VIPR

SRAC Publication No. 4605

November 2008

Algal Toxins in Pond AquacultureJohn H. Rodgers, Jr.1

Algal toxins can cause problems in the freshwater aquaculture of both vertebrates (fish) and invertebrates (shellfish). Such problems include:

•off-flavor(Tucker,2000;SRACPublicationNo.192),

•indirecttoxicitythroughchangesinwaterquality(SRACPublica-tion No. 466), or

•directtoxicity.

Algal toxins are organic molecules pro-ducedbyavarietyofalgaeinmarine,brackishandfreshwaters,aswellasonwetsoils(Falconer,1993).Theyareaprobleminaquaculturewhentheyare produced in sufficient quantities, withsufficientpotency,tokillcul-tured organisms, decrease feeding and growthrates,causefoodsafetyissues,oradverselyaffectthequalityoftheproduct(Shumway,1990).

Algal bloomsTheproductionofalgaltoxinsisnor-mallyassociatedwithalgalblooms,or the rapid growth and exception-allydenseaccumulationofalgae.Theterm Harmful Algal Bloom (HAB) is used to describe a proliferation of al-gae,orphytoplankton.Severebloomsofevennon-toxicalgaecanspelldisaster for cultured animals, because bloomsdepletetheoxygenintheshallowwatersofmanyaquaculturesystems.ThenumberofHABsaround

theworldisincreasing(Shumway,1990;Sundaetal.,2006),especiallyintheU.S.wherealmosteverycoastalstate is now threatened, in some cases bymorethanonespeciesofharmfulalgae.Scientistsareunsurewhythistrendisoccurring.Thecausesmaybenatural(speciesdispersal)orhuman-related (nutrient enrichment, climate change, and/or transport of algae in shipballastwater)(Johnk,etal.2008;Sundaetal.,2006).

Theeffectsofalgalbloomsvarywide-ly.Somealgaearetoxiconlyatveryhigh densities, while others can be toxicatverylowdensities(afewcellsper liter). Some blooms discolor the water (thus the terms “red tide” and “brown tide”), while others are almost undetectable with casual observation (Shumway,1990).

HABs can affect public health and ecosystemswhen:

•filter-feedingshellfish(clams,mussels,oysters,scallops)feedontoxicphytoplanktonandac-cumulate harmful toxins that are passedupthefoodchain;

•fish,shellfish,birdsandevenmammalsarekilledbyeating organisms that have consumed algaltoxins;

•light cannot penetrate the water, thus changing the function and structureoftheaquaticecosystem;

•discolorationmakeswateraesthet-icallyunpleasant;

•thedecayingbiomassofabloomdepletesdissolvedoxygen(espe-ciallycriticalinaquaculture);or

•bloomskillotheralgaeimpor-tantinthefoodweb(Coddetal.,2005b;Landsburg,2002).

HABs can cause serious economic lossesinaquacultureiftheykillcul-tured organisms or cause consumers concernaboutfoodsafety.Prelimi-naryestimatesshowthattheeffectofHABoutbreaksontheU.S.economyismorethan$40millionperyear,or$1billionperdecade(Landsburg,2002;Hudnell,2008).

Toxin-producingalgaemaybecomemore prevalent in the future (Sunda et al.,2006;Johnketal.,2008),especial-lyineutrophicfreshwatersystems.Thispublicationfocusesonalgaltoxins in freshwater pond aquaculture in the South and southeastern United States.Themostcommontoxin-pro-ducingalgaeinthisregionarecy-anobacteria, golden algae (Prymnesium parvum) and euglenoids.

Cyanobacteria: the blue-green algaeCyanobacteria(blue-greenalgae)in-habitfresh,brackish,marineandhy-persaline waters, as well as terrestrial environments.Cyanobacteriagrowinmanyhabitatsfromthermalspringstothearctic.Theyplayimportantrolesinthebiogeochemicalcycling1 Clemson University

of elements and in the structure, functionandbiodiversityofaquaticcommunities (from microbes through vertebrates).Somecyanobacteriacanreduce both N2andCO2. Some can convert N2 into NH3and,ultimately,into amino acids and proteins.

Cyanobacteriahavearelativelysimpleprokaryoticstructureandlackmembrane-boundorganelles(nucleus,mitochondria and chloroplasts). With murien in the cell wall and reproduc-tionbybinaryfission,cyanobacteriaarestructurallyandphysiologicallylikeothergram-negativebacteria,buttheyconductphotosynthesislikeplantsinaquaticsystems.Cyanobac-teria are much larger than other bac-teriaandmakeamajorcontributiontoworldphotosynthesisandnitrogenfixation(Coddetal.,2005a;Huismanetal.,2005;Hudnell,2008).

Cyanobacteriaoccurinunicellular,colonial and filamentous forms and most are enclosed in a mucilagenous sheath,eitherindividuallyorincolo-nies. As single cells, large colonies andfilaments(trichomes),blue-greenalgae can become the dominant algae innutrient-richwaters.Theycanformbloomssothickitappearsthatblue-greenpaintcoversthesurfaceofthe water.

Several species found in the South and Southeast produce substances that cause taste and odor problems in water supplies and aquacultural prod-ucts(Tucker,2000).Someblue-greenalgae,particularlyAnabaena and Mi-crocystis, produce toxins poisonous to fishandtowildlifeandlivestockthatdrinkcontaminatedwater.Therearealsodocumentedcasesofblue-greenalgal toxins harming people in other partsoftheworldwhodrankpoorlytreated water.

Cyanobacterial ecology in aquaculture ponds Cyanobacteriacancolonizeandrap-idlygrowtogreatmassesinaquacul-ture ponds. Factors that affect their growtharenutrientstatus,salinityor ionic strength, light conditions, turbulence and mixing, temperature andherbivory(Sundaetal.,2006).

Inaquaculturesituations,eukaryoticalgae (green, diatoms, etc.) can often growfasterthancyanobacteria.How-ever,cyanobacteriacanout-competealgae for nutrients, thrive with low dissolvedoxygen,andphotosynthe-sizemoreefficientlyatlowlightlev-els.Cyanobacteriaarelessaffectedbyturbidity,highconcentrationsofammonia and warm temperatures. Theycanseizetheadvantageineutrophicaquaculturesituations.Cy-anobacteria can affect the production ofzooplanktonandconsequentlytheproductionoffish.Theyalsoproduceallelochemicals that can inhibit com-petingalgaeandinvertebrategrazers(Gross,2003;Berryetal.,2008).

Thereiscompellingevidencethatcyanobacteriaandtheirtoxins(bothneurotoxins and hepatotoxins) af-fectzooplankton(cladoceransandrotifers) population structure, and thatthismayinfluencetheecologicalprocessesresponsibleforcyanobac-terialsuccess(Berryetal.,2008).Zooplanktongenerallyavoidcy-anobacteria as a food source (Gross, 2003),whichmeansthatzooplank-ton feed on algae that compete with cyanobacteria.Intheprocess,theyrelease essential nutrients, further fertilizingcyanobacterialgrowth.Duringcyanobacterialblooms,whenalternativefoodsourcesforzooplank-ton have been exhausted, Daphnia populationsmaydecline.Somezoo-plankton(Daphnia pulicaria, Daphnia pulex) species have adapted to survive in the presence of certain toxic cells (Sundaetal.,2006;Gross,2003).Thischangesthezooplanktonpopula-tiondynamics.Feedingpressurebyadaptedzooplanktononcyanobac-teriaisreducedbyfishpredation,which again releases nutrients that fuelcyanobacterialgrowth.Itmaybeprematuretoproposethatcyanobac-terialdominanceisguidedbycyano-toxin production. However, feeding deterrence is one of the roles sug-gestedforthesemetabolites(Berryetal.,2008).Whetherthecompoundscausingtoxicityanddeterrenceareoneandthesamehasrecentlybeenquestioned(Berryetal.,2008).Whiledaphnidsarekilledwhenfeedingon

toxic Microcystiscells,theyshownoselection between ingesting toxic or nontoxic cells, which indicates that microcystinsarenotresponsibleforfeedinginhibition(Berryetal.,2008).

Problems with cyanobacteria in aquaculture pondsCyanobacteriacanrapidlyovertakean aquaculture pond and contribute tounstableconditions.Cyanobacteriablooms can decrease fish production andkillfishbecauseofoxygendeple-tion.Cyanobacteriacanalsocauseoff-flavorandobjectionableodorinfish.

However,theroleofcyanobacteriaandcyanotoxinsinfishkillsandoth-er problems is not clear at this time. Therearemorethan1millionfishpondsintheSoutheastandmanyofthemhaverelativelyfrequentbloomsofcyanobacteriathatmayproducetoxins (e.g., Microcystis, Anabaena, etc.).Yetthereareonlyafewreportsoffishkillsthataredirectlyrelatedto algal toxin production (Zimba et al.,2001).Sothemerepresenceoftoxin-producingalgaedoesnotneces-sarilymeanthatenoughtoxinwillbeproduced to harm fish in culture.

Cyanobacterial toxinsCyanobacterialtoxinscanbeclas-sifiedseveralways.Theymaybeclassified according to their chemical structuresascyclicpeptides(mi-crocystinandnodularin),alkaloids(anatoxin-a,anatoxin-a(s),saxitoxin,cylindrospermopsin,aplysiatoxins,lyngbyatoxin-a)andlipopolysaccha-rides.However,cyanotoxinsaremorecommonlydiscussedintermsoftheirtoxicitytoanimals.Whilethereareseveraldermatotoxins(e.g.,lyng-byatoxinandaplysiatoxins),whichareproducedprimarilybybenthiccyanobacteria,mostcyanotoxinsareeither neurotoxins or hepatotoxins (Coddetal.,2005a).

Neurotoxins. Neurotoxins are or-ganicmoleculesthatcanattackthenervoussystemsofvertebratesandinvertebrates.Threeprimarytypesof neurotoxins have been identified: 1)anatoxin-a,analkaloid,inhibitstransmissions at the neuromuscular

junctionbymolecularmimicryoftheneurotransmitteracetylcholine(blockspost-synapticdepolarization);2)anatoxin-a(s)blocksacetylcholin-esterase (similar to organophosphate pesticides);3)saxitoxinsarecarbamatealkaloidsthatactlikecarbamatepesti-cidesbyblockingsodiumchannels.

NeurotoxinsareproducedbyseveralgeneraofcyanobacteriaincludingAnabaena, Aphanizomenon, Microcystis, Planktothrix, Raphidiopsis, Arthrospira, Cylindrospermum, Phormidium and Oscillatoria.NeurotoxinsproducedbyAnabaena spp., Oscillatoria spp. and Aphanizomenon flos-aquae blooms have been responsible for animal poison-ingsaroundtheworld(Carmichael,1997;Briandetal.,2003).

Neurotoxinsusuallyhaveacuteeffects in vertebrates, with rapid pa-ralysisoftheperipheralskeletalandrespiratorymuscles.Othersymptomsinclude loss of coordination, twitch-ing, irregular gill movement, tremors, altered swimming, and convulsions beforedeathbyrespiratoryarrest.

Hepatotoxins. Hepatotoxins are producedbymanygeneraofcy-anobacteria and have been impli-cated in the deaths of fish, birds, wildanimals,livestockandhumansaroundtheworld(Briandetal.,2003;Carmichael,1997).Thecyclichep-tapeptides,ormicrocystins,inhibiteukaryoticproteinphosphatasestype1andtype2A,resultinginexcessivephosphorylationofcytoskeletalele-mentsandultimatelyleadingtoliverfailure(Codd,2005b).Thesetoxinstargettheliverbybindingtheorganicaniontransportsysteminhepato-cytecellmembranes.Microcystinsarethelargestgroupofcyanotoxins,withmorethan70structuralvariants(MalbroukandKestemont,2006).Microcystinistheonlycyanotoxinforwhichthebiosyntheticpathwayand gene cluster have been identified (Huismanetal.,2005).Microcys-tinsareproducedinfreshwatersbyspecies of Microcystis, Anabaena and Planktothrix.Symptomsofpoisoninginfishincludeflaredgillsbecauseofdifficultybreathingandweaknessorinabilitytoswim.Channelcatfish,

Ictalurus punctatus, can become intox-icatedat~50to75µgmicrocystin/L(Zimbaetal.,2001).Allfishmaybekilledwithin24hoursofexposure.Atnecropsy,severelesionsmaybeobserved in liver tissues.

Onepotenthepatotoxin,cylindrosper-mopsin,isproducedbyCylindrosper-mopsis raciborskii,arelativelysmallcyanobacterium.Cylindrospermopsinisanalkaloidthatsuppressesglu-tathioneandproteinsynthesis.C. raciborskii has been in the South and Southeast for decades and is becom-ingmorewidespread.Mammals(suchashumans)arerelativelysensitivetocylindrospermopsinandmaybeaffectedwhentheyeatfishthathavebeenexposedtothetoxin.Astudyreporting the bioaccumulation of cylindrospermopsininmuscletis-sueoftheredclawcrayfish(Cherax quadricarinatus) and visceral tissues of rainbow fish (Oncorhynchus mykiss) shows that exposure could occur from farm-raisedfreshwateraquaticfoods.Fisharegenerallymoretolerantofalgal toxins than mammals and tend toaccumulatethemovertime(Carson,2000).AlthoughC. raciborskii has not yetbeenaprobleminaquaculture,itcould become a problem in the future.

Environmental effects on toxin productionTheeffectsofenvironmentalfactorson toxin production are much studied andwidelydisputed(Codd,2000;Coddetal.,2005a).Bloomsinthesamebodyofwatercanbetoxicornon-toxicfromoneyeartothenext.A different strain composition (i.e., toxicversusnon-toxic),whichcan-notbedistinguishedmicroscopically

if belonging to the same species, is a common explanation for this oc-currence. However, some species are knowntoproducehighorlowlevelsoftoxicityunderdifferentlaboratoryconditions.Thestimulusfortoxinproduction in such species is not known.Environmentalparameterssuchaslightintensity,temperature,nutrients and trace metals have been mimickedunderlaboratoryconditionsandtheireffectoncyanotoxinpro-duction investigated. Studies on light intensityarenotdefinitive,butitisknownthatintenselightincreasesthecellularuptakeofiron,whichmayberesponsible for more toxin production. However, low concentrations of iron leadtohighermicrocystinconcentra-tions(Huismanetal.,2005).Nutrientssuch as nitrogen and phosphorus are essentialforcyanobacterialgrowth.Phosphorusisusuallythelimitingfac-tor in ponds, so small increases in this nutrientmayinfluencetoxinproduc-tionsimplyasaresultofincreasingalgalgrowth.Generally,decreasedamountsofmicrocystin(producedbyAnabaena, Microcystis and Oscillatoria) andanatoxin-a(producedbyAphani-zomenon) have been reported under the lowest phosphorus concentrations tested(Watanabeetal.,1995).

Managing toxic cyanobacteriaMonitoring and diagnosing the problem. While not all blooms of toxin-producingcyanobacteriaresultintoxinproduction,mostdo.Oncea bloom is observed, the onset of toxicitywillberapid(hourstoadayortwo).Toconfirmtheproblem,adiagnostician will need fresh samples (unpreserved) of the water contain-

Figure 1. Microcystis aeruginosa (photos by John H. Rodgers, Jr.).

ingthesuspectedcyanobacteria(Rottmannetal.,1992).Asampleofbothsickanddeadfishwillalsobe needed, along with informa-tiononfishbehaviorandanyothersymptomsobserved.Youngfisharegenerallymoresensitivethanolderfish.Thediagnosticianmaylookforlesions on fish livers, although this is inconclusive as the sole method of diagnosis(Zimbaetal.,2001).

Treatment. Mostofthetime,manag-ingapondspecificallytopreventtoxicblue-greenalgaebloomsisnotjusti-fied, and the treatments themselves arerisky.Analgicideshouldnotbeappliedwithoutconsideringthesizeof the affected pond, the number and typeoffishatrisk,theageandcondi-tionofthefish,thesensitivityofthecyanobacteriumtotreatment,andthecostofthetreatment.Non-chemicaltreatmentsinclude1)physicalmixingandaeration,2)increasingflowrateorflushingtodecreasehydraulicreten-tion time, and 3) decreasing or alter-ing nutrient content and composition. Someoftheseoptionsmaynotbeviable at all sites and in all situations.

Prymnesiophytes: the golden-brown algaeThehaptophytegenusPrymnesium is comprisedmainlyoftoxin-producingspecies that form harmful blooms usuallyinbrackishwater(Westetal.,2006).BloomsofP. parvum have been responsibleforfishkillsandsignifi-canteconomiclossesinEurope,NorthAmericaandothercontinents.Texashas been hit with recurrent blooms in several reservoirs and rivers and TexasParksandWildlifehasofferedsome detailed advice regarding man-agementoptions(Sageretal.,2007).

Prymnesiophyte ecology Prymnesium parvumiscommonlycalled the “golden” alga. It is con-sideredtobeahaptophyteprotist(GreenandLeadbetter,1994).Itisarelativesmall(~10µm),generallyhalophilic organism that intermit-tentlyproducesanichthyotoxin.Thisorganismhasbeenimplicatedinnumerousextensivefishkillsin

brackishwatersandinlandwaterswithrelativelyhighmineralcontentonfivecontinents(OtterstromandSteemann-Nielsen,1940;Holdwayetal.,1978;JamesanddelaCruz,1989;Kaartvedtetal.,1991;Guoetal.,1996;Lindholmetal.,1999).

P. parvumcellscontainchlorophyllsa and caswellasyellow-brownac-cessorypigmentsandarecapableofphotosynthesis.However,theorgan-ism is thought to be a mixotroph that can feed on bacteria and protists (Skovgaardetal.,2003)andphagotro-phyhasbeenobservedincultures.P. parvum has a vitamin requirement in laboratoryculture(Droop,1954).

The Prymnesium toxins Prymnesium parvum produces at least threetoxins—anichthyotoxin(UlitzerandShilo,1966),acytotoxin(UlitzerandShilo,1970)andahemolysin(aproteinthatlysesredbloodcells)(Ulitzer,1973).Thesetoxinsarecol-lectivelyknownasprymnesinsandall can alter cell membrane perme-ability(Shilo,1971).Bloomdensitydoesnotcorrelatestronglywithtoxic-ity(Shilo,1981),probablybecausetoxicitymaybeenhancedbytem-peraturelowerthan30ºC(ShiloandAschner,1953),pHgreaterthan7.0and phosphate concentration (Shilo, 1971).

The P. parvumichthyotoxinaffectsgill-breathingaquaticanimalssuchas fish, brachiated tadpoles and mol-lusks(Shilo,1967).Itcausesgillcellstolosetheirselectivepermeabilityand,thus,makesthemvulnerabletoanytoxininthewater(UlitzerandShilo,1966;Shilo,1967).

Signs of intoxication Dense growths of Prymnesium par-vummaycolorthewateryellowtocopper-brownorrust.Thewatermayfoam if aerated or agitated. Affected fishbehaveerratically.Theymayaccumulate in the shallows and be observedtryingtoleapfromthewa-ter to escape the toxins (Sarig, 1971). Affectedfishmayhaveevidentbloodingills,finsandscalesandmaybecovered with mucus. Young fish are often most sensitive to the toxin. If fish are removed to uncontaminated waterintheearlystagesofintoxica-tion, their gills can recover within hours (Shilo, 1967). However, feeding andgrowthwillusuallybereducediffishsurvive(BarkohandFries,2005).

Aquatic insects, birds and mammals arenotaffectedbyP. parvum toxins. Thegoldenalgaisnotknowntoharmhumanseither,althoughdeadordy-ing fish should not be eaten.

Managing prymnesiophytes Monitoring and diagnosing the problem.IdentifyingPrymnesium parvum requires examining un-preserved, discrete water samples. P. parvumcanpassthroughmanyplanktonnetsandtheirstructurecanbealteredanddistortedbypreserva-tives or fixatives. P. parvum cells can be detected at low concentrations (~102cells/mL)usingfluorescentmi-croscopyonliveorreasonablyfreshsamples. P. parvum cell densities can bedeterminedusingahemacytom-eter(BarkohandFries,2005).

Prymnesium parvum N.Carteraresmall, subspherical, swimming cells about8to15µmlongwithtwoequalorsubequalheterodynamicflagella

Figure 2. Prymnesium parvum (photos by Dave Buzan and Greg Southard).

Haptonema

2 flagella

saddle-shapechlaroplasts

9.1 µm

12to20µmlongandashort(3to5µm),flexible,non-coilinghaptonema(Greenetal.,1982).Cellshavetwochloroplaststhatmaybe“c-shaped”andolivegreenincolor.Theyswimwith a smooth forward movement while the cell spins on the longitudi-nalaxisandflagellarpole. P. parvum cells have diagnostic calcareous scales that can be observed with electron microscopy(Greenetal.,1982).Expe-rienceisrequiredtoidentifythisalga.Westetal.(2006)havedevelopedaspecificmonoclonalantibodyusedinconjunctionwithsolid-phasecytom-etrytorapidlyquantifyP. parvum.

AbioassaycanbeusedtoestimateichthyotoxinproductionbyPrymne-sium parvum(Sageretal.,2007).Thisassayisusefulindecidingwhethertoapplyanalgicide.Theassayinvolvesexposing fish such as larval Pimephales promelas to the pond water in ques-tion, and to dilutions of the suspect water amended with a cofactor or promoter of P. parvum toxin.Ulitzerand Shilo (1966) discovered that the potencyoftheP. parvumichthyotoxinwasaugmentedbythecationDADPA(3,3-diaminodipropylamine)inlabora-torytestsbecauseitincreasedthesensitivityofGambusia to the toxicant. Thisbioassaycanidentifywatersthathave sufficient toxin (or are develop-ing sufficient toxin concentrations) to posearisktofishinculture.

Fordiagnosticanalysis,10-literwatersamples should be collected at least 6 inches below the surface because P. parvum is sensitive to UV radiation. Bothcellcounts(microscopy)andthetoxinbioassayareneededtoconfirmP. parvum, so unpreserved water samples must be shipped expedi-tiouslytothelab.

Treatment. TexasParksandWild-life has detailed advice for manag-ing Prymnesium parvum (Sager et al., 2007).Onemethodusedinisolatedpondcultureisapplyingammoniumsulfateandcoppersulfate(Barkohetal.,2003).Theammoniumsulfateconcentrations required to control P. parvum(~0.17mg/Lofun-ionizedam-monia)mayproduceun-ionizedam-moniaconcentrationsthatadversely

affectsomefish(Barkohetal.,2004).Ifnotcarefullyused,thecoppersulfatemaykilldesirablealgaealongwith the P. parvum and decrease food resourcesforthezooplankton,therebydisruptingfishfeeding.Neitherbarleystraw nor a commercial bacterial bioaugmentation product were effec-tive for controlling P. parvuminTexasponds(Barkohetal.,2008).Barleystraw extract was also ineffective in laboratorytests(Groveretal.,2007).Treatmentswithhighconcentrationsofammonium(0.72mgNH4-N/L)weresuccessful,thoughtheyposearisktonon-targetspecies.Repeatedtreatments of ammonium chloride and phosphoric acid were somewhat successful for controlling P. parvum growth in limnocorrals in aquaculture ponds(Kurtenetal.,2007),buttheyarealsohazardoustonon-targetspe-cies.

IntheChineseaquacultureofcarpspecies, suspended solids (mud), organicfertilizer(manure)anddecreasedsalinityhavebeenusedtocontrol P. parvum (Guo et al., 1996), with the best results from decreased salinityandammoniumsulfate.

When using an algicide, obtain all regulatoryapprovalsandpermitsand follow label instructions and re-strictionstocomplywithfederallaw.

EuglenoidsSince1991,severaloutbreaksoftoxic Euglena (Fig. 3) have occurred inNorthCarolinahybridstripedbass (Morone saxatilis x M. chrysops) production ponds, causing the loss ofmorethan20,000poundsoffish.

Relativelyrecentresearchhascon-firmed that Euglena species produce anichthyotoxininfreshwateraqua-culture(Zimbaetal.,2004).Thehy-brid striped bass mortalities in North CarolinawerecausedbyE. san-guinea,awidelydistributedspeciesinmanyshallow,relativelycalm,eutrophicfreshwatersystems.Thisspeciesalsokilledlaboratory-rearedchannel catfish, tilapia (Oreochromis niloticus) and striped bass. In confir-matorystudies,Zimbaetal.(2004)noted that cultures of Euglena granu-lata (UTEXLB2345)causedsimilarmortalitiesandsymptomsinchan-nel catfish and sheepshead minnows (Cyprinodon variegatus).

DiagnosisMicroscopicexaminationofawatersample can confirm the presence of Euglena since E. sanguinea is morphologicallydistinct.Thetypi-calprogressionofsymptomsfromexposure to Euglena toxin begins with the fish going off feed for no apparentreason.Within24hoursofcessation of feeding, the fish swim at or near the surface in an agitated or disorientated state, often with the dorsal fin extending out of the water or swimming on their sides and even upsidedown.Ifstepsarenottakenimmediatelyafterobservingthisstate,within24hoursthefishwillbedead.

Field observation of dead fish indi-catedrapidonsetofmortalitywithreddeningofgilltissue.Mortalityoflaboratory-rearedchannelcatfishoccurredwithin6.5minutesto2hours after exposure. No water qual-

Figure 3. Euglena sanguinea.

25 µm

itycharacteristics(ammonia,nitrate,pH,temperatureordissolvedoxygen)were abnormal or exceptional during the fish mortalities. Fish exposed to E. sanguinea in culture or to filtrate from cultures were disoriented rapidly.Theirrespirationwasac-celeratedandtheylosttheabilitytomaintain equilibrium. Although no distinct hemorrhaging was observed, gill tissue was reddened (Zimba et al.,2004).

Euglena toxin Based on behavioral changes in exposedfish,Zimbaetal.(2004)suggested that the euglenoid toxin functionsasaneurotoxin.Thetoxiniswatersoluble,non-protein,heatstable(30°Cfor10minutes),freez-ingstable(-80°Cfor60days),andlabiletooxidation.Euglenoidsshouldbe sensitive to several of the algicides available. If a toxic Euglena bloom oc-curs,trytominimizemixingofthewater because mixing will disburse the bloom throughout the pond. Aer-ateonlyifneededtosavethefishfromacuteoxygendepletion.Al-though Euglenasp.arenormallyverymobile, as a bloom progresses to the point that fish are disorientated, the algae seem to become concentrated in the downwind side of the pond.

In2002,workbyRowanandotherson a EuglenabloomattheTidewaterResearchStationinNorthCarolinashowed that potassium permangan-ateappliedatarateof2.5timesthepermanganate demand of the pond apparentlydetoxifiedthetoxinandeliminatedthesource.Lowerratesdetoxified the toxin but did not elimi-natethesource,andthesymptomsofagitation and disorientation recurred quicklyinexposedfish.Research-ersatUNC-Wilmingtonidentifiedthe alga as Euglena sanguinea and are attempting to isolate the toxin and studyit.

Mentionofacontroltacticfortoxin-producing algae does not constitute endorsementofanalgicideoranyothertacticforyourspecificsitua-tion.CheckwithyourlocalExten-sion agent regarding site specific permit requirements and restrictions.

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