86 × 32–50 µm (Lom and Dyková, 1992).

Prevention and control. There are no repor-ted methods for caged fish.

Cryptocaryonosis

Cryptocaryonosis is a disease caused bythe holotrich ciliate, Cryptocaryon irritans,a parasite belonging to the class Colpodea(order Colpodida) (Diggles and Adlard,1995). Only one species, C. irritans, isreported for the genus. However, intra-specific variants exist (Diamant et al., 1991;Colorni and Diamant, 1993; Diggles andLester, 1996b; Diggles and Adlard, 1997).The ciliate invades the skin, eyes and gillsof a suitable host, impairing the physio-logical functions of these organs. Its lifecycle is quadriphasic and includes a para-sitic phase on the fish (trophont), duringwhich Cryptocaryon feeds and can beobserved continuously revolving in the




fish epithelia. After growing for 3–7 daysto a maximum size of 300–400 µm, theparasite spontaneously leaves its host(as a protomont) and within several hoursencysts and starts dividing (tomont), even-tually producing up to 200 free-swimminginfective stages (theronts). Sizes and num-bers of theronts vary with the geographiclocations, fish host species and watertemperature (Colorni and Burgess, 1997).The theront life span is approximately 24 h,but its infectivity rapidly decreases after thefirst 6–8 h post-excystment (Yoshinaga andDickerson, 1994; Diggles and Lester, 1996a).

Host range. This ciliate protozoan showslow host specificity and is capable of infect-ing most marine teleosts. Host susceptibil-ity, however, may vary (Nigrelli andRuggieri, 1966; Wilkie and Gordin, 1969;Colorni, 1985). Grouper cultured in marinecages in Hong Kong were susceptible to theprotozoan infection; other fish species werenot (ADB/NACA, 1991). Cultured grouper,snapper and Asian seabass fingerling aresusceptible to this protozoan during theearly stage of cage culture (Chong and Chao,1986; Glazebrook and Campbell, 1987;Leong, 1994).

Geographic distribution. Although typicalof tropical seas, this parasite has a world-wide distribution that extends well into tem-perate environments (Diamant et al., 1991).

Diagnosis. The parasite burrows into thefish epithelia and appears macroscopicallyas pinhead-size whitish ‘blisters’, more con-spicuous on coloured fish and on the trans-lucent parts of the fins. Heavily infested fishmay frequently come to the surface, gaspingfor oxygen. Mucus production increases. Adefinitive diagnosis of cryptocaryonosis canbe made from the examination of a gill clipor a wet mount of fin or skin scraping forthe presence of the large, revolving ciliateprotozoans.

Prevention and control. The presence ofC. irritans in cage-cultured fish means thatthe cages are kept in too shallow waters. If

logistically feasible, the cages should bemoved into an area where sufficient depthand currents prevent the theronts from rein-fecting the fish (Colorni, 1987).

Diseases Caused by Metazoans

Monogenea

The monogeneans are gill and skin flukesfrequently encountered in mariculture sys-tems. Most monogeneans are host-specific,but some species have a wide host range.Monogeneans are hermaphroditic. Theirdirect life cycle, together with the availabil-ity of constantly stressed fish hosts in highstocking density environments, facilitatesfish-to-fish infestation (Paperna et al., 1984;Leong and Wong, 1987; Cone, 1995).

Capsalid monogeneans

Capsalid monogeneans are generally foundon the fish skin and under the scales, whilea few are found on the gills. They can moveactively on the body surface, feeding onepithelial cells and mucus. The body ofthese parasites is relatively large and flat,with a conspicuous muscular disc haptor atthe posterior end (Fig. 6.10). The haptormay be subdivided by septa. At the anteriorend is a pair of large disc-like adhesiveorgans. The intestinal caeca are diverticularand end blindly. Three genera, Benedenia,Neobenedenia and Megalocotyloides, arecommonly found infecting marine fishcultured in floating net cages (Table 6.4).

Host range. The capsalid monogeneanshave been reported from a wide host range inthe wild (Yamaguti, 1963; Paperna et al.,1984), in cultured marine fish and in marineaquarium fish (Nigrelli, 1943; Paperna andOverstreet, 1981; Leong and Wong, 1987;Ogawa et al., 1995a,b; Hla Bu et al., 1998).High mortalities associated with heavyinfestation of Benedenia epinepheli (Ogawaet al., 1995a) were reported in Japanese floun-der (P. olivaceus) in Shimane Prefecture andin black rockfish (Sebastes schlegeli) (with




an intensity of 900–1500 worms per fish) inYamaguchi Prefecture. Ogawa et al. (1995b)reported that 100% mortality of juvenileamberjack (Seriola rivoliana) in Okinawawas associated with N. girellae.

Some capsalid monogeneans appearto have low host specificity. For example,Ogawa et al. (1995a) reported that B.epinepheli was found in 25 fish host species,with tetraodontid fish being most sus-ceptible, as up to 3000 individuals of B.epinepheli were recovered from a singleindividual in Japan. In Malaysia, 13 speciesof cultured marine fish were found withcapsalid monogeneans (Benedenia lutjani,

B. epinpheli and Neobenedenia girellae).Both B. epinpheli and N. girellae werefound to be equally distributed on thegreasy grouper (E. coioides) and the Asianseabass (L. calcarifer). In general, serranid,sparid and lutjanid fish appear to be moresusceptible than other species. In the goldensnapper (Lutjanus johni) up to 60 B. lutjaniper infected host were counted. Tilapia cul-tured in cages in the marine environmentwere heavily infested by Neobenedeniamelleni in Hawaii and in the West Indies(Kaneko et al., 1988; Robinson et al., 1989;Gallet de Saint Aurin et al., 1990; Hall,1992).


Fig. 6.10. Capsalid monogenean commonly found on cultured marine fish.



Geographic distribution. The capsalidmonogeneans have a wide distribution pat-tern (Table 6.5). More benedenid specieshave been reported from the East Asia regionthan from other regions. This is probably duenot only to a greater variety of fish speciescultured, but also to the availability there ofmore diagnostic facilities.

Cultured fish infested with capsalidmonogeneans gradually withdraw fromthe group, quit eating and their bodiesgradually darken. Heavily infected fishswim erratically and rub against the net,which results in dermal ulceration andsubsequent bacterial invasion.

The active feeding of the monogeneanson mucus and epithelial cells leads tohaemorrhage, inflammation and mucushyperproduction (Paperna, 1991; Egusa,1992). The monogeneans often settle onand around the eyes, damaging the corneaand causing blindness (Egusa, 1992; Ogawaet al., 1995a; Colorni, 1998).

Prevention and control. The capsalid mono-geneans are found on a large variety of wildfish and it is difficult to prevent and controlthem in the cage environment. Despite theirsize (up to a few mm) the monogeneansmay go unnoticed. Whenever logistically


Fish species

Capsalid species 1 2 3 4 5 6 7 8 9 10 11

Benedenia epinepheliB. hoslinaiB. lutjaniB. monticelliB. seriolaeBenedenia spp.Neobenedenia girellaeN. melleniNeobenedenia sp.MegalocotyhoidesepinepheliM. convoluta

+−+−−++−++

+

+−+−−++−++

−

+−+−−−+−−−

−

+−+−−++−+−

−

+−+−−+−−+−

−

+−+−−+−−+−

−

+−+−−+−−+−

−

+−−−−−−−−−

−

+−−+−−−+−−

−

−−−−−−++−−

−

−+−−+−+−−−

−

(1) Epinephelus coioides; (2) E. malabaricus; (3) E. bleekeri; (4) Lutjanus johni; (5) L. argentimaculatus;(6) Lates calcarifer ; (7) Pinjalo-pinjalo; (8) Pagrus major; (9) Liza and Mugil spp.; (10) Prepchromis spp.;(11) Oplegnathus fasciatus.*Many more cultured marine finfish susceptible to capsalids are not listed here.

Table 6.4. Capsalid monogeneans found in various cultured marine finfish.*

Benedenid species East Asia Southeast Asia West Asia

Benedenia epinepheliB. monticelliB. seriolaeB. lutjaniB. hoshinaiBenedenia spp.Neobenedenia girellaeN. melleniNeobenedenia sp.Megalocotyloides epinepheliM. convoluta

+−+−+−++−++

+−−+−+−−+++

−+−−−−−+−+−

Table 6.5. Geographical distribution of various benedenid species in cultured marine fish.



feasible, a freshwater dip of 3–5 min shouldbe made to dislodge the parasites fromthe host (Leong, 1997; Zafran et al.,2000). The treatment kills the parasites,which turn white and become more visi-ble. Ellis and Watanabe (1993) reportedthat the egg, juvenile and adult stage ofN. melleni in cultured tilapia could beeliminated in a 5 day hyposalinity (15 g l−1 )treatment. Tropical cleaner-fish, such asthe wrasse (Thalassoma bifasciatum) andgobies (Gobiosonia genie, G. ocenops havebeen used to control N. melleni infectingseawater-cultured tilapia (Cowell et al.,1993).

Diplectanid monogeneans

Diplectanid monogeneans are found onlyon the gills of fish hosts, feeding on mucus.Two genera of diplectanids are found toinfest cultured marine finfish: Diplectanumand Pseudorhabdosynochus.

Host range. The diplectanid monogeneanshave been reported from a wide varietyof fish hosts (Beverly-Burton and Suraino,1981; Kritksy and Beverly-Burton, 1986;Leong and Wong, 1987; Hla Bu et al., 1999).In the tropical environment, they are com-monly found on cultured serranids, sparidsand centropomids (Table 6.6).

Diplectanid species are very host-specific and do not infect other fish species.Pseudorhabdosynochus epinepheli, Pseudo-rhabdosynochus lanteuensis, Pseudorhab-dosynochus coioidesis and Diplectanumgrouperi are found only in serranids, whereasPseudorhabdosynochus lateis, Pseudorhab-dosynochus monosquamodisci and Diplec-tanum penangi (Fig. 6.11) are found only incentropomids. Diplectanids are not knownto infect cultured lutjanid fish.

Geographic distribution. The geographicdistribution of diplectanid monogeneans incultured marine fish is shown in Table 6.7.


Fish species

Diplectanid speciesDicentrarchus

labraxEpinephelus

coioidesE.

malabaricusE.

bleekeriLates

calcarifer

PseudorhabdosynochusepinepheliP. lanteuensisP. lateisP. monosquamodisciP. coioidesisDiplectanum penangiD. grouperiD. aequansD. laubieri

−

−−−−−−++

+

+−−+−+−−

+

+−−+−+−−

+

−−−+−+−−

−

−++−+−−−

Table 6.6. Diplectanid monogeneans found in various cultured marine finfish.

Diplectanid species East Asia Southeast Asia West Asia

Pseudorhabdosynochus epinepheliP. lanteuensisP. lateisP. monosquamodisciP. coioidesisDiplectanum penangiD. grouperiD. aequansD. laubieri

++−−+−−−−

+++++++−−

−−−−−−−++

Table 6.7. Diplectanid monogeneans found in various culture locations.



More diplectanids are reported in culturedmarine fish from Southeast Asia but due tothe numerous transfers of live fish from oneregion to another, similar reports are to beexpected from East Asian regions, wheremany exotic marine finfish were recentlyimported by fish farmers.

Diagnosis. Fish infected with diplectanidmonogeneans do not show conspicuoussigns; haemorrhage, hyperplasia and fusionof lamellae at the points of attachmentare commonly observed (Oliver, 1977;Giavenni, 1983; Hla Bu and Leong, 1997).The body of diplectanid monogeneans iselongated and characterized by a large flathaptor with squamodiscs at the posteriorend.

Prevention and control. It is difficult toprevent the introduction of diplectanidsinto the culture system, especially whenfingerling and juvenile fish are obtainedfrom the wild. Freshwater treatment, whichworks effectively on benedenids, is noteffective against diplectanids. The popula-tion size of diplectanids may be controlledin culture systems through appropriatestocking density of the fish in each cage.

Dactylogyrid monogeneans

Dactylogyrid monogeneans are parasiteson the gills of cultured snapper. They aremucus feeders. One genus, Haliotrema, hasbeen reported from cultured lutjanids(Leong and Wong, 1987, 1989; Liang andLeong, 1992; Leong, 1994).

Host range. The monogeneans found invarious cultured marine finfish are shown inTable 6.8. They show restricted infectivity offish host and are found mainly on lutjanidfish, with the exception of Haliotrema


Fig. 6.11. Diplectanum penangi, a monogeneanworm infecting the Asian seabass, Lates calcarifer.

Fish species

Dactylogyrid species 1 2 3 4 5

Haliotrema johniH. noncalcarisHaliotrema sp. AHaliotrema sp. BHaliotrema sp. CHaliotrema sp. EHaliotrema sp. FHaliotrema sp.Haliotrema epinepheli

+−++−−+−−

++++++−−−

+−−−−−−+−

−−−−−−−−−

−−−−−−−−+

(1) Lutjanus johni; (2) L. argentimaculatus; (3) L. russelli; (4) Pinjalo-pinjalo; (5) Epinephelus coioides.

Table 6.8. Dactylogyrid monogeneans found in various cultured marine finfish.



epinepheli, which is found on serranids aswell.

There are nine known species ofdactylogyrids found in various species ofcultured marine snappers, all belonging tothe genus Haliotrema (Table 6.8). The meanintensity of infection of Haliotrema johni(Fig. 6.12) in cultured golden snapper (L.johni) (mean range of 162–409 per fish) wasfound to be an order of magnitude higherthan that in wild snapper (33 per infectedfish) (Leong and Wong, 1989). Furthermore,the prevalence and mean intensity of infec-tion of H. johni in cultured disease finger-ling golden snapper (90–97%; 107–314 perinfected fish) were much higher than thosein wild golden snapper (8–60%; 13–29 perinfected fish) (Leong and Wong, 1987). InPenang, Malaysia, Haliotrema noncalcariswas found in all cultured mangrove snapper(Lutjanus argentimaculatus), with a meanrange intensity of 45–58 per infected fish.Both Haliotrema sp. A and Haliotrema sp. Bwere also dominant numerically in bothgolden and mangrove snappers (Liang andLeong, 1992).

Geographic distribution. The dactylogyridsare commonly found in golden and man-grove snapper cultured in Southeast Asiaand in East Asia (Hong Kong).

Disease signs and pathology. Modera teinfection of dactylogyrids in cultured finfishdoes not show significant clinical signs.In heavy infection, however, the foreheadof the golden snapper is often devoid ofscales and with epidermal lesions from therepeated rubbing against the net in responseto the irritative action of the parasite (Chongand Chao, 1986). The histopathology ofdactylogyrids on cultured marine finfishhas not been reported.

Prevention and control. It is not possible toprevent fish from being infected by thesemonogeneans. Reducing stocking densityof juveniles in the cage would probablyreduce the build-up of population size ofmonogeneans in the fish. In heavily infectedgolden snapper, a formalin treatment of300 ppm for 30 min significantly reducesH. johni (48%) and Haliotrema sp. (78%),while treatment with fresh water reducedHaliotrema sp. by 91% (Liang and Leong,1992). Dipterex and malachite green werefound to be ineffective in reducing the popu-lation size of these monogeneans (Liang andLeong, 1992).

Microcotylid monogeneans

Microcotylid monogeneans are gill para-sites in which the haptor has numerousclamps that are important for taxonomicidentification. Some clamps are situatedon long stalks, while others are found onthe body surface at the posterior end. Themouth of microcotylids is adapted for bloodsucking.

Host range. The microcotylid monogen-eans have been reported on a wide range ofhosts in the wild (Yamaguti, 1963) and oncultured marine fish (Paperna, 1991; Egusa,1992). The microcotylids reported in cul-tured marine fish are shown in Table 6.9.Only a few of the many species of cultured


Fig. 6.12. Haliotrema johni, a monogenean infect-ing cultured golden snapper (Lutjanus johni).



fish have been reported to be infected bythe microcotylids, which display a certaindegree of host specificity.

Geographic distribution. The geographicdistribution of microcotylid monogeneans isshown in Table 6.9. None of them has beenfound in Southeast Asia.

Disease signs and pathology. Culturedmarine finfish infected by microcotylids donot always show clinical signs. There werefew or no pathological changes in greymullets, European seabass and gilthead sea-bream infected with microcotylids (Paperna,1991). Conversely, in other cultured fish,such as yellowtail and red seabream, mortal-ity in the cages has been directly attributedto the heavy infestation of these flukes.An average of 85 Heteraxine heterocercawere counted per infected yellowtail (Egusa,1992). A large amount of mucus is secretedwhen the parasite is present in high num-bers, gill filaments are destroyed, and haem-orrhage due to parasite feeding activitycan cause severe anaemia (Egusa, 1992). Par-asitized fish often suffer from a concurrentbacterial infection.

The microcotylids have a flat bodyand are relatively large, reaching 17 mm inH. heterocerca on yellowtail and 20 mmin Heterobothrium tetradonis on puffer fish(Egusa, 1992). Very little is known abouttheir development. The optimum tempera-ture for eggs of H. heterocerca to hatch is18–25°C. At 25°C, approximately 4 days arenecessary but it was found possible to

induce hatching between 10 and 28°C(Matsusato, 1968). The spawning period ofBivagina tai extends from November toJanuary and eggs hatch in approximately8.5 days at 18.5–19.5°C (Fujita et al., 1969).

Prevention and control. Preventing theintroduction of microcotylid monogeneansinto cage culture systems is difficult when-ever wild juvenile marine finfish are usedfor stocking. Finfish infected with microco-tylids have been successfully removed withimmersion in hyposaline water (Okamoto,1963; Akazaki et al., 1965; Fujita et al.,1969), sodium pyrophosphate–hydrogenperoxide but not by oral administration ofbithionol (Okamoto, 1963; Akazaki et al.,1965; Fujita et al., 1969). In addition,freshwater immersion was successful inremoving Choricotyle sp. in seabream(Egusa, 1992).

Sanguinicolid digeneans

Digenean species are endoparasitic andrequire one or more intermediate hosts(mostly snails) for the completion of theirlife cycle. The first larval stage emergingfrom an egg (miracidium) is ciliated andfree-swimming and develops into the sporo-cyst and redia stages, eventually producingcercariae and metacercariae. The parasite ismost lethal, particularly to juveniles, whenthe metacercariae migrate within the fishbody. The adult digeneans live in piscivorebirds.


Microcotylid species Fish host Culture sites

Bivagina taiChoricotyle elongataHeterobothrium okamotoiH. tetradonisHeteraxine heterocercaMetamicrocotyle cephalusMicrocotyle mugilisMicrocotyle sp.M. chrysophryeiM. labrachisPolylabris sp.

Pagrus majorPagrus majorPagrus majorTakifugu rubripesSeriola quiqueradiataMugil spp.Mugil spp.Lutjanus russelliSparus aurataDicentrarchus labraxSiganus spp.

East AsiaEast AsiaEast AsiaEast AsiaEast AsiaWest AsiaWest AsiaEast AsiaWest AsiaWest AsiaWest Asia

Table 6.9. Microcotylid monogeneans found in various cultured marine finfish.



Only digenean species belonging to thefamily Sanguinicolidae have been reportedto cause mortality in cultured marine finfish(Ogawa and Egusa, 1986; Herbert et al., 1994;Ogawa and Fukudome, 1994; Harisson,1995). Heterophyiid metacercariae have alsobeen reported in the muscles of marine fish,particularly in the mullets (Liza spp. andMugil spp.) (Egusa, 1992).

The infective stage of sanguinicolidspenetrates the fish host eventually gainingentry and settling into the vascular system.The flukes as well as their eggs are normallyfound obstructing the blood flow in the gillarteries, ventral aorta and the heart.

Host range. The sanguinicolids reported invarious cultured marine finfish are shown inTable 6.10. So far, only cultured carangid(Seriola sp.), seabass, grouper and snapperhave been reported to be infected with fourgenera of sanguinicolids, comprising fivespecies. Surveys by Ogawa et al. (1989,1993) and Ogawa and Fukudome (1994)revealed that nearly all the culturedSeriola spp. examined were infected byParadeontacylix spp. All seabass from PulauKetam, Selangor, Malaysia, larger than 10 gwere found to be infected by Cruoricola lates(Herbert et al., 1994), while 63% of 19examined seabass weighing between 18 and1073 g in Penang were infected (Harisson,1995). According to Herbert et al. (1994), themajority of C. lates are found in the venulesaround the stomach, pyloric caeca, intestineand excretory bladder. In Penang, 70% ofcultured greasy grouper (E. coioides), with aweight range between 52 and 364 g, wereinfected by the sanguinicolid, Pearsonellum

corventum, with a mean intensity of eightper fish (Harisson, 1995).

Geographic distribution. The few sanguini-colids are reported to show a limited geo-graphical distribution, in accordance withthat of their host (Table 6.10). Paradeonta-cylix spp. are found in East Asia, whereasCruoricola sp., Pearsonellum sp. and Car-dicola sp. are found in Southeast Asia.Without any doubt, however, increasedawareness will widen the geographic distri-bution as well as the variety of hosts inwhich these worms have been detected.

Diagnosis. No particular signs are observedin fish infected with sanguinicolids, exceptthat the fish die with open mouth and flaredopercula (Ogawa and Fukudome, 1994).Field observations indicate that affected fishgasp for oxygen and die soon after being fed,suggesting that they require more oxygenwhen actively competing for food (Ogawaet al., 1989). Heart and gills are the mainorgans affected by the sanguinicolids. In thegills, hyperplasia is extensive, especially inthe area around encapsulated eggs, resultingin lamellar fusion. Eggs lodged in the hearttissue may form nodules, most of them in theventricle, where muscle cells atrophied, butdid not become necrotic (Ogawa et al., 1989).

Prevention and control. There are no knownmethods for controlling sanguinicolids infish cultured in cages. Fish caught in thewild become infected in their naturalhabitat. As all seabass fingerlings culturedin Southeast Asia are hatchery-produced,


Fish host

ParasiteSeriola

quinqeradiaLates

calcariferEpinephelus

coioidesLutjanus

spp.Culturedsite

Paradeontacylix grandispinnisP. kampachiCruoricola latesPearsonellum corventumCardicola sp.

++−−−

−−+−−

−−−+−

−−−−+

East AsiaEast AsiaSoutheast AsiaSoutheast AsiaSoutheast Asia

Table 6.10. Sanguinicolid blood flukes in cultured marine fish according to geographical location.



C. lates infects the fish once they are movedinto the cages.

Diseases Caused by Crustaceans

Crustaceans belonging to the Branchiura,Copepoda, Isopoda and Amphipoda arefrequently found on the body surfaceand/or gills of caged marine fish. Some, likeArgulus spp., glide freely on the body sur-face, while others anchor themselves to thehost.

They do not require an intermediatehost for their transmission. The maturefemale lays eggs, which develop into free-living nauplii and copepodid larval stages.All larval stages undergo several moultingsfrom one stage to another before metamor-phosing into adults in a suitable fish host.

Host range. The number of parasitic crusta-ceans reported from cultured marine finfishare relatively few and are shown in Table

6.11. The only branchiuran reported isArgulus sp. infecting grey mullet (M.cephalus), milkfish (C. chanos) and Asianseabass (L. calcarifer) (Paperna and Over-street, 1981; Chong and Chao, 1986; Arthurand Ogawa, 1996). A. scutiformis wasreported from Takifugu rubripes (Egusa,1992). The life history of marine argulidshas not been reported.

Most of the copepods reported arecaligids, which could cause epizootics inthe farms. A large population of yellowtailwas infected with Caligus spinosus, whichcaused serious injuries to the fish hostin Japan (Fujita et al., 1968), and Caliguspatulus in milkfish cultured in the Philip-pines (Lavina, 1977; Jones, 1980; Lin, 1989).In Malaysia, cultured groupers (E. coioidesand E. malabaricus) are often infested byCaligus spp., which are also found in cul-tured snapper and seabass, and by Ergasilusborneoensis (see Leong and Wong, 1988;T.S. Leong, unpublished data). Izawa (1969)reported that the developmental stages ofC. spinosus in cultured yellowtail included


Parasite crustacean Fish host Cultured site

Alcirona insularisAega sp.

Argulus scutiformis

Caligus spinosusC. patulusCaligus sp.Ergasilus borneoensisElaphognathia sp.Gnathia sp.

Gnathia piscivoraLemathropus latisLernaea cyprinaceaNerocila sp.Pseudocaligus apodusP. fugusJassa sp.Microjassa sp.Lembos sp.Stenothole sp.

Epinephelus sp.Lates calcariferL. calcariferChanos chanosMugil cephalusTakifugu rubripesSeriola quinqueradiataChanos chanosEpinephelus coioides, L. calcarifer, Lutjanus johniE. coioidesM. cephalusL. calcariferC. chanosL. johniM. cephalusL. calcariferC. chanosE. coioides, L. calcarifer, L. johniM. cephalusT. rubripesE. coioides, L. calcarifer, L. johniE. coioides, L. calcarifer, L. johniE. coioides, L. calcarifer, L.johniE. coioides, L. calcarifer, L. johni

CaribbeanSoutheast AsiaSoutheast AsiaSoutheast AsiaCaribbeanEast AsiaEast AsiaSoutheast AsiaSoutheast AsiaSoutheast AsiaWest AsiaSoutheast AsiaSoutheast AsiaSoutheast AsiaWest AsiaSoutheast AsiaSoutheast AsiaSoutheast AsiaWest AsiaEast AsiaSoutheast AsiaSoutheast AsiaSoutheast AsiaSoutheast Asia

Table 6.11. Parasitic crustaceans found in cultured marine finfish.



two nauplius stages, one copepodid stage,three chalimus stages and two juvenilestages before the copepod metamorphosedinto an adult.

The isopod, Nerocila sp., has beenfound in grouper, seabass and snapper inSingapore and Malaysia, whereas Aega sp.has been detected in seabass in Thailand(Chong and Chao, 1986; Ruangpan, 1988)Larval stages of gnathiid isopods were alsofrequently encountered in grouper, seabass,milkfish and mullets (Paperna and Por,1977; Leong and Wong, 1988).

The amphipods, Lembos sp., Microjassasp., Jassa sp. and Stenothol sp., are found ingrouper, seabass and snapper cultured inMalaysia (Leong et al., 1998).

Geographic distribution. As indicated inTable 6.11, parasitic crustaceans, particu-larly the caligids and isopods, are widelydistributed especially in Southeast Asia.Fish mortality has been attributed tothe presence of large numbers of thesecrustaceans.

Diagnosis. The nature and severity ofpathogenic effects depend on the interactionbetween the host and the parasite. Some ofthese parasites are mobile and cause lessdamage than those that are stationary, asthe latter firmly anchor themselves to thehost.

Argulids, however, though motile,do cause considerable injury to the hostbecause they tend to remain in one spot for along period of time. The pointed styles ofargulids pierce the skin while feeding onmucus. Furthermore, acting as a cephalo-thoracic suction cup, they exert a great pres-sure with their body. The presence of largenumbers of argulids results in haemorrhageas well as thinning of the epithelial cells.

Many parasitic crustaceans on the gillsattach themselves by grasping or anchoring.The epithelial cells are generally reducedor lost, resulting in the inflammation andthickening of the local epithelial layer,haemorrhage, haemolysis, hyperaemia andhyperplasia. These signs are evident inthe gills of grouper infested with E.

borneoensis and Asian seabass infested withLernathropus latis.

Mortalities caused by copepods havebeen reported for Caligus spineus on yellow-tail in Japan (Fujita et al., 1968), Pseudo-caligus apodus on grey mullets in Israel(Paperna and Lahav, 1974), Caligus patulusin milkfish in the Philippines (Lavina, 1977)and Pseudocaligus fugus in puffer fish inJapan (Arthur and Ogawa, 1996).

The isopod, Aega sp., caused mortalityin juvenile Asian seabass L. calcarifer inThailand (Ruangpan, 1988) and an unidenti-fied isopod on yellowtail in Japan (Kubotaand Takakuwa, 1963). The larval stages ofgnathiid isopods have been found in Asianseabass, snapper and milkfish in Malaysiaand Thailand (Leong and Wong, 1988) andGnathia piscivora in mullets in Israel(Paperna and Por, 1977). The gnathiids feedon fish blood and can cause severe anaemiawhen present in large numbers.

Prevention and control. Parasitic crusta-ceans are generally introduced along withfish caught in the wild for culture, butseveral of them are transmitted by wildfish around the cages. Prevention, therefore,is difficult. Organophosphate insecticidesare commonly used for treatment. Fujitaet al., (1968) successfully treated yellowtailinfected with Caligus elongatus by meansof 50 s immersion in 100 ppm solutionof Dipterex. Freshwater dip proved to beeffective for Caligus sp. in cultured grouperand snappers in Malaysia, and C. elongata inred drum (Landsberg et al., 1991). Otherchemicals that have been used includeformaldehyde, hydrogen peroxide andivermectin.

Concluding Remarks and CurrentPerspectives

Like other aquaculture systems, cage aqua-culture uses resources and produces wastes.Certain types of site habitats are particularlysensitive to cage aquaculture developmentand the impacts of cage fish farming on theaquatic environment can exert with time a




negative feedback effect on cage operations(Beveridge, 1996).

Many species of wild fish are attractedby the cage structures, for shelter and abun-dant supply of food. They often gain accessinto the cages through the mesh, whilefarmed species manage to escape into thesurrounding environment. The mingling offish populations creates new opportunitiesfor disease transfer (Diamant and Colorni,1995; Colorni, 1998) and the interactionsbetween cultured and feral fish mayhave important ecological implications.Translocated species may carry exoticdiseases that could spread and devastateindigenous wild populations or may bethemselves extremely sensitive to a localpathogen. In any case, the introduction oflarge numbers of caged fish to a system tendsto have dramatic effects on disease agents. Ithas become increasingly apparent that highstocking densities of caged fish cause ‘patho-gen loading’ in the surrounding area, wherepatterns of occurrence, prevalence andpathogenicity change greatly.

Only a limited number of therapeuticdrugs are licensed for use in fish. Whendrugs are used, costs are usually high andresidues may remain in the fish flesh aftertreatment, which means a long withdrawalperiod before the fish can be marketed. Also,accumulation of therapeutics in waste prod-ucts can compromise water quality. Use ofantibiotics, in particular, may not onlyenhance the development of resistant strainsof bacterial populations but may also sup-press the immune system of the fish (Adamset al., 1997).

Considerable effort has been made inrecent years to develop effective, safe andeconomical vaccines for numerous bacterialand viral diseases. Since in vitro cultureof the causative agent or its inactivation isnot always feasible, subunit vaccines havebeen prepared using recombinant technol-ogy. Here, the pathogens’ antigenic determi-nants that elicit a protective host responsehave been identified and isolated, molecu-larly cloned and expressed in the bacteriumEscherichia coli or the yeast Saccharomycescerevisiae. Using biotechnology for thegrowth of these organisms, expressed

‘foreign’ antigenic proteins can be producedin bulk. The food is the most practical deliv-ery system of these products to caged fish,requiring no extra labour and no handlingstress. However, oral vaccines have so farproved disappointing, providing protectionthat is generally weak and of short duration,presumably because protective antigenicdeterminants are destroyed in the fishforegut. Encapsulation of vaccines is neededto ensure that the essential antigenic deter-minants reach the second gut segment ina non-degraded and immuno-stimulatoryform (van Muiswinkel, 1995).

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6 infectious diseases of warmwater fish in marine …marine and freshwater fish (wolf, 1988)....

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