5 Non-infectious Disorders of Coldwater Fish · Non-infectious Disorders of Coldwater Fish 175 Fig....

5 Non-infectious Disorders of Coldwater Fish

David J. SpeareDepartment of Pathology and Microbiology, Atlantic Veterinary College,

Charlottetown, Prince Edward Island C1A 4P3, Canada

Introduction

The use of cage culture technology forthe commercial on-growing of finfish hasproven to be economically efficient andit continues to expand. Part of whatseparates this production approach fromland-based technologies is the range ofnon-infectious diseases that confrontproducers and health professionals. Theprincipal Achilles’ heel of cage cultureis the minimal degree of control, beyondthat afforded by cage site selection, overenvironmental phenomena.

Coldwater cage culture is dominated bythe production of salmonid species suchas Atlantic salmon (Salmo salar), chinooksalmon (Oncorhynchus tshawytscha) andsteelhead trout (Oncorhynchus mykiss)in marine environments. The objectives ofthis chapter are to focus on non-infectiousdiseases that interact with this segment ofthe finfish aquaculture industry. Commer-cial cage culture of flatfish species, cod andother marine coldwater species is develop-ing in importance, as is cage culture ofrainbow trout and Arctic charr (Salvelinusalpinus) in freshwater lakes or brackishwater bays. Some of the conditionsdiscussed are also appropriate to thedeveloping culture of these coldwaterspecies.

Failure of Juvenile Salmon to Adaptto Marine Culture

The phase in which salmon smolts aremoved from their freshwater rearing sites tothe marine cage culture on-growing site is aperiod of high risk. This is also the case fortransfer of steelhead rainbow trout juvenilesfor on-growing in marine cages (Oorschotand Boon, 1993). The Atlantic salmonhatchery industry has largely geared itsactivity towards production of a seawater-ready smolt in 1 year from egg hatching.This S1 smolt comes from the upper-modalgrowth population of juveniles in a hatch-ery, and is judged for seawater-readinessbased on anatomic, behavioural and physio-logical characteristics. Variations on thetheme exist. For example, entry of smolts toseawater can take place during their firstautumn (S0.5), second autumn (S1.5) orsecond spring (S2). As yet there is noconsensus on mortality rates to be expectedwith each regime; however, autumn entrysuccess is usually less than for spring entry.Chinook salmon, depending on the strainbeing used, can be put to seacages asS0 smolt (i.e. entry in the spring of theyear the eggs hatched). However, thispractice has been anecdotally implicated asthe cause of higher mortality rates, particu-larly from infections with Renibacterium

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salmoninarum (the causative organismof bacterial kidney disease) during theremainder of the marine production cycle.

A number of factors can lead to smoltmortalities soon after fish are transferred toseawater. With spring transfer of S1 Atlanticsalmon smolts, a mortality rate during thefirst month post-transfer of up to 3% may notbe regarded as unusual. This derives from aninability of some juveniles to adapt properlyto sea water. Mortality patterns after seawa-ter entry can vary dramatically, and theiranalysis can be used to point to potentialaetiologies. For instance, when mortalitiesoccur shortly after seawater introduction,this usually points to problems stemmingfrom fish handling and transport methods.Acute patterns of mortality shortly aftershipment frequently stem from anoxic con-ditions developing during transportation.The window of opportunity just prior tosmolt movement has been viewed as aperiod in which health checks, treatment,vaccination, grading and inventory assess-ment can take place. Handling of fish is astress that results in elevated oxygen con-sumption in the periods following handling(Davis and Schreck, 1997). Transporting fish

to cage sites after handling may compoundthe oxygen debt that fish experience, espe-cially since high loading rates (to reducethe weight of transported water) of fishare frequently used during shipment. Acutepost-transfer mortality is also linked tothe physiological and osmotic demands thatdevelop if smolts are handled so roughly thatscale loss occurs. Smolts are particularlyprone to losing scales, and this in turncreates significant osmoregulatory problemson introduction to seawater. Smolt loss canalso occur if newly introduced juvenilesencounter strong currents. In reviewingdiagnostic case material from AtlanticCanada (Aquatic Diagnostic Services casearchives 1990–1997, University of PrinceEdward Island, Canada), there have beenseveral submissions of smolts with severeskin lesions from net abrasions andexertional muscle necrosis (Fig. 5.1) follow-ing their introduction to marine cages wherewater current was excessive. The type andpattern of muscle damage are interestingin that ‘fingerprint lesions’, which can bemisdiagnosed as nutritional deficiency, canpersist in survivors. Early muscle lesionsinclude various forms of degeneration, such

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Fig. 5.1. Section of epaxial musculature from an Atlantic salmon post-transfer smolt several weeks afterintroduction to a cage site with excessive water current speed. Extensive satellite cell, myoblast andfibroblast proliferation have replaced areas vacated by muscle fibre necrosis and dissolution. Regenerativefibres, with characteristic nuclear rowing (arrows indicate several examples), are abundant. H&E stained.



as segmental and discoid myofibrillarchanges. Fibre necrosis is followed bymineralization. Survivors show a range ofmuscle changes including presence ofmacrophages removing cellular debris,proliferation of satellite cells, myoblastelongation and fibre regeneration (Fig. 5.1).

The scale and scope of post-transfermortalities are of concern to the cage cultureindustry. In vertically integrated operationsthere is considerable opportunity to coordi-nate protocols aimed at reducing transferstress. This can involve more precise timingof pre-transfer activities (vaccinating,grading), the timing of transfer itselfand avoiding delays during transfer.Protocols for safe smolt transfer, takinginto account pre-shipment, shipment andpost-introduction activities, have beendeveloped (see Pennell, 1991, for specificinformation).

In contrast to the acute mortality peaks,which can reflect transportation problems, amore gradual onset of post-transfer mortalityis widely (but anecdotally) attributed to theproblem of partial adaptation of non-smoltsto the marine environment. These fish do notdie at the time of transfer, but fail to regulatetheir blood electrolyte levels effectively.These fish are highly stressed, they darkenand hang listlessly at the water surface andtowards the edges of cages. Over an extendedperiod, they undergo advanced body

condition deterioration and often succumbto infectious diseases including those nottypically problematic in marine environ-ments, such as costiasis (Figs 5.2 and 5.3).The role of these stressed fish asbioamplifiers of disease such as sea liceinfestations, furunculosis and vibriosis isfelt to be an important factor in theepizootiology of disease outbreaks. The term‘lice-magnets’, to describe the effect of thesefish prior to sea lice epizootics, has beencoined in reference to this effect.

The rapid changes in environmentalindices experienced by smolt at seawaterentry have been linked with the develop-ment of epithelial hyperplastic plaques(Nowak and Munday, 1994) and increasednumbers of mucous cells (Franklin, 1990) onthe gill filaments of Atlantic salmon. Envi-ronmentally induced precursor lesions areoften cited as predisposing causes forinfectious gill conditions. With relevanceto marine culture of salmonids, these post-entry lesions are proposed to create a favour-able environment for the establishment ofParamoeba sp. infections responsible foramoebic gill disease (AGD) in Tasmania(Nowak and Munday, 1994). An idiopathicgill condition known as clubbing and necro-sis gill syndrome (CNG), which may alsoact as a predisposing factor for AGD, hasrecently been described for Atlantic salmonsmolt in brackish water cage sites in

Non-infectious Disorders of Coldwater Fish 173

Fig. 5.2. Section of gill taken from a ‘pinhead’ Atlantic salmon smolt several weeks after seawater transfer.Virtually all lamellae are fused to adjacent lamellae in a pattern typical for costiasis. H&E stained.



Tasmania (Clark et al., 1997). During CNG,fish have diminished feed response andaffected fish have pale gills due to excessivebranchial mucus production. As yet, thespecific environmental conditions res-ponsible for the genesis of these branchialhyperplastic responses have not been deter-mined. Similar changes have not yet beendescribed in other parts of the world whereAtlantic salmon production takes place.

Pathophysiological Effect of RoutineAquaculture Practices

During on-growing in cages, routineaquaculture practices can contribute to fishstress and physical damage. Grading andtransferring fish between cages is a neces-sary but risky task. Dip nets and mechanicalpescolators can damage fish. Farmers aregenerally hesitant to move or grade fishduring warm water periods because of theincidence of infectious disease problemsthat occur post-handling. It is not knownwhether this link between handling andoutbreaks of infectious diseases stems fromthe effects of physical trauma or physio-logical stress or both.

Grading and population splitting is anecessary event. Infrequent grading and theresultant increased variability of fish size

will accentuate differences in specificgrowth rate during the remainder of the pro-duction cycle. Harvesting a cage that has aspread in size and condition affects market-ing (Huguenin, 1997). A general solution isto complete grading procedures duringspring and autumn, such that fish arerelatively undisturbed during periods ofwarmer water.

Performing net changes to removebiofoulants is another situation in whichstock are either moved or stressed. Organicgrowth on netting increases during warmertemperatures. Net cleaning or net changingduring warm weather is considered to bestressful to stock. However, failure to cleannets predisposes cages to reduced water flowthrough them, but conversely increases theamount of current-induced net deformationdue to heightened resistance to current flow.The latter can reduce the habitable volumeof a cage.

An interesting problem reported byWilliams et al. (1995) is an ocular degenera-tion that develops in cage-cultured halibutafter handling. The ocular changes includegas- and fluid-filled cysts in the ocularchoroid (= posterior uvea). This lesion isusually combined with damage to the ocularchambers, uveal structures and lens. Thelesions closely resemble those of ocular gasbubble disease, and Williams et al. (1995)

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Fig. 5.3. Scanning electron micrograph of a gill lamellar surface, which is colonized by flagellatedprotozoans with a morphology typical of Ichthyobodo necator.

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have suggested that the trauma of handlingmay cause gases in blood to come out ofsolution. They proposed that some marinespecies may be uniquely predisposed tothis, due to relatively high levels of carbonicanhydrase within the ocular choroid. Thismay generate excess local oxygen produc-tion within the body of the choroid itself.Conditions favourable for the productionof typical gas bubble disease as seen onland-based facilities supplied with groundwater are unlikely to occur for sustainedperiods at sea cage sites. As such, typical gasbubble disease is not reported for cage-cultured fish.

Oil adjuvants in fish vaccines havebecome widely used for cage-culturedsalmon (Poppe and Breck, 1997). In easternCanada, their use has been standard practicesince the occurrence of coldwater vibriosis(Hitra disease) in the early 1990s. Reducedgrowth rates after the use of an oil-adjuvanted vaccine have been noted andmay be attributed to chronic active peri-tonitis and production of fibrotic visceraladhesions (Lillehaug et al., 1992; Poppe andBreck, 1997) (Fig. 5.4). Poppe and Breck(1997) also noted that the degree of

post-vaccination side effects varied widelybetween farms and within the same fishpopulation. Additionally, where the vaccineis inadvertently administered into thegut wall, severe granulomatous enteritisextending from the serosal surface throughto the mucosa can develop, and in somecases lead to leakage of gut contents intothe peritoneum and death from acuteperitonitis.

Behaviour-related Problems

Damage to fins, skin and eyes can resultfrom the hierarchial activities typical ofsalmonids. These problems are less fre-quent in Atlantic salmon compared withchinook salmon. Determining whether thiscorrelates to different degrees of domestica-tion is complicated since evidence can begenerated for both increased and decreasedaggression resulting from domestication(Ruzzante, 1994). Selecting broodstockbased on growth rate may be inadvertantlyselecting for feeding-related agonisticbehaviour if access to feed is determinedby aggressive interaction and competition


Fig. 5.4. Severe granulomatous reaction affecting the peritoneum and stomach wall of an Atlantic salmonseveral months after vaccination with a preparation containing an oil-based adjuvant. Persistent dropletsof oil (small arrows) and the site of invasion of the granulomatous response into the muscle wall of thestomach (large arrow) are shown. H&E stained.



(Ruzzante, 1994). Extending from this itis perhaps curious to note that aggressionbetween salmon is often found to beinversely dependent on stocking density.This may be related to the suppression ofhierarchial establishment at high densities.

Territorial behaviour of Atlantic salmoncan result in bite wounds on the tail fin,peduncle region, anal fin and vent, presum-ably as one fish is pursued by another.Wounding, and ulcers that develop from sec-ondary infections, have an economic effectthrough downgrading of the final product ifhealing is not complete or if scarring and/ormelanization occurs. Abrasions can alsodevelop from surface leaps, in which fishcontact and become abraded from surfacenetting. Furevik et al. (1993) noted that 6%of surface leaps caused fish to contact pennetting. Culture techniques being developedfor Atlantic halibut may also lead to abrasionproblems. Martinez Cordero et al. (1994)have found that halibut will congregate onthe cage bottom rather than occupy the watercolumn. During rough weather, when seacage bottoms heave, this could result in netabrasions although observations show atleast some halibut leave the cage bottomduring rough weather.

Conditions Relating to OxyradicalProduction

Modern methods of feed manufacturinghave drastically reduced the problems asso-ciated with nutrient imbalance and stabilityof ingredients. However, the impreciseknowledge of fatty acid requirements offish, combined with the use of high fat dietsto deliver protein-sparing metabolic energy,and the demands of marine coldwater fishfor polyunsaturated fatty acids (PUFAs)as membrane lipid components (Winstonand Giulio, 1991) create problems stem-ming from feed storage (Hertrampf, 1992).Rancidity, resulting in the productionof malonaldehyde, develops during theexposure of PUFAs to oxygen.

In a pattern similar to the multiple pre-sentations of fat oxidation in other domestic

species, there are many clinical and patho-logical disease presentations that link backto the problem of antioxidant defencesbecoming exhausted by oxyradical pro-duction. There are quantitative differencesbetween species for the major antioxidantenzymes – superoxide dismutate, catalaseand glutathione peroxidase (Winston, 1991)– which may contribute to the differingclinical patterns relating to feed rancidity.Contributing to the overall oxyradicalproduction/free radical quenching balancesheet are dietary factors such as the amountand saturation profile of fat components,storage factors contributing to rancidity andrelative abundance of feed-additive stabiliz-ing compounds such as tocopherol,carotene, ascorbic acid and glutathione(Winston, 1991). Variable sparing or contrib-uting effects within this mix of componentsmeans that studies on isolated componentsvary considerably. As an excellent exampleof this, Frischknecht et al. (1994) comparedthe lesions attributed to deficiencies invitamin C, vitamin E and also the twoin combination. Rainbow trout deficient ineither had suppressed growth, anaemia,muscle dystrophy and haemosiderindeposition in the spleen. With the additionof vitamin E only, similar signs developedalong with deformations of the vertebralcolumn and spontaneous haemolysis. Also,fish of different ages showed differences inthese lesions.

A significant rancidity-related problemin farmed fish is lipoid liver disease. This istypically linked to auto-oxidation of fats infish feeds (Roald et al., 1981; Saraiva et al.,1986). In addition to appetite suppression,clinically affected fish manifest signs stem-ming from red blood cell destruction and, onfurther examination, have large friable palelivers due to macrovesicular lipidosis andceroid deposition (Fig. 5.5). Cell-membranedegradation products can be found in otherorgans, and are especially abundant inthose areas with a large resident phagocytepopulation such as peritubular networks ofthe kidney (Fig. 5.6). Hepatocellular necro-sis can occur when fish with lipoid liverdisease are exposed to sudden heightenedoxidative stress.

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Pansteatitis, a condition noted in rain-bow trout in which inflammatory cells arepresent in any fat storage area, occurs introut reared in brackish water and fed rancidfeeds. A condition of fat cell necrosis inAtlantic halibut, which affects subdermaladipose tissue, has also been linked to animbalance of dietary oxidants and antioxi-dants (Bricknell et al., 1996). This diseaseis curious since a specific region of fatdeposition is targeted, and multinucleated

macrophages within the inflamed degener-ate fat stores are characteristic. In a lessdirect manner than for the conditions citedabove, increased oxidant stress arising frominadequate vitamin E levels has been shownto increase the clinical effects of salmonpancreas disease (SPD) as it occurs inAtlantic salmon (Ferguson et al., 1986a,b;Raynard et al., 1991).

In contrast to the epizootiologicalpresentation of SPD, acute heart failure or


Fig. 5.5. Section of liver from a fish with hepatic ceroidosis. Hepatocytes are uniformly enlarged due tointracytoplasmic accumulations of ceroid and lipid. H&E stained.

Fig. 5.6. Section of a kidney from a fish with lipoid liver disease. Macrophages of the peritubular capillarynetwork are enlarged (arrow points to an example) due to accumulations of ceroid and othercell-membrane breakdown products. H&E stained.



cardiomyopathy syndrome (CMS) typicallyoccurs in fat fast-growing salmon thathave spent at least one sea winter in cages(Amin and Trasti, 1988; Ferguson et al.,1990; Grotmol et al., 1997). Fish oftendie during feeding (Grotmol et al., 1997)and on necropsy an enlarged and sometimesruptured atrium with haemopericardiumis detected. Death may be from cardiactamponade (Ferguson et al., 1990). Thepathology includes development ofthrombi in the atria, acute myocardial lysis,the presence of debris-laden subendocardialmacrophages and endothelial damage (Fer-guson et al., 1990). Because the diseaseaffects rapidly growing fish and becausethere is myocardial damage with somesimilarity to that noted in SPD, nutritionaland specifically oxidant factors have beenspeculated as playing a role. However,Grotmol et al. (1997) have recentlyidentified an endotheliotropic nodavirusthat reacts with antibodies raised to thestriped jack nervous necrosis virus. There-fore, it may be that nutritional factors have amodulating effect on CMS presentation, asthey do for SPD. It is interesting to note thatAtlantic salmon, during periods of stress,accumulate adrenaline in atrial tissue, per-haps due to potent local uptake mechanisms(Fløysand et al., 1992). Endogenous adrena-line in excessive amounts is known tobe cardiotoxic (Carlsten et al., 1983), andpoikilotherms manifest this by necrosis ofspongy myocardium.

Myointimal hyperplasia leading tocoronary arteriosclerosis is a commoncondition in wild and cultured salmon, andhas been shown by Saunders et al. (1992) tobe linked to rapid growth rates of salmon asopposed to being an effect of sexual matura-tion. Whether this lesion is influenced bycomposition of dietary fat is still unknownbut this remains an active hypothesis.

Intertwined with the effects of oxidativestresses contributed by high fat diets arethose scenarios that can arise when dietaryantioxidants are deficient in the diet. Theclinical repercussions of vitamin E, vitaminC or selenium deficiencies are rarelyclassical in clinical presentations, and,as detailed by Frischknecht et al. (1994),

experimental data suggest that manifesta-tions are dictated by factors such as watertemperature and fat content of diet and inter-actions between antioxidant componentsthemselves.

Gastrointestinal Impaction

Water-belly syndrome (WBS) is a prob-lem for several species of cage-rearedsalmonids, but especially for marine-rearedrainbow trout (Staurnes et al., 1990) duringperiods when salinity is high and watertemperature is low. Changes to feedingprogrammes, and in particular the use ofextruded pellets with a higher fat and carbo-hydrate content, have been cited as riskfactors (Staurnes et al., 1990). Affected fishare easily detected based on gross appear-ance. On dissection they have a massivelydistended stomach filled with water (Fig.5.7). Reductions in the thickness of theabdominal wall led Staurnes et al. (1990)to conclude that the condition generallydevelops over a considerable period of timeand that recovery is uncommon.

A differential diagnosis for WBSincludes the gastric impaction and muralgastritis that develop in salmon due to theconsumption of wood chip debris. Millerand Black (1992) noted that in areas wherewood chips are hauled in open barges, con-siderable amounts are spilled during loadingand transport. Fish that have been trained toeat pellets will also respond to floating orslowly sinking wood chips. The indigestibil-ity of wood chips causes them to accumulatein the stomach where they act in the typicalfashion of a foreign body, blocking thetransit of other ingested particles from thestomach. At one farm, Miller and Black(1992) noted that 80% of salmon had woodydebris (mostly bark) in their gut, andattributed 90% of the farm’s mortality ratesto the effects this was having on the fish.Curiously, in an attempt to deflect theingress of floating wood chips into the cagesby the use of a skirting net, they found aneffect opposite to that expected. The skirtingnet restricted the velocity of surface watercurrents moving through the cages so that

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contact time between fish and debris wasincreased.

Conditions Relating toCage Site Location

Cage-cultured fish are a physically con-strained population within an environmentthat is partially changeable due to currentsand tides. Avoidance of detrimental envi-ronmental factors is therefore restricted tothe limited space and depth within the con-fines of the cage. Accordingly, site selectionis a critical process and should, ideally,examine meteorological, locational andbiological characteristics (Huguenin, 1997).

One of the more significant obstaclesfacing expansion and sustainability ofmarine cage culture is the availability of suit-able sites (Huguenin, 1997). For example, ineastern Canada, there are limited numbersof sites that are sufficiently protected fromsevere weather while simultaneously havingenough current flow to avoid summertimeheating and slack-tide anoxia, or wintersuperchill. In other areas, problems ofmultiple use of water resources have broughtaquaculture into conflict with other stake-holders. As an example of the detrimentaleffects for fish farming, aquaculture siting isfrequently in areas that are near commercialmarine traffic. There have been several

recent incidents of oil spills from tankers (anexample being the Shetland Island ‘Braer’incident in the early 1990s), which haveraised alarm bells about what should beexpected when an oil slick comes intocontact with farms. The outcome from acrude oil spill is difficult to predict, since, asreviewed by Alkindi et al. (1996), a numberof processes occur after the spill, whichaffect the fate of the hydrocarbon mix andtherefore the ultimate mix of toxins. As aresult, the aftermath of an oil spill (and/orany other commercially shipped aquatictoxin) will largely be unpredictable.

Autointoxication is also a concern atlease sites where fallowing has not occurred,where currents are minimal and where thedistance between the bottom of cages and thesea bottom is minimal. Benthic degradationand, specifically, deposition of protein-richorganic debris from salmon farm sedimentsis of concern to aquaculturists and environ-mentalists. As anoxic conditions developwithin accumulating debris, conditionsbecome favourable for the production ofhydrogen sulphide. Off-gassing of hydrogensulphide and/or release of anoxic water andhydrogen sulphide due to current-induceddisturbance of the deposits are believed to beresponsible for the condition known as sitesouring (Munro, 1990; Papoutsoglou et al.,1996). Population signs related to sitesouring include reduced growth rate and


Fig. 5.7. Marine cage-cultured rainbow trout with massively distended gastrointestinal tract due towater-belly syndrome.



increased disease problems of stock (Kiemeret al., 1995). In studies on the effects ofchronic exposure of Atlantic salmon smoltsto sublethal concentrations of hydrogensulphide, Kiemer et al. (1995) found thatit caused progressive gill hyperplasia,coupled with degeneration and necrosisof hepatocytes. Hydrogen sulphide is alsocapable of binding to haemoglobin andinhibiting the oxygen uptake in a mannersimilar to that induced by exposure tonitrite. The combination of gill pathologyand reduced oxygen loading kinetics ofhaemoglobin may perhaps act synergisti-cally on growth performance.

Cage sites in well-protected shallowsites, such as partially enclosed bays, runthe risk of periodic high temperatures andmarginal to lethal dissolved oxygen levelsoccurring during slack tides. Additionally,Oorschot and Boon (1993) implicated highermetabolic requirements for osmoregulationat elevated water temperatures as a con-tributing cause to summer mortality inmarine-cultured rainbow trout. Conversely,in eastern Canada, dramatic mortalities haveoccurred because of superchilling (Fletcheret al., 1988). This problem generally occursin mid- to late winter, on cloudless nightswhen air temperature plummets to below−20°C. As high tide begins to recede, water,which has superchilled (having cooled tojust below its freezing temperature but notyet undergone ice crystal formation), drawsback towards lease sites. As fish contactthis unstable superchilled water, their bodytemperature drops to a level where bloodand body fluids will freeze. Superchillphenomena can lead to mortality of all stockon a farm.

In general, site selection is an importantprocess that should consider temperatureprofiles during summer and winter, thelikelihood of declines in dissolved oxygenat slack tide, plankton bloom history,current speed at slack and peak tides, theabundance and type of predators, shelterfrom wind and storms, and the likelihood ofexposure to upwelling currents (see Pennell,1992, for practical review and specificguidelines).

Algal Blooms

Toxic algal blooms are a cause of cata-strophic losses to marine cage cultureoperations and globally their incidence orrecognition is on the rise. The mechanismsof interaction between algae and finfish thatcontact algal blooms are highly variable.Additionally, the inter-relationship of envi-ronmental factors that promote blooms arecomplex and challenging to model (Perryet al., 1989), as is predicting the timing ofdiatom aggregation and subsequent masssedimentation phenomena characteristicof bloom declines (Passow, 1991). Environ-mental variables control not only thegrowth habits of the algae, but also themotility, morphology (for example, trans-formation from unicellular to colonialhabit) and rates of secretion of carbohydratecomplexes (Tomas, 1978; Luttke, 1979).The upwelling of ocean currents, whichbrings about nutrient enrichment and rapidchanges to water temperatures, is a commonfactor promoting algal blooms. Historicaloccurrences of coastal upwelling phenom-ena and algal blooms are important criteriafor cage operation site selection.

Morphological characteristics of somediatoms appear to aid their ability to causedisease. For example, the chain-formingdiatoms Chaetoceros concavicornis andChaetoceros convolutus (Albright et al.,1993) and some non-chain-forming Core-thron spp. (Speare et al., 1989) diatomspossess setae and spinules (barbs). Thesebrittle spear-like projections emerge fromthe diatom and form a silica-rich web-likestructure around the body of the frustule,which assists the buoyancy of the diatom(Fig. 5.8). Inadvertently, however, the setaeare important morphological features,which aid pathogenicity. The setae projec-tions cause the diatoms to become retainedin the sieve-like arrangement of inter-filamental and interlamellar spaces of thegill (Speare et al., 1989) (Fig. 5.9). The colo-nial nature of the Chaetoceros diatoms,which may be an advantage to the diatomwith respect to sedimentation rates (Fryxell,1978), probably further enhances their

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pathogenicity, since a flexible chain ofsetae-bearing diatoms is more likely tobecome entrapped or snared during passagebetween gill lamellae.

There has been considerable interest indetermining the pathophysiological effect ofdiatom blooms on fish, in order that thera-peutic and supportive measures can be put

in place once a bloom overruns a cage site.The clinical signs of salmon during exposureto a Chaetoceros sp. bloom are largely thoseof anoxia brought about by abundantmucous discharge on to gill lamellae(Albright et al., 1993). A similar phenome-non was reported by Hishida et al. (1997)to explain the cause of death of marine


Fig. 5.8. Scanning electron micrograph showing the arrangement of the spine-like setae emerging fromthe corona of a Corethron sp. diatom. Material was collected from the gill of a marine cage-cultured cohosalmon during an algal bloom.

Fig. 5.9. Section of gill with epithelial hyperplasia surrounding entrapped diatoms (arrows). H&E stained.



cage-cultured yellowtails during a bloomof the marine alga Chattonella marina.Additionally it has also been shown thatC. marina produces oxygen radicals espe-cially during exponential growth phases(Ishimatsu et al., 1996a). Whether there isa causative relationship between oxygenradical production and hypersecretion ofmucus is as yet not precisely defined(Ishimatsu et al., 1996b).

In clinical cases relating to the effectsof exposure to Chaetoceros spp., there is aprotracted time course of mortality and poorgrowth performance. This appears unrelatedto the acute branchial reactions to the algaeand more probably reflects the progressivepathology evoked by entrapment of thesilica-rich frustules and setae within gilltissue in a manner similar to that proposedfor Corethron spp. (Speare et al., 1989).The specific lesions include a randommultifocal pattern of branchial lamellarand filament fusion, with layers ofsquamous-transformed epithelial cellsencircling captured diatom elements. Migra-tion of leucocytes, originating from lamellarpillar channels and the gill filament’s centralvenous sinusoid, towards the pockets oftrapped diatoms is common (Speare et al.,1989) and mechanistically understandableconsidering the antigenic nature of manyforms of silica (Lugano et al., 1982). Growthfactors released by the leucocytes presum-ably have a role in evoking the epithelialhyperplasia that accompanies diatomentrapment.

Recognition of the chronic physiologi-cal disturbances, which persist in fish afterexposure to an algal bloom, is critical inmanaging the health and performance ofrecovering populations. Feeding and cagemanagement decisions need to takethis recovery time-lag into consideration.For example, these fish may have littlerespiratory-function reserve. Therefore,unexpected mortalities may occur afterroutine practices such as grading or netchanges. Furthermore, Albright et al. (1993)noted that cage-cultured Pacific salmon hadreduced resistance to common indigenousbacterial pathogens following exposure tosublethal concentration of Chaetoceros spp.

Whether this is a manifestation of stress,or a more specific mechanistic pathway isunknown.

The possible role that other setae-bearing diatoms, not typically recognizedas problematic, may have on the health ofcage-cultured salmon has been raised. Forexample, Bruno et al. (1989) noted thepotential role that Distephanus speculumand Chaetoceros debile may have. Addition-ally Kent et al. (1995) demonstrated severegill lesions in fish exposed to a bloom domi-nated by the chain-forming Skeletonemacostatum and two species of Thalassiosira,which possess barbless setae. This suggeststhat diatom monitoring programmes thatare put in place to alert fish farmers ofdiatom bloom status need to track adiverse range of organisms since many ofthem may prove to have negative effects onfish health.

Heterosigma carterae (Heterosigmaakashiwo, Olisthodiscus luteus) has beenreported as a significant cause of cata-strophic fish mortality in many parts ofthe world including the Pacific Northwest.Unlike the setae-bearing diatoms whoseaction on the gills appears to be mechanical,H. carterae appears to affect fish by releasinga toxin. Supplemental oxygenation does notimprove fish survival and the diatom doesnot provoke gill lesions (Black et al., 1991).Fish experimentally exposed to this algaappear anaesthetized (Black et al., 1991) andthis may reflect the action of a brevetoxin(neurotoxin), which has been identifiedfrom H. akashiwo samples from a red tide inJapan (Khan et al., 1997).

A toxin affecting permeability of gillepithelium is also believed to be themechanistic link between algal bloomsof the phytoflagellate Chrysochromulinapolylepsis (Prymnesiophyceae) and massivemortalities of cage-cultured Atlantic salmonon the Norwegian coast (Underdal et al.,1989). These authors reported that a combi-nation of low salinity, high temperaturesand high nutrient content created conditionsbelieved to be conducive to the bloom.Additionally, the pathophysiological effectof the algal cells on the fish was affected bysalinity (Underdal et al., 1989), suggesting

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that the elaboration of toxin was under tightenvironmental control.

Exposure to microcystin hepatotoxinsreleased into the environment from blue-green algae has been implicated as the causeof gill and liver damage in feral brown troutin Scotland (Rodger et al., 1994). It is alsosuspected to be the cause of net pen liverdisease (NPLD), a syndrome that yields aunique pattern of liver damage in cage-cultured Atlantic salmon along thePacific Northwest (Kent et al., 1988; Kent,1990). NPLD lesions include markedhepatocellular pleomorphism with abun-dant megalocytes (Fig. 5.10), some of whichare multinucleated. Megalocytosis persiststo some degree even in livers of fish that arein a recovery/hepatocellular regenerativephase (Kent, 1990). The syndrome is mosttypical when it affects Atlantic salmonduring their first year in seawater, beginningin summer and leading to persistentmortality rates. In some situations, cumula-tive mortality has reached 90% (Kent, 1990).The effect of this condition on growth ratesand production performance of fish has notyet been defined, although recovery from

NPLD can occur if fish are moved to cleanseawater (Kent, 1990).

Sunburn

Effects of solar ultraviolet (UV) exposurehave been recognized as the cause of classicsunburn lesions on the dorsum of cage-cultured fish. Additionally, the so-called‘summer syndrome’ of cage-cultured Atlan-tic salmon, which begins as a discrete focusof skin necrosis on the dorsum and caudalpeduncle (Rodger, 1991), but which can fur-ther develop into severe ulceration accom-panied by secondary infections, is nowbelieved to be linked to solar UV exposure(McArdle and Bullock, 1987; Rodger, 1991).Summer syndrome is generally a problemfor salmon during their first summer at sea,and Rodger (1991) advanced the hypothesisthat rapidly growing post-smolts wouldhave many epidermal cells undergoingDNA synthesis or mitosis making them vul-nerable to UV. This is supported in part infindings by Bullock and Roberts (1992) thatepidermal cells migrating to cover sites of


Fig. 5.10. Section of a liver from an Atlantic salmon with net pen liver disease. Hepatic megalocytosis istypical. Note extremely hypertrophied nuclei (arrows). H&E stained. (Photo courtesy of M.L. Kent, PacificBiological Station, Department of Fisheries and Oceans.)



repair were most vulnerable to UV. Ingeneral, this may explain why fish sufferingfrom epidermal parasitism (particularly sealice, which frequently target the epitheliumcovering the dorsal cranium) are also morevulnerable to sunburn.

Epidermal changes induced by exces-sive UV exposure begin as a pattern of single-cell epithelial necrosis, with necrotic cellsscattered throughout the epidermis. Thisleads to epithelial oedema and separationof the basal layer of epithelial cells fromthe subjacent basal lamina. Dermal changesinclude degeneration of melanocytes(McArdle and Bullock, 1987). Whether ornot the initial cellular injury will lead to tis-sue changes such as hyperplasia, ulcerationor secondary infection is dependent on thedegree of injury and the types and number ofopportunistic pathogens.

Predators

Direct and indirect losses due to actions ofpredators are perhaps the most significantcauses of fish mortalities in cage culture(Moring, 1989) and are often anecdotallycited by aquaculturists as a significant con-straint to production. This is not surprisingconsidering the attractiveness of a cageculture site to predators, and the oftenminimally effective defence afforded bypredator netting.

Avoidance of predators needs to beone of the major criteria used during siteselection. Historical biological data andobservations are often useful in determiningthe local abundance of predators – for exam-ple, locations of seal colonies. Unfortu-nately, because of the rich biota thatdevelops around cage culture lease sites,attraction of feral animals is unavoidable.The interaction of wildlife and farmed fish isa major point of criticism used by detractorsof fish farming. Common predators includeaquatic mammals such as sea lions, sealsand otters, in addition to predatory oropportunistic species such as ospreys,eagles, herons, kingfishers and gulls(Moring, 1989).

Methods used to reduce predator losseshave involved cage nettings (over cage sur-faces to deter birds and as a skirting to determarine mammals), visual and acoustic scar-ing devices, dogs, nightwatchmen, trappingand, in some cases, killing. The economicconsequences of predation are numerous.The costs of fish being killed and eaten, orescaping through predator-caused pen tears,would be relatively straightforward to cost-analyse. However, it is usually impossible togather the data to determine the extent oflosses. These losses then become part of theunaccounted-for ‘shrinkage’ phenomenonof cage inventory (Moring, 1989). Woundsinflicted upon fish are also a concern. Sealswill often swim rapidly into the nettingand grab hold of and chew off parts of fishthat they encounter. Carss (1993) noted thatherons commonly dropped fish while tryingto pull them through cage nets. The presenceof these injuries provides access for primarypathogens. Seal attacks are particularlyproblematic, since their occurrenceincreases during periods of colder watertemperature. Cold water temperaturegenerally acts to delay wound healing andthese persistent wounds become sites forinfection. In addition, fish with wounds aredowngraded at the time of marketing. Aspart of an environmental assessment ofaquaculture, an excellent synthesis of theimpact of predation and methods to limitpredation, as practised in British Columbia,has been produced by Iwama et al. (1997)

In addition to the costs associated withfish being wounded or killed, the presenceof predators frequently stresses the fish tothe point where they cease feeding. Farmerscite the presence of predators as a commonprecursor to outbreaks of infectious diseasessuch as vibriosis and furunculosis, suggest-ing that the fish are stressed when they sensepredators nearby.

Neoplastic Conditions

Historically, the development of tumoursin animals has been considered a non-infectious disease event, which arises due

184 D.J. Speare



to either random or provoked cellulargenetic defects. However, within thiscategory, the role of infectious agents isincreasingly becoming recognized, anddrawing the line between environmentaland microbial contributions to oncogenesisis becoming more difficult.

The epizootiology of several types ofcommon tumours supports the idea ofrandom genetic or developmental eventsas the underlying cause. At the processingline, such disorders as multiple hepaticcysts (Bruno and Ellis, 1986) and polycystickidneys are sometimes noted. These cystsare generally fluid filled and, in fish as inmammals, may have their origins in failureof component cells (such as biliary duct cellsand renal tubular epithelium) to properlymaintain cellular polarity. Vectorial pro-cesses involved in normal secretion aretherefore disturbed (Molitoris and Nelson,1990) and cysts may form due to the result-ing secretions. Nephroblastomas, tumoursemerging from the surface of the posteriorkidney, in which poorly developed sectionsof the nephron are formed, are also notedwith regularity in market-ready salmon.These tumours seem to have little or noeffect on growth performance, although thetumour can grow to massive size.

Thyroid hyperplasia and neoplasia alsooccur in farmed fish (AVC case archives).

Differentiating responsive hyperplasia of thethyroid gland from a benign neoplasticprocess can be difficult. This differentiationis often critical since many causes ofthyroid hyperplasia stem from nutritionaldeficiencies, which must be corrected.Epizootiological considerations are usefulin this regard, as well as monitoring theresponse (such as regression of follicularhyperplasia) to dietary management. Spon-taneous thyroid carcinoma also can occurin cage-cultured salmon. The histologicalappearance can include bizarre cellularformations in which the diagnosis of theircellular origins may be impossible withoutthe use of immunohistochemical markers.Hepatic tumours may be single animaldisease phenomena, but when they occur ingroups of farmed fish, other factors such asfeed contamination with aflatoxins (Nunezet al., 1991) should be investigated.

Haemic tumours are well representedin cage-cultured salmon. Spontaneouslymphosarcoma has been intermittentlydiagnosed in Atlantic and chinook salmoncultured in Canada (AVC case archives), aselsewhere in the world, and is characterizedby infiltration of many organs, and par-ticularly the renal interstitium, by smalluniform-sized lymphocytes (Fig. 5.11).Whether these tumours reflect spontaneousgenetic mutations, or develop due to the


Fig. 5.11. Section of a kidney from an Atlantic salmon in which the inter-tubular portions have been over-run by a population of monomorphic lymphocytes. This pattern is typical for lymphosarcoma. H&E stained.



interaction of the host genome with an infec-tious agent such as a novel or endogenousretrovirus, is as yet unknown. Based on theepizootiology, however, it would appearthat typical salmon lymphosarcoma is notinfectious. In contrast to this, Kieser et al.(1991) have reported an outbreak of anepitheliotropic lymphoblastic lymphoma incoho salmon. Its histological picture con-trasts with spontaneous lymphosarcoma bythe relative immaturity of many of the neo-plastic cells. At a population level, it con-trasts remarkably in that progression of thedisease within the population occurred.

Plasmacytoid leukaemia (PL), alsoknown as ‘marine anaemia’, is a haemicneoplasm, which principally affectscage-cultured chinook salmon. Fish with PLhave massive numbers of plasma cellsand plasma cell precursors, including manyplasmablasts in mitosis. These cells arewidely distributed in the fish and, inparticular, infiltrate organs such as thekidney, spleen, liver, retro-orbital areas andthe lamina propria of the gut (Kent et al.,1990). PL contrasts with typical lymphosar-coma and the epitheliotropic lymphoblasticlymphoma in that its infectious nature hasbeen repeatedly demonstrated (Kent andDawe, 1990; Newbound et al., 1993)although the exact nature of the infectiousagent remains controversial. Nevertheless,its waxing and waning nature within farmedpopulations suggests that its expression asa clinical disease entity may be tied toenvironmental conditions and/or the pres-ence of other disease conditions. Furtherdetails on PL are presented elsewhere in thisvolume.

Disease Conditions Relating to theUse of Medications

There are relatively few scientific reportsdealing with the adverse effects of medica-tions applied to fish in cage culture. How-ever, this lack of reporting does not reflectthe observations that are frequently madeby aquaculturists and fish health profes-sionals. Indeed, several of the bath

treatments directed at sea lice are appliedin such a manner that behavioural signsof toxicity are routinely noted and used tosignal that the treatment period shouldbe terminated. Treatment-induced fishkills, especially those attributed to theeffects of organophosphate-based sea licetreatments, can be quite extensive (Rothet al., 1993). This has prompted a search fororganophosphates with wider therapeuticmargins, in addition to other methods of sealice control.

Bath treatments in cage-culture situa-tions are problematic because of difficultiesin calculating the volumes of water in cagesfitted with tarpaulins. Additionally, theunderlying disease conditions and pre-treatment stress levels of target fish can leadto results that are unexpected based oncomparisons with scientific data, the latterbeing typically generated from exposure ofhealthy fish under optimum environmentalconditions. Reduction of dissolved oxygenconcentrations, during field treatments,is particularly important with respectto organophosphate treatments, since,although brain acetylcholinesterase (AChE)levels recover after organophosphate expo-sure (Morgan et al., 1990), low oxygen levelsat the time of treatment cause a greater andmore persistent suppression of AChE (Høyet al., 1991). The latter problem may makefish vulnerable to the toxic effects of a regimeof repeated organophosphate baths (Høyet al., 1991).

Bath treatment of fish with highconcentrations of hydrogen peroxide hasrecently been used as an alternative toorganophosphates for treatment of salmonwith sea lice (Bruno and Raynard, 1994).However, depending on the concentrationused, the water temperature and theexposure time, hydrogen peroxide has thepotential to cause mortalities (Bruno andRaynard, 1994) stemming from extensivebranchial epithelial necrosis and conse-quent branchial oedema (Johnson et al.,1993a; Kiemer and Black, 1997) (Fig. 5.12).As an alternative to bath treatments for lice,ivermectin (an avermectin compound) hasbeen used successfully when incorporatedinto the feed (Johnson and Margolis, 1993).

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Although Johnson et al. (1993b) noted adifference in toxic effects between speciesof salmon, they were unable to correlatehistopathological changes with the toxicity.

The incorporation of antibiotics intofeed can lead to feed refusal or reduced feed-ing rates (Hustvedt et al., 1991), particularlyif the feeding rate is low and, consequently,the concentration of antibiotic in the feedis relatively high on a percentage basis.Whether antibiotics can directly be associ-ated with fish deaths is difficult to deter-mine; however, Hiney et al. (1994) noted anincreased mortality rate in Atlantic salmonduring a treatment with the fluoroquinoloneantibiotic ‘flumequin’. Intuitively it shouldalso be expected that diseases may alter therates of antibiotic metabolism and clearance.This phenomenon has been largely unex-plored; however, it was suspected by Bruno(1989) to explain the development of pat-terns of liver pathology in fish suffering fromfurunculosis and being treated with oxytet-racycline. Bruno (1989) suggested that theantibiotic may have had an anomalous effecton the livers due to compromised antibioticexcretion.

Summary

Non-infectious disorders of cage-culturedfish can stem from many sources. They may

lead to distinct clinical entities or playa role in the pathogenesis of infectiousconditions. In general, because of the fixednature of cage culture operations, environ-mental factors that may cause disease orstress will continue to be major consider-ations when cage sites are being selected.Current research into non-infectious dis-orders, despite the importance of theseproblems to aquaculture bioeconomics,is relatively fragmented and typically doesnot attract research money in a mannercomparable with funding for infectiousdisorders

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