NSW DPI

Diagnosis, Treatment & Prevention of THE Diseases of the Australian Freshwater Fish Silver Perch (Bidyanus bidyanus) Fisheries Research and Development Corporation

Fisheries Research and Development Corporation

Phil Read • Matthew Landos • Stuart J. Rowland • Charlie Mifsud Diagnosis, Treatment and Prevention oF THE Diseases of the Australian Freshwater Fish Silver Perch (Bidyanus bidyanus)

Phil Read, Matthew Landos, Stuart J. Rowland & Charlie Mifsud

Fisheries Research and Development Corporation DISCLAIMER FOR FURTHER INFORMATION The information contained in this publication is Grafton Aquaculture Centre based on knowledge and understanding at the time PMB2, Grafton NSW 2460 of writing (April 2007). However, because of advances Ph 02 6640 1690, or in knowledge, users are reminded of the need to port stephens fisheries Centre ensure that information upon which they rely is up Locked Bag 1, Nelson Bay NSW 2316 to date and to check currency of the information Ph 02 4982 1232 with the appropriate officer of New South Wales Department of Primary Industries or the user‘s independent adviser..

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© State of New South Wales through NSW Department of Primary Industries (April 2007). You may copy, distribute and otherwise freely deal with this publication for any purpose, provided that you attribute NSW Department of Primary Industries as the owner.

ISBN 978 0 7347 1792 4 JOB NUMBER 5938 table of contentsdiagnosis, treatment & prevention of the diseases of the australian freshwater fish silver perch (bidyanus bidyanus)

Acknowledgements … 3 Fungal diseases … 34 Disease problems in purging systems … 62 saprolegniosis – Saprolegnia parasitica Introduction … 4 epizootic Ulcerative Syndrome (EUS, Red Spot Disease) – Aphanomyces invadans Aquatic plants and fish health … 64

Anatomy of silver perch … 6 Bacterial diseases … 39 Chemical use and legislation columnaris – Flavobacterium columnare (January 2007) … 65 Diagnostic techniques … 9 Tail rot syndrome goldfish ulcer disease – Information required to prevent, Diseases and pathogens … 16 Aeromonas salmonicida nova diagnose, treat and control disease … 67 streptococcosis – Streptococcus iniae Ecto-parasitic protozoans … 16 mycobacteriosis – Mycobacterium spp. chilodonellosis – Chilodonella hexasticha Calculations, treatments and aeromonad dermatitis – Aeromonas spp. ichthyophthiriosis (white spot, ich) – dose rates … 70 epitheliocystis Ichthyophthirius multifiliis Formalin ichthyobodosis – Ichthyobodo necator Viral diseases … 50 medicated feed Trichodinosis – Trichodina sp. epizootic haematopoietic necrosis (EHN) alkalinity and copper sulfate Tetrahymenosis – Tetrahymena sp. Potassium permanganate salt Myxozoan infections … 24 Miscellaneous non-infectious diseases, disorders and Trichlorfon Henneguya spp. conditions … 51 withdrawal periods

Hypoxia s Ecto-commensal ciliates … 26 Hydrogen sulphide poisoning Ambiphyra spp. Notifiable fish diseases … 77

gas supersaturation (Gas bubble disease) t en con Monogeneans … 27 noxious algae Glossary … 78 le o f a b le t Lepidotrema bidyana cloudy eyes and red tails •

1 |

Physical abnormalities p Copepods … 29 References and further reading … 80 abdominal swelling (bloat) anchor worm – Lernaea spp. nutritional disorders Ergasilus spp. aggression Cestodes and nematodes … 32 acknowledgements

The authors would like to thank and Tomlin, Steve Vidler, Roger Camm, Trevor Peter Selosse, Ken Bock, Les Rava, Paul acknowledge the members of the native Walshe, Gary Webb, Bob Overguard, Robertson, Matthew Hollis, Kevin Clark, fish hatchery and silver perch industries Charles Faulkner, Mike Beveridge, Sam Peter Boyd, David Glendenning, Nathan for their input and information over the Clift, Jeff Guy, Ric Mailler, Andrew Pratt, Ferrie, Todd Rowland, Leo Cameron, years, in particular Mark Scifleet and Ian Grant Webster, Tom Sole, Geoff and Luke Ferguson, Joanne Murray, Ralf Charles. Ben Pope, Ian Brunton, Rob Bartley, Jahrling, James Lang, Peter Dickson, Ross Burton, Brian Taylor, Stan Moore, Matt Parker, Brendan Palmer, Nat Sewell, We also thank the following who Michael Hickey, Bruce Sambell, Warwick Joel Crispin, Daniel Kratz, Andrew Ford, allowed access to their facilities and Reakes and Mike Murphy. Tony McClymont and Steve Pepper. shared their knowledge of fish diseases; Paul Trevethan, Alan and John Hambly, We thank Dr Gordon Beakes (UK), This disease manual was prepared as Noel Penfold, Calvin and Lisa Terry, Bruce Professor Iva Dykova (Czech Republic), part of a project that was funded by Malcolm, Ray Partridge, Roger Munzel, Dr Craig Hayward (University of the former NSW Fisheries, including the Trevor Pontifex, Andrew Yazbek, Craig Queensland) and Dr Brett Ingram Aquaculture Initiative, the current NSW and Parry Anderson, Nic Arena, Steve (Department of Primary Industries, Department of Primary Industries, and Grammer, Nick Lambert, Grantley Blake, Victoria) for their work and contribution the Fisheries Research and Development Jim Cliffe, Lindsay Fraser, Ainsley Pope, on specific diseases and parasites, and Corporation (FRDC). We thank Bill Lindy Trudgeon, Marcia Thompson, Patrick Tully (NSW DPI) for his efforts and Talbot, Dr Nick Rayns, Dr Geoff Allan Ron and Peter Randall, Bruce Rhoades, contributions to photographic editing, and Ian Lyall for their support and Graham Bailey, Steve Wood, Gary Webb, sketches and diagrams. encouragement. We acknowledge and Dennis Bressan, Dennis Cole, Albert are grateful for the support of the silver The authors acknowledge the effort and Cooke, Nathan David, Colin Dickson, perch industry by FRDC. input of staff at the Narrandera Fisheries Michael Gilbert, Bob Hamilton, John Centre, Wollongbar Agricultural Institute Heslin, Roger Kershaw, Mat Kilham, Chris and the Grafton Aquaculture Centre. Lawson, Rob McCormack, Peter Moore,

In particular, we thank Dr Richard s Gay Passfield, Ross Thompson, Laurie Callinan, Stephen Thurstan, Mark Nixon, k nowle d gemen t ac •

3 | p introduction

Silver perch (Bidyanus bidyanus) is mid 1990’s and is based primarily on expansion of the silver perch grow-out an Australian native freshwater fish aerated, earthen ponds. There is some industry since the mid 1990’s has seen a endemic to the inland Murray‑Darling production in recirculating aquaculture corresponding increase in the incidence River System (Fig. 1). Hatchery systems (RAS) and cages, and these of diseases, plus several new diseases techniques were developed at the intensive systems have potential for and pathogens including a winter Narrandera Fisheries Centre (formerly significant production in the future. fungal disease, gill flukes, and various the Inland Fisheries Research Station) Some silver perch farms have achieved syndromes and conditions. The common in the late 1970’s, and transferred to a high survival and production under diseases of silver perch are caused by new commercial industry in 1982. The commercial conditions; however, for protozoans, monogeneans, fungi and routine production of fingerlings by success, farms must have a good supply bacteria. Diseases have had a significant government and private hatcheries over of high quality water, a reliable power impact on commercial production the past 27 years has provided a solid supply for aeration and pumps, be through induced stress on fish, loss of foundation for the development of a geographically located in a region that growth and production, death of stock grow-out industry. enables fast growth and good health, and high costs of treatments. and be well managed. Research at the Grafton Aquaculture In 2001 – 2005, a project entitled Centre in the early 1990’s demonstrated Diseases of silver perch under culture ‘Development of a Health Management that silver perch is an excellent species conditions have been previously Strategy for the Silver Perch Aquaculture for pond culture with high survival, fast described by Ashburner (1983), Rowland Industry’ was undertaken to study the growth and high production rates. An (1983), Rowland and Ingram (1991) diseases and health management of industry has been developing since the and Callinan and Rowland (1995). The silver perch. Major outcomes were: identification of new and important diseases; development of control and preventative methods for most diseases; and a health management strategy for the industry based on three separate t ion in t ro d uc •

4 | p

Figure 1 Silver Perch (Bidyanus bidyanus). Source: Patrick Tully diagnosis, treatment & prevention of the diseases of the australian freshwater fish silver perch (bidyanus bidyanus) publications, ‘Health Management Plan for Silver Perch Culture’, ‘Hatchery Quality Assurance Program for Murray Cod (Maccullochella peelii peelii), Golden Perch (Macquaria ambigua) and Silver Perch (Bidyanus bidyanus)’ and the manual ‘Diagnosis, Treatment and Prevention of the Diseases of the Australian Freshwater Fish Silver Perch (Bidyanus bidyanus)’. This manual has been prepared as an easy-to-use publication with numerous photographs of diseased fish and pathogens that will facilitate the prompt diagnosis and appropriate treatment of silver perch diseases. Its use in conjunction with the health management plan, should reduce the incidence and severity of disease outbreaks, leading to improved survival and performance of fish, and increased production, efficiency and profitability of silver perch farms. t ion in t ro d uc •

5 | p p|6 • anatomy of silverp erch difficult to locate andare sited in S reproductive systems. andendocrine perch alsohave lymphatic, nervous, Silverbody andthenbackto theheart. it passesunderlow pressure to the to thegills fromby where theheart single circuit, withbloodbeingpumped cardiovascular system consists ofa adaptation to anaquatic life. The mammals, withdifferences reflecting teleosts are similarto thosefound in liver,systems (heart, kidney, etc) of the oesophagus. M withbladder whichlacksaconnection some fins, scalesandaswim ctenoid possessbonyand typically spinesin includes silver perch, ismore advanced spiny‑rayed fish. The latter group, which two maingroups, thesoft‑rayed and Teleosts canlooselybedividedinto the largest group withinOsteichthyes. terms, andconstitutein evolutionary Teleosts are thehighestbony fishes to theClassOsteichthyes orbony fishes. Silver perch ( ANATOMY ome organs, likethepancreas are Bidyanus bidyanus ost oftheorgan of SIL ) belongs VER Source: Patrick Tully featuresExternal ofsilver perch. Figure 2 caecae ( mesenteric fat between thepyloric Source: Patrick Tully andPhil Read Gross anatomy oftheviscera ofsilver perch. Figure 3 are poikilothermic (cold blooded)are poikilothermic operculum nostril gill rakers gill lamellae lateral line pectoral fin pectoral heart PERCH Figs. 2 spleen pelvic fin stomach liver nape and pyloric caeca 3 ). Silver perch gall bladder urogenital aperture intestines anus temperature. Fins are median(dorsal, is determined by theenvironmental animals, i.e. theirbodytemperature gonad swim bladder dorsal fin(spinous) trunk muscle kidney caudal peduncle caudal anal fin caudal muscle caudal dorsal fin(soft) caudal fin caudal diagnosis, treatment & prevention of the diseases of the australian freshwater fish silver perch (bidyanus bidyanus) caudal and anal) or paired (pectoral Epidermis – cellular‑epidermal material, protection against the environment; and pelvic). The skeleton (Fig. 4) is sloughed cells, and mucus secreted to sensory receptors; excretory, some made up of the skull, vertebral column the surface; immuno‑active properties; respiratory functions; dermis contains and the fin skeleton. The skull has a assist in osmoregulation and swimming; many pigment cells containing melanin complex arrangement of bony plates protects against abrasion; primary (Fig. 5). (neurocranium) which still allow flexibility and surrounds the olfactory, optic and otic areas. The lower section of the skull (branchocranium) consists of bones associated with the jaw, pterygiophores operculum and gill arches. caudal vertabrae skull

External Features Opercula – bony cover which serves to protect the gills and assist with respiration. Lateral line – pressure sensory organ having epidermal pores; runs bilaterally ribs from head to caudal fin. vertabrae Fins – bony/spiny and soft‑rayed; assist with locomotion, positioning and Figure 4 aggressive behaviour. Main skeletal features of silver perch. Source: Patrick Tully and Phil Read p erc h

epidermis sensory organ

scale silver opening of lateral line canal

scale dermis o f om y t ana •

7 | p

lateral nerve muscle

Figure 5 Diagrammatic representation of a section through fish skin. Source: Phil Read (adapted from Storer et al. 1972) p|8 • anatomy of silverp erch production andperception.production andpositioning; soundbuoyancy pressure changes;assistswithbody watersac filledwithgases;detects physical protection ( layer ofcells; assistsinosmoticcontrol; growth covered rings; by anepidermal excretion ofsalts)( and ionicbalance ofwater, (absorption osmotic of maintenance dioxide; carbon excretion ofnitrogenous wastes and area; uptakeofoxygen andsurface Swim bladder(gasbladder) Gills Scales Source: Phil Read Ctenoid scalesfrom theflankofamature silver perch andthecaudalpeduncle ofajuvenile fish. Figure 6 Respiration Internal adult

–

main respiratoryorgan; large – calcified, flexible plates with Features Fig. 7 Fig. 6 ).

). – thin‑walled generating newbloodcells. systemcirculatory capableof filter; stomach withintheabdominalfat; red‑coloured organ located nearthe Gall bladder Gall Liver Spleen to thegills,arteries organs andbody. distributes blood viathoracic cavity; ventricle); posterior to gills inseparate Heart Kidney nitrogen excretion. andregulation;blood cell destruction nutrient andtoxins from absorbed gut; stores carbohydrates and fats; processes to assistdigestion;produces enzymes posterior kidney. wastes from theblood;anterior and ion resorption; removal ofnitrogenous balance; proteinblood osmolarity and production toproduction assistinlipiddigestion.

–

–

large, paletanto red incolour;

– – two chambered (atriumand flat, strap‑like, dark, excretion ofwater to maintain

– dark, mottledgreen; biledark, juvenile rounded. ovaries pink/creamangular; coloured, white/cream coloured, flattened/ from thedorsalabdominalwall; testes response. nutrients, gasesandwastes; immune and short anaerobic burstsofpower.and short white muscleutilisedfor aerobic activity girdle,pectoral bones;red and accessory true bone, skull, column, vertebral ribs Pyloric caecaePyloric Stomach Musculoskeletal system Gonads Intestine Blood secretes andacid. mucus, enzymes termination ofoesophagus;digestion; control; lipidandprotein regulation. digestion. Source: Phil Read Silver perch gills (×100 mag.). Figure 7

–

hyper‑osmotic; transfer of –

– – sex organs; paired; suspended digestion; osmoregulatory firm, sac‑like organ sac‑like atfirm,

– finger‑like pouches; – skeleton of perform on‑farm, diseasediagnosis. on‑farm, perform The following equipment isneededto Diagnostic diagnostic • • • buckets, airstones andairpump. C orpithingspike.knife coverslips, cuttingboard andkilling and blades, microscope slidesand scissors,sharp‑pointed scalpel includingforceps, kit Dissection 400×). magnification, 40×,100×,200×and and 40×lensmagnification (final stage, 10×ocularwith 4×,10×,20× with powered light source, moveable Binocular compound microscope ast net, seinenetandhandnets; T ools

techniques the following features. checked daily, thosewith inparticular Ponds, cagesandtanksshouldbe Obser • • • • variations e.g. Poor water orsudden quality summer temperatures); feedingHigh rates (>60kg/ha; ponds); fingerling densities(particularly stocking High harvested; partially R ecently (within2weeks) stocked or Recent water exchange; blooms algae blue‑green scum, surface Heavy High ammoniaandhighpH (>4°C in24hrs) temperature in decreases Sudden Very hightemperatures (>30°C) Low dissolved oxygen (DO)(<3 ‘Crash’ ofalgalbloom v ation mg/L) displayed by fishare: signsthe more common andimportant of diseaseorpendingdisease. S changes inthewater could beindicative any unusualsigns infishorunexpected culture andseason.I facility infection, size, ageandcondition offish, between diseases, levels of infestation or behavioural signs, andthesecanvary Diseased fishdisplay many physical and Source: Phil Read Diseased silver perch schooling inincoming water. Figure 8 Signs • • • • • edges, aerators ( Fish congregating nearthesurface, by some, manyactivity orallfish; L V Bird predation; e.g. flashing; Fish abnormally, swimmingoracting oss ofappetite aluable broodfish. – Fig. 8 reduced feeding ); n general, ome of

p|9 • diagnostict echniques p|10 • diagnostict echniques Ensure: water withcalibrated quality meters. unusual signs isto immediately monitor of theobservation after The firstaction W • • • • • ater acceptable ranges. minimum ormaximumlevels, or temperature (10–30°C (<0.1 DO (>3 Presence orabsence offeed ingut. dead fish. I M and discoloured organs; bulging eyes, red brains orenlarged eroded patchespale ordark, ofskin, Fish withunusualcolouring; may be ncreasing or numbersofmoribund oribund ordeadfish; oribund quality mg/L), pH(6 mg/L), ammonia

monitoring – 9.5) and ), theseare

Source: Phil Read S Figure 9 4 fish) ( Fish shouldbesampled(minimum following conditions: Sampling water M • • • • • • ampling fishusing acastnet. anagement (if <6.0 pH). A Exchange water; I S behaviour (over 1–3days); Sudden decrease infeeding fish; M ncrease aeration; top feeding; dd limeto increase low pH ortalities and/or moribund (sick) and/ormoribund ortalities Fig. 9 quality

fish ) after observation ofthe observation ) after

of

sub‑optimal

Source: Guy Jeff S Figure 10 • • evering thegill arch to remove gill tissue. temperature). (>15°Cwatersummer andspring autumn, during more, particularly Fish unsighted for 2weeks or colour; standpipes orropes), abnormal or rapid swimming, rubbingon column orinwater currents, circling fish positionedhighinthewater ‘gasping’at pondedgesorsurface; (‘flashing’; fish ‘listless’ andor A bnormal swimmingbehaviourbnormal Source: Phil Read and gill raker [gr lamellae[pl] Single gill arch showing primary Figure 11 bacterial diseases.bacterial andsomefungal ecto‑parasitic procedures are usedto diagnose theexamination.during The following the fishandwilltherefore beunseen ordetachrapidly frommay bekilled recommended assomeecto‑parasites U deathimmobilisation offish. soonafter parasites are prone to detachingand/or behind headorpithingbrain) assome (severing ofspinalcord immediately immediately following euthanasia examination shouldcommence (use water from pond).M containers having aerated pondwater for necropsy shouldbeheldin Live, preferably fishcollected moribund Ex tissue sing anaestheticsfor euthanasiaisnot amination gr ] [arrows].

of

gill icroscopic

and

skin pl diagnosis,

Gill examinationGill Source: Guy Jeff S Figure 12 • • • • • eparating gill lamellaefrom agill arch. trea higher magnification (100×). examine thetissueat low (40×),then the primary gill lamellae( the primary gill archsever from thecartilaginous place onaslideandusingscalpel, gill ( gill arch (2cuts)andremove >10mmof scissors, sever thewhite, cartilaginous theopercular coverlift andusing lamellae to spread ( apply light pressure to encourage the lay acoverslip over thematerial and water); not usechlorinated tapwater or pond of distilledwater to thegill lamellae(do discard thegill arch andadd2–3drops tmen Figs. 10 & tionpreven of and – large fish: 11 ); ); Fig. 13

the diseases of Fig. 12 ); );

the australian Gill examinationGill Source: Phil Read Healthy gill tissuebeneath acover slip. Figure 13 • • • • • • • examine thetissue. tissue is ‘flooded’; raised endofthecoverslip until the add drops ofwater beneath the ofthegill arch);due to thethickness coverslip willberaised offtheslide lay acoverslip onthe sample (the drops ofdistilledwater; attached) onaslideandadd2–3 gillplace arch thegill (cartilaginous others; separate onegill anddiscard the remove asetofgills; using scissors, sever agill arch and cover to reveal thegills; using scissorsremove theopercular freshwa ter fish – silver small fish(<10 h perc (b idyanus bidyanus g): )

p|11 • diagnostict echniques p|12 • diagnostict echniques Fin clipexamination: Skin examination:Skin Source: Guy Jeff S Figure 14 • • • • • craping the skin to obtainasample.craping theskin examine as described forexamine asdescribed gill tissue. add 2–3drops water, coverslip and to theslide; remove from thescalpel skin/mucus scraping. and prepare for itasdescribed skin suchasraggedabnormalities edges) offinsthat demonstrate any portion remove asmallpiece ofcaudalfin(or facing upwards ( scrape alongthesideofbody using ascalpelandlight pressure, position thecaudalfinonaslide; Fig. 14 ); ); ideally include moribund specimens.ideally includemoribund be representative ofthepopulation and the sample(organs orwholefish)should exceed 7 buffered formalin. Tissue shouldnot in10%neutralshould besent preserved is greater than3hours, thespecimens within3hours.laboratory I unfrozen provided theywillarrive at the should bekeptonwet ice andsent possible, freshly euthanasedspecimens I suitable andreliable for diagnosis. laboratory. M diagnostic disease fish a to delivered samplesoffishshouldbeon‑farm, W L fish f delivery oflive specimensisnotf delivery aboratory hen thediseasecannotbediagnosed

for mm in thickness. I mm inthickness.

disease oribund fishareoribund themost

submission

diagnosis f thedelay n allcases

of

Live specimens: Iced specimens: • • • • • • do notfeed to fishprior transport deliver samplespersonally; preferably or overnight transport air‑tight container; seal;watertight bags; 1 4to 6fishinstrong plasticpackage deliver within3hrs. place container inawatertight and cover with ice; place thesampleinaplasticbagand wrap fishinadampclothortowel; ⁄₃ pondwater, ²⁄₃pure oxygen; P (<30 P • • • • reserved specimens reserved specimens for smallfish. tissue isincluded;fixtissue/organs as a5 ensuring lateral lesions line);sampleany skin of withsection spleen, brain, skin liver, intestine, heart, stomach, (anterior andposterior kidney, gill, remove outorgans fat anddissect tissue. use 10timesthevolume offixative to 10% neutral buffered formalin; place samplesinaplasticbottlewith sever organs); from thevent to thegills (donot using scissors, openfishgutcavity g): mm margin ofnormal – – large fish: small fish diagnosis, Frozen specimens: meets recommended standards. with your courier to ensure packaging under IATA regulations. transport Check clearlypriortoand labelled submission packaged inthree containers watertight Preserved are specimens required to be • • • trea following poisoning. thesuspected freeze samplesassoonpossible most fishdiseaseinvestigations). two majordiagnostic tools usedin histopathology ormicrobiology (the frozen tissuesare oflittleusefor analysis andsomeforms ofvirology; recommended for toxicological tmen & tionpreven of

the diseases of

the australian submissions: Information to accompany laboratory • • • • • • • • • storage ration;diet; size andmanufacturer; water source swimming; abnormal ‘flashing’ clinical signs e.g. poorfeeding; rate perday beganandmortality date mortality density stocking e.g. pond, raceway cage, tank, facility ofproduction size andtype temperature; DO;ammonia;salinity water includingpH; quality species offish;ageandsize date name; address; phonenumberand freshwa ter fish silver h perc (b idyanus bidyanus )

p|13 • diagnostict echniques p|14 • diagnostict echniques will be processed and further examined.will beprocessed andfurther Specimens received at thelaboratory Source: Matt Landos colonies growingBacterial onabloodagarplate. Figure 15 L • • • • aboratory pathogens andchangesintissue. stained; microscopically examined for in’ to assesssinglecell depthsections; decalcified andindividualtissues ‘cut Histopathology conditions. environmental changes;weather changes indiet;chemicaltreatments system changese.g. newtanks; exchange; fishdelivery e.g. grading; water harvesting; (past2weeks)recent husbandry

Procedures

– fixed orfresh tissues Source: Matt Landos gill ofnormal structure.Histological section Figure 16 • • Bacteriology Virology viruses. immunological tests to identify including PCR,sequencingand fish cell lines;moleculardiagnostics ( colonies for antibiotic susceptibility screening ofbacterialof bacteria; for culture); identification bacterial only (donotsubmitfixed tissue lesions;fresh tissuefluids; alsoskin kidney, spleen,brain, peritoneal specific media;targeted organs Fig. 15 ).

– viral culture onvarious

– bacterial culture onbacterial – Source: Matt Landos silver perch gills. showing hyperblasticHistological section [arrows] Figure 17 ‘ diseases andpathogens silver perch culture involve thecommon disease. M requiredskills to accurately diagnose common pathogens, anddevelop the tissues, helpinidentification ofthe the recognition andabnormal ofnormal healthy anddiseasedfishwillfacilitate However, the regular samplingof microscopic imagesischallenging. farmer, interpreting physical signs and To theneworinexperienced fish steps usedto investigate fishdiseases. andgill biopsiesare thefirstskin andaconcise evaluationquality of tanks, regular monitoring ofwater offish,pondsandDaily observation the obvious! stagesofaninvestigationearly lookfor Learning signs ’ and ost diseaseoutbreaks in

to

diagnose

recognise – during theduring

disease

the

( will dependuponotherclinicalfindings the interpretation oftheirsignificance present withoutcausingclinicaldisease; tissue canhave parasites andbacteria andgill lamellae. Skin the secondary causing cell growth andfusionbetween shows hyperplasia andhypertrophy, epithelium. Diseasedgill tissueoften changes inpigment orthickeningofthe haemorrhaging, ulceration, erosion, canincludehyperaemia,Changes inskin signs causedbyovert systemic disease. organisms, orthemanifestation of invasion ofpathogens orother occasionally difficultduesecondary the aetiological agent(s), orcauses, is a diseaseevent; however, determining andgill tissueare commonskin during Changes intheappearance ofboth Source: Phil Read Gill fluke[arrow] Figure 18 Figs. 16,17,18,19,20,21 – a large parasite. and 22 ). diagnosis, Chilodonella hexastichaand Chilodonella [c matter [om],andtheparasites Trichodina sp[t W Figure 19 Source: unkown lamellae [s [p Silver perch gills; primary Figure 20 Source: Phil Read temperature (>5°Cover fluctuations (pond water tea turning colour), large in water e.g. quality analgae ‘crash’ meters. Suddenchangeshigh‑quality monitored onaregular basisusing temperature, pHand T always controllable. preventing disease;however, itisnot M et mount ofgill tissueshowing [arrows] organic aintaining water in iscritical quality trea tmen om ] [arrows]. & tionpreven of c W t ater (DO quality AN) shouldbe ] and secondary ] andsecondary

the ] (×100mag.). diseases of

the australian p

s ] , Source: Phil Read air bubbles [b W Figure 22 Source: Phil Read changes [arrows] to cell structure. W Figure 21 water quality. following ofpoororchanging periods ofpondsshouldbedailyobservation common, andinfections are particularly and disease. Protozoan andfungal low DO(<3mg/L)cancausestress 24 hrs), high T et mount of skin showing [arrows]et mount ofskin scales[s et mount ofgill tissueshowing abnormal b freshwa ] andparasites [p ter p AN fish ’s of andperiods silver h perc ]. (b idyanus bidyanus s ], ], )

p|15 • diagnostict echniques p|16 • diseases and pathogens organisms. perch culture thanany othergroup of Protozoans causemore diseasesinsilver injury, andsomemay produce toxins. mucus, whileotherscausephysical protozoans feed onthecells and ofgill tissue. S particularly they greatly impairtheepithelium, W such asciliaorflagellafor locomotion. fission andhave specialisedorganelles organisms that reproduce by binary Protozoans are usuallysinglecelled Ecto‑p diseases hen present inlarge numbers, arasitic protoz

and ome oans p athogens Chilodonella hexastichaChilodonella M treated to avoid quickly large losses. of 10–30°C.Needsto bediagnosed and spring, andover thetemperature range autumn,winter and early particularly fingerlings. O lossesofsilverserious perch, especially numbers. The parasite cancause cause arapid increase inparasite months before predisposing conditions 1–2 organisms on5fish)over of aperiod parasite may exist inlow numbers(e.g. usually progresses however, rapidly; the in ponds, cagesandtanks. The disease disease chilodonellosisinsilver perch I Chilodonellosis nfestations oftheprotozoan ay have stage. acyst utbreaks inallseasons, causethe Chilodonella hexastichaChilodonella P Signs length, 20–40 dorso‑ventrally flattened; 50–70 protozoan; ovoid shaped; to kidney • • • • • • • athogen appearance may haveSkin mottledand/orgrey Emaciation R edges and nearsurface position, often L Flashing L rates mortality Chronic and/or to acute morbidity ethargy, swimmingslowly, head‑up oss ofappetite agged fins µm wide. isaciliate µm in of individuals often clumpedongillof individualsoften tips. movement at low temperatures; groups slowgliding motion;often orlittle higher magnification. Characteristic appears granular; cilianoticeable at slide preparation. C prompt examination required following morerendering detection difficult; become immotileordetachcan quickly at least 4fishfrom pond. The organism to examineof anoutbreak;important diagnosis stages difficultintheearly individual fishcansometimesmake loads ( parasitic light or heavy have may fish but also skin ( but alsoskin magnification. Found mainlyongills M Diagnosis Source: Stuart Rowland Source: Stuart (×100 mag.). mucus[arrows] hexastichaChilodonella inskin Figure 23 icroscopic examination at 100× 100 µm Fig. 25 ); large variation between Figs. 23 ytoplasm often and 24 ). I nfested diagnosis,

Ponds/cages: Tanks: Treatment Source: Phil Read lamellae (×200 hexastichaChilodonella ‘grazing’ [arrow] gill Figure 24 • • • • trea purging) and/orformalin 25 5 repeat following day. ponds after 3–4 weeks.ponds after effectiveness; may needto re‑treat pond fishto gaugetreatment usually sufficient; re‑examine aeration for 4–5days; onetreatment formalin 25–30 needed); flushwell oncompletion. treatment; aerate well (oxygen, if during observe orfry); (not larvae formalin 150 well; nofeeding. and repeat thefollowing aerate day; continuous bath for at least8 10 g/L saltcontinuous (including g/L salt(NaCl)for 60min,flushand tmen & tionpreven of

mag.). mg/L for 60minutes 100 mg/L, maintain 24 µm

the diseases of mg/L h, flush

the australian

h activity onponds. activity having notrash fishandprevent bird overstock. I notwater Do andnutrition. quality moved between ponds. M to andfishbeingarrivals thefarm, to prior stocking,fingerlings new prophylactically (2–5 Quarantine andtreat allfish P Source: Phil Read gill lamellae (×100mag.).[arrows] primary infestationHeavy hexasticha ofChilodonella on Figure 25 • revention (e.g. June thenagaininA 25–30 prophylactic for broodfish: formalin freshwa mg/L winter/early spring f possible, usesource water ter fish silver g/L salt),including h perc aintain good (b ugust) idyanus bidyanus )

p|17 • diseases and pathogens p|18 • diseases and pathogens life‑cycle temperature‑dependent, less temperature‑dependent, life‑cycle stages;stages ofand free‑swimming ( treated. Hasacomplex life cycle diagnosed andNeeds to bequickly in autumnassociated withoutbreaks. in water temperatures to/below 15°C infestation. O spot develop against future immunity freshwater ofwhite fishthat survivors is someevidence inotherspeciesof mortality. A can progress rapidly and cause100% in ponds, tanksandcages. Disease white spotorich.O multifiliis the ciliate protozoan, diseases ofsilver perch. I One ofthemostcommon andserious 5 1 and2 the parasitic protozoan Ichthyophthirius multifiliis; Diagrammatic representation of thelife of cycle Figure 26 Source: Patrick Tully (white Ichthyophthiriosis Fig. 26 – tomites released; 6 – 6 ) involving attached, encysted trophonts; 3

5 , cause the disease known as, causethediseaseknown spot ffects fishofallsizes. There ccurs year round; decrease , ich) – – tomont; 4 theronts. ccurs insilver perch 4 1 Ichthyophthirius

nfestations of

– tomites; 3 2

( (1,000 protozoan; trophonts, 50–1,000 than 4days, >24°C;more than5 Ichthyophthirius multifiliis P Source: Phil Read Silver perch infested withwhite spot. Figure 27 to fishusingapenetrating gland. granular appearance, 20–50 theronts that are oval orround shaped, released infestive asfree‑swimming, division into numerous tomites; then equipment (suchasnets)tomonts; leave onsubstrate fishandencyst and chemicals. stagessusceptible tofree‑swimming stage; onlywithout afree‑swimming reproducing underneathepithelium <7°C; someevidence ofparasite Figs. 27 athogen µm =1 and 28 mm) attach to fish ); mature trophonts isaciliate µm; attach

µm weeks, Signs Source: Phil Read Trophonts attached to theheadofasilver perch. Figure 28 • • • • • • • • • ( on pondbottom, standpipes, ropes) Flashing strong (often andrepeated L sides ofponds Positioned inwater currents and/orat cases) Opaque to white eyes (advanced cases) W mortality Chronic and/or to acute morbidity and fungalinfections bacterial lesionsandsecondary Skin ormottling markings skin M R Figs. 29 ethargy andlossofappetite agged fins, skin raised andbrokenagged fins, skin ild skin haemorrhaging; striated haemorrhaging; ild skin hite nodules on skin (advancedhite nodulesonskin and 30 ) clearer cytoplasm thantrophonts.clearer cytoplasm uniform cilia;theronts ciliated, usually in immature individuals;bodywith mature trophonts, nucleus spherical macronucleus sometimesvisiblein ‘swirling’ motion;horseshoe‑shaped granularusually dark withslow be present onlyongills; cytoplasm skin epithelium( skin usually embeddedundergill and 40 gill tissue. Parasites readily seenat M Diagnosis Source: Phil Read ‘flash’ on asubmerged pipe. Silver perch infested withwhite spotaboutto Figure 29 icroscopic and examination ofskin –100× magnification. Trophonts Figs. 31 and 32 ); can diagnosis,

Ponds/cages: Tanks: Treatment Source: Phil Read Silver perch ‘flashing’. Figure 30 • • • trea aeration if necessary; or aeration ifnecessary; DO dailyandprovide additional Rates Calculations, Treatments andDose until disease controlled (seechapter maintain levels between 25–30 water temperature <25°C formalin 30 30°C for 10 days. todecrease lengthoflife cycle–raise temperature manipulation to up to 20days; aerate well; nofeeding; until disease controlled, may befor salt (NaCl)2–5 tmen ); aeration continuous, monitor & tionpreven of mg/L initially(when g/L saltcontinuous

the diseases of ), then mg/L

the australian

Source: Phil Read macronucleus insomeparasites [arrow] (×100mag.). on silver perch gills; note ‘horse infestationHeavy ofIchthyophthirius multifiliis Figure 31 Quarantine infected pondsincluding stocking. M to prior andnewfishonfarm fingerlings prophylactically (2–5 Quarantine andtreat allfish P • revention copper (ascopper sulfate, C low DO decay ofalgaecancausedangerously copper sulfate isanalgacide, the Treatments Rates andDose >50 copper mustbe treatment, alkalinity treatment until diseasecontrolled; for 0.2 concentration between 0.1and free C initially, thenmonitor andadjust 0.1–0.2 freshwa mg/L; continuous aeration during mg/L (seechapter u + . mg/L, recommend 0.2 ionlevels dailyto maintain aintain goodwater quality. ter fish silver g/L salt),especially h perc Calculations, -shoe’ shaped (b ). C idyanus bidyanus uSO aution: mg/L 4 )

)

p|19 • diseases and pathogens p|20 • diseases and pathogens de‑silt pondsbetween crops. de‑silt simultaneously by and thisparasite. Dry than onepondortankto beaffected I any pondortank. tanks whenwhite spotisdiagnosed in fishinallpondsandobserve/monitor to holddiseasedfish.Closelyknown water exchange whensource water aquatic birds spreading disease. N equipment, vehicles, water; prevent Source: Phil Read mucus and scales(×100mag.). skin Ichthyophthirius multifiliis trophonts [arrows] in Figure 32 t iscommon for more il monitoring. parasites overlooked andisoften during ichthyobodosis. I protozoan that causesthedisease aquaculture systems ( have beencommon inrecirculating densities intanksandcages. O and larger fishheldat highstocking dangerous for fingerlingsparticularly known as known ( latter usuallyfeeding ongill tissue mobile form oranattached form; the Ichthyobodo necator Ichthyobodo necator Source: Phil Read systems withpoorwater quality. Ichthyobodo necator, canbecommon intank Disease causedby theprotozoan, Figure 33 grow‑out ofsilver perch inponds. Epizootics have beenuncommon during disease over awidetemperature range. (originally Ichthyobodosis Fig. 34 ). Ichthyobodo necator Costia necatrix Ichthyobodo necator

called t isoneofthesmallest (previously exists inadetached,

Fig. 33 C ) isaflagellate ostiosis)

). ). causes utbreaks is attached form, pear‑shaped ( attached to ofbody; ventral part flattened, 10–20 form, dorso‑ventrally kidney‑shaped, Ichthyobodo necator P Source: Phil Read (×400 mag.). Ichthyobodo necator [arrow] attached to gill tissue Figure 34 Signs resistance in S • • • • • • • ome evidence inotherfishesofsalt athogen L Hyper‑ventilation R Flashing skin Fish may have a ‘bluish’ sheento the sloughing M and/ormortality Chronic morbidity ethargy andlossofappetite agged fins 100 ucus secretion andepidermal µm I. necator µm insize. Two flagella free‑swimming . . Fig. 35 ). ).

secondary lamellae. secondary betweenhyperplasia, particularly gill epithelium( seen at 100–400×magnification on to see;attached pear‑shaped parasites around tissuesample;flagelladifficult rapid motion;often swimmingflicking Free‑swimming form may exhibit a – prompt examination offresh tissue. parasites detachfrom often hostskin; M Diagnosis Source: Phil Read (redrawn from Hoffman, 1967) Diagram ofIchthyobodo necator . Figure 35 Tanks: Treatment • • icroscopic examination ofgill and aerate water well; nofeeding. flush andrepeat 1or2days; after formalin 25 and repeat following and/or day; salt (NaCl)10–13 mg/L, continuous bath, Figs. 34and36 g/L for 60min,flush ); gill diagnosis, stock. R tanks. R incagesand andnutrition quality toprior stocking. M prophylatically, especiallyfingerlings Quarantine andtreat allfish P Ponds/cages: Source: Stuart Rowland Source: Stuart protozoan (×1000mag.). Ichthyobodo necator [arrows], aflagellated Figure 36 • • revention egularly sample,egularly examine andmonitor trea treatments may berequired. inRAS usually sufficient inponds;repeated aeration for 4–5days; onetreatment repeat 1or2days; after maintain 24 formalin 25–30 needed); flushwell oncompletion treatment; aerate well (oxygen if during observe orfry); (not larvae formalin 150 50 tmen µm educe stress andovercrowding. & tionpreven of mg/L for 60minutes mg/L, may needto aintain goodwater

the diseases of

the australian h fry in larval rearing ponds. inlarval fry condition. C debilitated withotherdiseasesorinpoor juvenile fishthat are overcrowded, loadings, andiscommonly found on organic high and quality water poor Trichodinosis associated isoften with intheshort‑term. high level mortality in large numbers, butrarely cause andfingerlingsinfect silver perch larvae (>100 inlargebut seldomcausemortalities ciliated protozoans, disease causedby infestations ofthe Trichodinosis isarelatively innocuous Trichodina Trichodinosis freshwa g) silver perch. spp. are widelydistributed, ter ommon on post‑larvae andommon onpost‑larvae fish silver Trichodina Trichodina h perc (b idyanus bidyanus spp. can )

p|21 • diseases and pathogens p|22 • diseases and pathogens with a spinning motion ( browses often over andgill surface skin tooth‑like withinthebody; structures circularperimeter; arrangement of ofciliaaroundwith afringe the saucer‑shaped, 25–100 Signs Trichodina P Source: courtesy ofwww.fishdisease.netSource: courtesy denticles [d Trichodina sp. showing [arrows] cilia[c Figure 37 • • • • • • • athogen ©WCS d 30 Head‑up, swimmingnearsurface L Flashing ofopercula andflaring Frayed erosion, fins,skin dark skin Excess mucusproduction Emaciation and/ormortality Chronic morbidity ethargy µm ]. spp. are circular, µm indiameter Figs. 37 ] and and

c 38 ). inconsequential. I (e.g. 1–3parasite/field ofview)is of viewmay require treatment. infestations to above 20parasites/field Tanks: Treatment ( andfintissueand common onskin easily recognised at 100×magnification M Diagnosis Source: courtesy ofwww.fishdisease.netSource: courtesy Trichodina sp. S Figure 38 • • Fig. 39 canning electron micrographcanning electron (SEM)of icroscopic andgill; examination ofskin at least 8 formalin 25 salt (NaCl)10 ); observation oflow numbers); observation h; aerate water; nofeeding. mg/L, continuous bath for g/L for 60min; ncreasing levels of

Ponds/cages: Source: Stuart Rowland Source: Stuart (×100 mag.). Trichodina sp. aparasitic ciliated protozoan Figure 39 overcrowding. well‑fed andfry, andreduce larvae implementing water exchange. M maintaining orincreasing aeration, and poor water by reducing quality feeding, to prior stocking.fingerlings Eliminate prophylactically (2–5g/Lsalt),especially Quarantine andtreat allfish P • • revention formalin 15–20 copper (ascopper sulfate, C usually sufficient for ponds;or aeration for 4–5days, onetreatment 4–5 days treatment. after sufficient; monitor water for quality treatment, onetreatment shouldbe >50 0.2 100 , alkalinity mustbe mg/L, alkalinity mg/L, continuous aeration during µm mg/L, maintain 24 uSO

aintain 4 )

h ulceration. organs causingswelling, necrosis and parasite canpenetrate muscletissueand such ascarp, catfish, andsalmon,the advanced casesinotherfishspecies a highorganic loadinthewater. I associatedin silver with perch fry appearance to farms. however, itis rarely aproblem on disease tetrahymenosis insilver perch; saprophytic ciliates that causethe Tetrahymena Source: Phil Read [arrows];characteristics cilia [c Tetrahymena sp. –diagram with key Figure 40 ( largeroften (up100 but are usuallymore pear‑shaped and Tetrahymenosis Fig. 40 Tetrahymena ). S evere losseshave occurred spp. are free‑living Chilodonella hexastichaChilodonella spp. are similarin µm inlength) ], caudal cilium [cc

n cc diagnosis, c

]. ]. to the ‘gliding’ of movement isoften ‘spiralling’ compared 50–100 symmetrical, ovoid body30–60 Signs Tetrahymena P Source: Stuart Rowland Source: Stuart Tetrahymena sp., aciliated protozoan (×200 mag.). Figure 41 appearance of cytoplasm ( appearance ofcytoplasm ciliates. M • • • • • • athogen ay beconfused withnonpathogenic trea Emaciation W L swelling, ulceration, andnecrosis Epithelial damage, e.g. localised Excess mucusproduction and/ormortality Chronic morbidity oss ofappetite andlethargy hite patches orspotsonskin tmen µm long; evenly‑distributed cilia;µm long;evenly‑distributed & tionpreven of ispyriform orradially C. hexasticha 300 µm

the diseases of Fig. 41 . Granular µm wide, ). ).

the australian movement; penetration of magnification; relatively fast ‘gliding’ gill tissue;parasite recognisable at 100× M Diagnosis overcrowding. I P Ponds/cages: Tanks: Treatment perch. however, few for casesreported silver into muscleororgan tissuespossible; mprove reduce stress water and quality; • • revention icroscopic and examination ofskin at least 8h;aerate water; nofeeding. formalin 15–20 formalin 25 infections may bedifficultto treat. systemic ponds; for sufficient usually aeration for 4–5days; onetreatment freshwa ter fish mg/L, continuous bath for silver mg/L; maintain 24 h perc Tetrahymena (b idyanus bidyanus h

)

p|23 • diseases and pathogens p|24 • diseases and pathogens There isevidence spore‑producing, histozoic plasmodia. lamellae were invaded by multiple severely compromised; mostsecondary disease was controlled. was Gillfunction (40/day) over two weeks before the (300–450 of infection rate (>90%offishaffected) However inoneepizootic, ahigh oraffectgrowth.not causemortalities perch andlight infectionsusuallydo myxosporidians causingdiseaseinsilver hosts. There have beenfew records of different life stagesandintermediate hosts. They are obligate parasites with found offish worldwide inavariety M Source: MattLandos spore Henneguya sp.– showing histological the section Silver perch gills severely compromised by Figure 42 My any speciesofmyxosporidians are Henneguya x -producing histozoic plasmodia. oz oan g) resulted inchronic mortality

sp. onsilver perch infections Henneguya 500 µm spp. utilise caudal appendages( 40 to 50 size canvary, 8to15 Signs M P Source: Prof.Iva Dykova, Institute ofParasitology, Republic Czech magnificationHigh ofHenneguya spores. Figure 43 at temperatures >20°C. M known. the speciesinfectingsilver perch itnot host intheirlifecycle. The lifecycle of annelids (worms) asanintermediate • • • • • athogen yxosporidian ( Poor growth andemaciation Gills grossly thickenedwithnodules L individual orsmallgroups Fish listlessat pondsurface; Chronic fishmortality oss ofappetite µm; two polarcapsulesandtwo ost infestations have occurred Henneguya µm ×4to10 10 Figs. 42,43 µm spp.), spore and µm, tail 44 ). as per description aboveas perdescription ( preparation ofplasmodium,spores in resolving plasmodia;squashed responsein shape, marked inflammatory ~ plasmodium ( magnification; brown/tan dark encysted M ( with mildlynodularappearance Grossly thickenedgill lamellartissue Diagnosis Source: Prof.Iva Dykova, Institute of Parasitology, Republic Czech polar capsules [pc]. showing internal spores [arrow] eachwithtwo ofHenneguyaHistological section plasmodia Figure 44 plasmodia. ‘Ich’. ofspores Nomotility orencysted plasmodium could beconfused with Fig. 45 80–150 icroscopic examination ofgills, 100× ). µm indiameter, ovoid to round Fig. 46 pc 50 µm ); intra‑lamellar, Fig. 47 ); );

Treatments notwell defined; Ponds/cages: Treatment Source: Phil Read by themyxosporidian, Henneguya sp. Silver perch gills; grossly visiblechangescaused Figure 45 on aregular base. Disinfect tanksystems andequipment 2 years); control intermediate hosts. 1to pondsregularly (every and de‑silt appropriate densities;dry stocking M microscopically.examine asub‑sample Quarantine fishbefore stocking, P • revention aintain goodwater and quality days. 2–3days;after aerate 24hfor several spore stages;re‑treatfree‑swimming outbreaks by targeting formalin, 25 mg/L may control diagnosis, Source: Phil Read (×100 mag.). Henneguya plasmodiaonsilver perch gills Figure 46 trea tmen & tionpreven of

the diseases of

the australian Source: Phil Read W Figure 47 et mount ofHenneguya spores (×400mag.). 100 freshwa µm ter fish silver h perc (b idyanus bidyanus )

p|25 • diseases and pathogens p|26 • diseases and pathogens (scopula) incolonies often ( orgill tissuebyattach to aholdfast skin identified as silver perch; to date allcaseshave been ciliates have rarely beenrecorded on Species ofsessile, ecto‑commensal Source: Phil Read (redrawn from 2000&Hoffman, 1967) Noga, sp.Diagram ofAmbiphrya ofkeycharacteristics Figure 48 bacterial andfungalinfection( bacterial and/oroffermetabolic function asite for could potentially impedegasexchange, industry. Large numbersonthegills with thisparasite inthesilver perch have ofproblems beennoreports forhost primarily attachment. There organic matter inthewater andusethe The parasites feed and on bacteria Infestations Ecto‑commensal Ambiphyra Ciliate spp. Parasites Fig. 48

Fig. 49 ). ). ). colonial. Noobvious motility. some length; somespeciessolitary; mostrange 40–100 mid‑body; girdlesome specieshaving ciliary Signs spiral ofciliaat posterior end( attached eitherby stalkorscopula; or goblet‑shaped,Bell elongated ciliates; P Source: Unknown parasite onsilver perch gills (×100 mag.). sp.,Ambiphrya aciliated, ecto Figure 49 • • • athogen Flashing Emaciation infestations) (heavy Hyperventilation - commensal Fig. µm in 50

); ); for allspecies species notneeded;treatment thesame at 100× magnification; identification to tissue;easilyrecognisablefin andskin M Diagnosis Source: Brett Ingram and oral cilia [c sp.,Ambiphrya showing [arrows] scopula [s Figure 50 Tanks: Treatment • • icroscopic examination ofgill (mainly), species may beresistant. prolonged immersionat 5 salt 10 2–3 formalin 25 days; aerate water; nofeeding. g/L (NaCl)for 60minor s ] (×200mag.). mg/L, retreat after c g/L; some ] ] minimise the risk ofrecurrence.minimise therisk exchange) to alleviate theproblem and improve water (aeration quality and have ahighconcentration ofbacteria; organically‑polluted water that could Presence isindicative of P Ponds/cages: • revention treatment 2–3days after ifnecessary. 24 formalin 15–20 h aeration for 4–5days, repeat mg/L, maintain diagnosis, Source: Prof. Iva Dykova, Institute ofParasitology, Republic Czech monogenean Lepidotrema bidyana [arrows]. ofgill showingHistological section the Figure 51 to skin (juveniles). Heavy infestations Heavy (juveniles). to skin haptor organ to gills (adultflukes)and Gill flukesattach usingtheirposterior, andontofarms from farms wildfish. the transfer ofpathogens between measures to beimplemented to avoid for quarantine stringenton-farm pathogens withlive fishandtheneed demonstrates ofmoving therisk occur onmostfarms. This rapid spread last 10years, andtheparasites now over thedistributed intheindustry tanks. They have become widely on silver perch inponds, cagesand are commonly found(Dactylogyridae) in particular in particular M Monogeneans onogeneans (skin andgill flukes),onogeneans (skin trea tmen 100 µm & tionpreven of Lepidotrema

the

bidyana diseases of

the australian ( have alsobeenrecorded onsilver perch group inthefamilyGyrodactylidae agents. I tanks isdifficultwithcurrent therapeutic Source: Stuart Rowland Source: Stuart (×100 mag.).the adult andtheinternal larva sp.Gyrodactylus showing [arrows] haptors [h Figure 52 to fungal and bacterial diseases( to fungalandbacterial predisposingwith gill thefish function, growth, tissue damageandinterference cause stress, poorfeeding response and silver perch; however, theparasite may influkes have notcausedmortalities (>15 parasites perfieldofview) Eradication of Fig. 52 freshwa ). nfestations ofasimilarparasitic h ter fish L. bidyana silver h perc from pondsand (b idyanus bidyanus Fig. 51 ] on ). ). )

p|27 • diseases and pathogens p|28 • diseases and pathogens Source: Phil Read attached to silver perch gill tissue (×100mag.). Lepidotrema bidyana, alarge mongenean gill fluke Figure 53 Signs without causingproblems orstress. numbers ofparasites may bepresent eyespots andheadorgans obvious; low develop into gravid adultswithin7 days; stage (oncomiracidium); juveniles can infestiveeggs hatch asafree‑swimming released to theaquatic environment; oviparous, producing eggswhichare 600 W P • • • • • athogen orm‑like parasite,orm‑like adultsupto 100 infestations) Emaciation (heavy, prolonged L Gill hyperplasia andgills skin Excessive on mucusproduction Flashing oss ofappetite µm in length; attached posteriorly; µm inlength;attached posteriorly; µm

stretch andrecoiling motion. showand juvenilescharacteristic (skin) Tanks: insignificant level. reduce monogeneannumbersto an may berequired to eradicate or Up to three treatments, 21 days apart of pondcontamination witheggs. on water temperatures anddegree (an organophosphate), depending treatment withformalin ortrichlorfon perch between 5and30days after M Treatment magnification ( examination ofgill at 40–100× Easily identified; microscopic Diagnosis • • onogeneans can re‑infest silveronogeneans canre‑infest formalin 150 feeding; or formalin 30 mg/L, aerate water, no Fig. 53 mg/L, 30minute bath; or ); bothadults(gill) areas. ( Ponds/cages: hydroxide [ pondsregularly andusecalciumDry regular treatments drying. andperiodic persistent intanksystems necessitating fluke numbers. M water quality. Frequently monitor gill indicators ofpoorwater quality, improve to stocking. Gillflukesare usually formalin), prior especiallyfingerlings prophylactically (2–5 Quarantine andtreat allincoming fish P C • • • • revention aO maintain 24 monitor DOdaily. formalin 30 indefinite bath; 0.5 trichlorfon following or day; salt 15 ingredient indefinite bath; or 0.25 trichlorfon ) liberally onany persistently, damp g/L, 1 C a ( mg/L (whenwater <25°C OH) h aeration for 4–5 h bath, repeat active ingredient,mg/L active onogeneans canbe mg/L active 2 ] orcalciumoxide g/L plus30

mg/L days;

), silver perch. parasitic copepods, as adultsonthehost. The freshwater, stages before attaching andmaturing egg, naupliiandcopepodid larval complex life cycle, developing through C Ergasilus C opepods are crustaceans witha opeods spp. have been recorded on Lernaea spp. and diagnosis, common ( carp high incidence ofanchorworm because the M Source: Phil Read attach below the epidermis. A Figure 54 the host( processes for themselves securing to A fish become concentrated. A water sources andnative whencarp static or slow‑flowing in increase may fungal infections. Numbersofparasites or areas bacterial often for secondary been recorded. A poor feeding response andgrowth has however,without causingmortality; individual fishinhighnumbers(100’s) the eastern drainage. Parasites caninfest perch (andotherfreshwater species)in parasite hasalsobeenrecorded onsilver oftheparasite.carriers However the Lernaea n anchorworm headshowing organs useto nchor worms possessanchor‑like trea tmen urray‑Darling Basinmay have a Fig. 54

& spp. ( anchor tionpreven of Cyprinus carpio ). Silver perch in farms ttachment sites are

the diseases of

worm) nchor ) are often

the australian

posterior end( sacs greenish, conical orovoid at up to 20 two to adultfemale four horns; soft wormlike; cephalic segment with temperature dependant. disappears, presumably dying;life cycle to copulation, female attaches; male several developmental stagesprior copepodids 4–16 1–3 presence ofsmall, red lesions. Lernaea Source: Parri &Craig Anderson a silver perch dorsal fin. Lernaea sp. [arrow] tissueof attached to thesoft Figure 55 flesh offish( A P M but theparasite canoccur year round. worm ismore common insummer, athogen nterior endofadultfemale in buried arketability offishinfestedarketability with days, into naupliusmetamorphose freshwa iscompromised dueto the mm inlength;paired egg ter Fig. 55 fish Fig. 56 silver days, completion of ); bodycylindrical, ); eggshatch h perc (b idyanus bidyanus )

p|29 • diseases and pathogens p|30 • diseases and pathogens grossly visible. stages, suchascopepodids may notbe examination ofgills; smallimmature nares; M cover ray such assoft tissue, mouthand onareas often having skin, ‘softer’ scale recognisable by eye attached to gills and features offish;gravid females easily M Diagnosis Signs Source: Phil Read egg sacs [es] [arrow]. Lernaea sp., aparasitic copepod with Figure 56 • • • • acroscopic examination ofexternal Flashing Emaciation andpoorgrowth site ofattachment ( andredHaemorrhaging lesionsat naked eye A nchor worms visibleto clearly icroscopic andmacroscopic Fig. 57 es )

Ponds/cages: Tanks: Treatment Source: IanCharles causedbyHaemorrhaging thecopepod Lernaea sp. Figure 57 • • • • • larval stagesof larval prevent by re‑infestation emerging repeated treatments required to for 28days. indefinite bath; 7days repeat every 0.5 trichlorfon salt 10 ingredient, indefinite bath; 0.25 trichlorfon forceps; removal ofindividualparasites with g/L, 1 h bath, repeat daily. active ingredient,mg/L active Lernaea mg/L active . reservoir freereservoir andother fish. ofcarp ensure water source andstorage improvement inwater density; quality; lowering toprior stocking; ofstocking Quarantine andprophylactic treatment P revention with gill function ( with gill function severe gill damageandinterference parasite’s claspingattachment causes attached to theadultfemales. The to theappearance ofwhite eggsacs as described often ‘gill maggots’ due on silver perch farms. Ergasilids are I Ergasilus Source: courtesy ofwww.fishdisease.netSource: courtesy Ergasilid sp. [arrow] attached to gills. Figure 58 secondary bacterial orfungalinfections. bacterial secondary tissue causedby ergasilids canleadto were recorded inponds. Damageto gill attached to thegills. Nomortalities Parasitesstressed harvest. during were relatively poorgrowth andwere easily ofinappetence,long periods recorded challenged,nutritionally displayed Fish(species unknown). were suffered ergasilid a heavy infestation pond‑reared, silver perch (>500 Ergasilus nfestations ofthecopepod, sp., have rarely beenrecorded

s p. Fig. 58 ). I n onecase, g) diagnosis, eggs ~100/sac, 0.05 attached white eggsacs, length,1–2 1 mm;female having posteriorly antennae (usedfor locomotion), length, 1 cephalothorax andabdomen,Distinct P Source: courtesy ofwww.fishdisease.netSource: courtesy head, thorax, abdomen andeggsacs [esarrow]. Ergasilid sp. showing bodywithgrasping antennae, Figure 59 ( colour onmaturity darkens rakers andgills. females enter gill andattach cavity to stage;copulation at free‑swimming developmental stagesviamoulting; nauplius; several copepodid cycle, egg hatching to free‑swimming athogen mm length;large, paired, claw‑like trea 1 tmen µm & tionpreven of es mm diameter,

the diseases of Fig. 59 ). Life

the australian mm; Signs forms may notbegrossly visible. tissue at 40×magnification; immature maggots’; easilyrecognisable ongill M Diagnosis • • • • • • • • acroscopic examination ofgills, ‘gill Gill hyperplasia S S Patchy/blotchy, skin dark offins Haemorrhaging Poor growth L Flashing oss ofappetite trong to reaction ‘light’ anaesthesia tress following handling freshwa ter fish silver h perc (b idyanus bidyanus )

p|31 • diseases and pathogens p|32 • diseases and pathogens use of high quality feeds.use ofhighquality improvement inwater density; quality; lowering toprior stocking; ofstocking Quarantine andprophylactic treatment P Ponds/cages: Tanks: Treatment • • • revention ingredient, prolonged immersion. 0.5 trichlorfon 3 days. salt (NaCl),10 ingredient; or 0.25 trichlorfon g/L continuous for mg/L active mg/L active

slender and cylindrical bodyhavingslender andcylindrical nematodes are by characterised a Source: Phil Read in theintestine ofsilver perch. Large (~ Figure 60 systems ( the anusofsilver perch heldinpurging have protruding beenreported from cestodesribbon‑like (speciesunknown) musculature ofsomefish.L are commonly found intheviscera or stages(plerocercoids)nematode larval fish.S or predatory The finalhostcanbepiscivorous birds (e.g. copepod, nymphs, insect worms). with at leastoneintermediate host parasitesBoth have similarlife cycles of many vertebrates includingfish. endoparasites inhabitingtheintestine and roundworms respectively) are C Cestodes estodes andnematodes (tapeworms 40 cm)cestode found (speciesunknown) Fig. 60

and ). C

nematodes ome cestode and omparatively, ong, white,

of Barcoo grunter ( silver perch andaspeciesofthegenus been found inthedigestive of tract Nematodes have (speciesunknown) tapered endsandnotruesegmentation. Camallanus Source: Phil Read I Figure 61 colour. cuticle; upto 10 slender, body, cylindrical covered with adhesive grooves Nematodes: (bothria). scolex (head)notpronounced having whiteribbon‑like; to cream colour; C P ( parasitised by cestodes andnematodes. growth for was reported silver perch ntestinal (~2cm)nematode (speciesunknown). Figs. athogen estodes: upto 40 61 and , hasparasitised thegut 62 ormal behaviour). Normal and mm length;red in Scortum cm; bodylong,

barcoo ) identification. to areference for laboratory definitive identify species. S size, andsegmentation) required to physiological features (scolex, shape, M or larvae. in determining thepresence ofeggs mounts offaecalmatter may beuseful Large worms wet identified grossly; Diagnosis Signs Source: MattLandos Camallanus sp. [arrow] attached to thegutwall. barcoogrunter) showing thenematode (Scortum oftheintestine ofBarcooHistological section Figure 62 • • S W wollen abdomen orms protrudingorms from vent ( icroscopic examination of 200 amples shouldbesent µm Fig. 63 diagnosis, ) birds andturtles. parasites, includingcould becarrying oxide. M using calciumhydroxide orcalcium R P V off‑label prescription from aregistered animals (non-fish)may beusedunderan in otherfood producing speciesof Chemicals whichhave registration M an A which are registered, of orthesubject There are currently notreatments Treatment Source: Matt Landos the anus of asilver perch. Nematode protruding (speciesunknown) from Figure 63 eterinary Surgeon. eterinary revention egularly dry, de‑silt egularly and dry,disinfect ponds de‑silt edicines A trea ustralian Pesticides and tmen inimise access ofanimals that & tionpreven of uthority ( uthority APVMA

the diseases of V ) permit. eterinary eterinary

the australian freshwa ter fish silver h perc (b idyanus bidyanus )

p|33 • diseases and pathogens p|34 • diseases and pathogens of aquatic fungi. to treat becauseofthecomplex biology Fungal infectionsare inherently difficult damage and/orimmuno‑suppression. inducedoften by stress, physical pathogens, withinfectionsbe secondary of fish. They are generally considered to matter. Fungi pathogens are important ondeadorganicopportunistically of saprophytic organisms that feed freshwaters. They form alarge group Class O Fungi orwater mouldsbelongto the Fungal omycetes andare ubiquitous in

diseases Source: Phil Read large silver perch. The fungus, parasitica Saprolegnia , growing on Figure 64 rapid (4–6days). and epizootics canbesevere and been recorded insomepondsonfarms, hasfronts inwinter; 100%mortality ( rapid decreases inwater temperatures temperatures <16°C,usuallyfollowing The fungus, (>250 saprolegniosis, usuallyaffectslarger diseaseinsilver perch,important winter damage to theepidermis. Anew, handling, removal ofmucusand silver perch are common rough after in silver perch. Fungal infectionsin causes thediseasesaprolegniosis Saprolegniosis A pril – A g) fish( ugust) associated withcold Saprolegnia parasiticaSaprolegnia Fig. Saprolegnia parasiticaSaprolegnia 64 ) andisprevalent at ,

and gills oflive fish( assist spores attachment to hostskin water; hooked, hair‑like may projections zoospores (sporulation); spores motilein hyphae (20 organic matter ( decreasing water temperatures (<16°C appearstopathogenicity increase with and gills. fungalinfectionsoftheskin superficial 8°C following atemperature decrease (12to (25 fingerlings has beenrecorded onsilver perch Source: Phil Read caudal fin ofsilver perch. stageofsaprolegniosisEarly [arrow] onthe Figure 65 ( mycelial growth andgills onskin water mould;whiteOpportunistic P Fig. 65 athogen ) over two days. I ); often coloured); often by trapped µm diameter) release mm length)heldintanks Fig. 66 t isassociated with Figs. 67 ); club‑shaped and 68 ); ); ). Signs Source: Phil Read contaminated with organic matter. S Figure 66 • • • • • • aprolegniosis ofthegill tissue;mycelium opercula stages) (early tissueonthedistalendof soft Fungal plaquesattached to the orgills (advanced stages) skin W stages) (early Light fungal growth oncaudalfin abdomen (early stages)( abdomen (early onundersideofHaemorrhaging Focal stages) (early areas ofpaleskin isolated) surface, (fish at pondedges, incurrents, on A bnormal swimmingandbehaviourbnormal hite ‘cotton wool‑like’ patches on Fig. 69 ) diagnosis, terminal. by fungus;gill infectionsare usually andgill infectedthe amount ofskin recovery relatedchemotherapy; to infections show resistance to Treatment difficult, many fungal Treatment stages. (mycelium) notsoobvious inearly 100× magnification; fungalgrowth with zoospores; easilydiagnosed at widths (10–30 andgills; fungalhyphaeskin ofvariable growth. M white to green‑brown coloured fungal gills; areas, paleand/orhaemorrhagic M Diagnosis Source: Dr GordonSource: Beakes Dr ofNewcastle (University Tyne, upon UK) micrographElectron parasitica ofSaprolegnia spores. Figure 67 acroscopic and examination ofskin trea tmen icroscopic examination of & tionpreven of µm); sporangium often

the diseases of

the australian Tanks: • • • on M daily (usedto control saprolegniosis eggs, formalin 1,000 bath; treatment, continuous, indefinite eggs, salt2 larvae, maintain >20°C; elevated temperature may assist, bath (adults, juveniles, larvae); treatment, continuous, indefinite salt (NaCl)2–5 freshwa urray cod eggs). ter fish g/L preventative silver g/L preventative h perc mg/L for 15 (b idyanus bidyanus mins )

p|35 • diseases and pathogens p|36 • diseases and pathogens Ponds/cages: Source: Matt Landos parasiticaSaprolegnia oogonium. Figure 68 • • supplemented; or aeration continuous and Rates Calculations, Treatments andDose 25–30 maintaining levels between water temperature <25°C formalin 30 2–5 recirculation system withat least clean toprior beingheldinavery formalin 100 bathed inahighconcentration of saprolegniosis. Fish needto bedip only way to avoid amajorlossfrom the isoften harvest emergency g/L salt. ), until diseasecontrolled; mg/L daily(seechapter mg/L initially(when mg/L for 30minutes, ), then diseases; reduce feeding; reduce high treatfish free ofecto‑parasites; parasitic temperatures to fall<18°C;ensure start late summer/autumnwhenwater or reduce predisposing stressors rate ofinfectionintanks. Eliminate S P Source: Phil Read saprolegniosis. of silver perch stagesofthedisease –early M Figure 69 • alt bath (2–5 revention ild haemorrhaging onthelowerild haemorrhaging abdomen copper (ascopper sulfate, C period ofwinter.period up to andthroughout thehighrisk degree ofprevention ifusedregularly > 50 mustbe treatment;during alkalinity controlled; continuous aeration 0.1 and 0.2 copper concentrations between free C initially, thenmonitor andadjust 0.1–0.2 mg/L. C u + mg/L, recommend 0.2 ionlevels dailyto maintain mg/L until disease g/L) prevents orslows opper may provide some uSO mg/L 4 )

clean pondsbetween crops. anddaily any deadfish(oreggs);dry to 16°Cinlate autumn/winter; remove temperaturesbe beneficialafter decline applications offormalin orcopper may saprolegniosis isaproblem, weekly where damage;onfarms winterand skin crashes ofalgalblooms;avoid handling good water quality, especiallyfollowing especially large (>500 Source: Matt Landos parasiticaSaprolegnia growing [arrow] onfish feed. Figure 70 the fungus)( substratesfertile for colonisation of organic matter, includingfeed are organic load in ponds(deadfishand Fig. 70 ); reduce biomass g) fish;maintain the fish develop large, deep, necrotic necrotic deep, large, develop fish the silver perch canbesignificant when rates are common. M in juvenile (<100 can causehighmorbidity, particularly waterhave supply. asurface Epizootics onsilverperiodically perch that farms organic load). The diseasecanoccur water (low salinity, quality low pH,high high rainfall andsubsequent declineof the latter usuallyfollowing of periods A fishin lossesoffarmed cause serious Queensland. toThe fungusisknown NSWandsouth‑eastern north‑eastern locatedfarms incoastal regions in The aquatic fungus, Source: Phil Read The fungus, Aphanomyces invadans, causingEUS(red spotdisease)onsilver perch. Figure 71 invadans (EUS, Epiz sia and estuarine fishinA sia andestuarine ootic red , causesEUSonsilver perch

spot

ulcerative g) fish;100%infection

disease) Aphanomyces ortalities injuvenileortalities

ustralia; syndrome diagnosis,

secondary bacterial infections. bacterial secondary significant potential forcavity; leavesoften adeep, crater‑shaped Saprolegnia parasiticaSaprolegnia A P invadans hallmark overhallmark therepaired area. from ofscalesa infection,withwhorls in larger silver perch recover that often ulcers. The diseaseislessofaproblem on bodyandcaudalregions ( generally reaction; chronic inflammatory ulcers (4–25 causes smallto large red lesionsand that andmusculature; penetrate skin and athogen typical watertypical mould, trea 72 tmen ); sloughingofnecrotic tissue ; differs from mould typical & tionpreven of mm diameter); severe and , inhaving hyphae Aphanomyces

the diseases of Figs. 71

the australian

Signs Source: Phil Read perch. Deep, necrotic ulcer Figure 72 • • • • • • Small red lesionsandulcers (10 signs)(early Focal raised scales areas ofpaleskin, L isolated) edges, incurrents, onsurface, A and/or morbidityFish mortality Deep, red ulcers inflammation (myositis) causingmuscletissuesuperficial, oss ofappetite infections) (heavy bnormal swimming(fishatbnormal pond freshwa ter fish – EUS onajuvenile silver silver h perc (b idyanus bidyanus mm), )

p|37 • diseases and pathogens p|38 • diseases and pathogens diameter, amongstmusclefibre ( presence offungalhyphae, 12–18 ulcers;muscle tissueunderlying examination (x100mag.) of ‘squashed’ ulcers inadvanced cases. M necrotic muscle) skeletal (exposing red lesions, smallulcers to large, deep small,patches singlescale‑sized ofskin, I Diagnosis Source: Phil Read invadans zoosporangia. Diagrammatic representation ofAphanomyces Figure 73 nitially, macroscopic examination; pale icroscopic Fig. 73 µm in ). Ponds: Tanks: zoospore stage. theinfectiousinfections through killing The following assistinreducing new quality. silver perch improvement after inwater R treatmentNo known ofinfected fish. Treatment • • • • ecovery hasbeenrecordedecovery inlarge of advanced cases infingerlings; ponds proven beneficialinrecovery to newabove) andre‑stocking treatment harvest, (asemergency tank). de‑stocked (chlorinatelower density stocking transfer offishto cleantank, 5 salt (NaCl)10 and 50 formalin, 25 g/L indefinite bath. mg/L, 1 mg/L continuous bath g/L 1 h bath; or h bath, then

P A zoospore stagesofthefungus. be sufficient to eliminate infectious environment for 7–10days islikelyto water inafish-freeSpelling surface pondsregularly. dry good water quality; or containing infected fish.M rivers andcreeks witha ‘fresh’, inflood source water. notpumpwater Do from high rainfall leadingto a ‘fresh’ in matter, days ofextremehotweather, especially highorlow pH,highorganic of ecto‑parasites,poorwater quality, predisposing conditions; infestations one orcombinations ofthefollowing O densities andhighbiomasses. revention void excessively highstocking utbreaks to occur known under improve water quality. ulcers) hashelpedfishhealnaturally; signs (smalllesionsto mediumsized oflarge fishhaving earlyre‑stocking aintain perch. uncommoninfections are insilver very infections.to bacterial S appear to berobust andlargely resistant related to poorhandling, silver perch perch. However, otherthanconditions diseases have insilver beenreported rough handling. To date, seven bacterial stress suchaspoorwater and/or quality result from directly environmental diseases infish.M causecommon anddamagingbacteria organelles andcandividerapidly. S are simple, donotcontain complex play akeyrole innature. cells Bacterial of small, ubiquitous organisms that form alarge,Bacteria diverse group B acterial

diseases ost bacterial diseasesost bacterial ystemic ome diagnosis, columnare Source: Phil Read infectioninsilverColumnaris perch bacterial fry. Figure 74 usually higherat temperatures >20°C. range oftissuetoxins; is pathogenicity established, through ofa production columnaris. columnare The bacterium, The bacterium, and highorganic loads. conditions associated withlow DO injury, otherdiseaseandcrowded stressful precursors suchasphysical silver perch, butusuallyfollowing andmature infingerling mortalities in silver perch, althoughithascaused mortalities. The diseaseisnotcommon can rapidly infectfishcausinghigh common inthepondenvironment and has aworldwide is distribution, C olumnaris trea 1 cm tmen canbeinvasive once , causesthedisease & tionpreven of Flavobacterium columnare Flavobacterium

the Flavobacterium diseases of

the australian

prevalent at temperatures >20°C. conditions colonising gills andskin; mechanism; preference for aerobic flagella,motileby glidinglacking rod; 0.4 Slender, filamentous gram negative P Signs • • • • • • athogen Ulcers with ‘yellowish’ pigmentation yellow to white necrotic edge Gill infection,eroded lamellaewith Frayed anderoded fins red periphery L 75 head andcaudalregions ( Erosive lesionson andnecrotic skin mortality Chronic or to acute fishmorbidity esions ‘whitish’ colour, with inflamed, freshwa ) µm diameter, 4to 10 ter fish silver h perc (b Figs. 74 µm length; idyanus bidyanus and )

p|39 • diseases and pathogens p|40 • diseases and pathogens Tanks: Treatment fungalinfection. have secondary hence thenamecolumnare; lesionsmay colonies giving a ‘haystack’ appearance usuallycongregatebacteria into having glidingmotion; characteristic asslenderrodsmagnification; bacteria andgill); 1,000×mounts oflesions(skin M Diagnosis Source: Phil Read columnare. perch Flavobacterium caused by thebacterium, ulcerationDeep onthecaudal peduncleofsilver Figure 75 • icroscopic examination ofwet sensitivity testing isrecommended.sensitivity this antibiotic; however, laboratory organism iscommonly sensitive to daily; loadandre‑treat bacterial This aeration, water exchange to ‘dilute’ maintain low light levels, good 10 20–30° at days 7 ingredient, oxytetracycline 20 days at <20°C,continuous bath, mg/L active C or or Ponds: • • • • matter; total KM organic high with ponds in required 2 higher C prolonged immersion,maintain level; copper (ascopper sulfate) 0.2 50–100 as feed additive for 10days, in systemic infections, oxytetracycline when water colourless orlight brown; 6 to 8 during treatment.during be >50 mustupon total alkalinity, alkalinity potassium permanganate (KM swabbed with20%iodinesolution. lesions onindividualfishcanbe fungal infections. may assistin recovery by preventing salt (NaCl)2 mg/L a.i.,higherlevels may be mg/L, KM mg/L; continuous aeration mg/kg fish/day. uSO g/L continuous bath 4 dosagesdependant nO nO 4 4 becomes inactive notto exceed

mg/L nO 4 )

<18°C; upto 30kg/m A P stocking levels (e.g.stocking upto 40 tank systems andmaintain appropriate quality. Ensure rapid solidsremoval in procedures; maintain goodwater organic harvest loadingduring (>28°C avoid at hightemperatures harvesting exposure to any oflow periods DO; revention void poorhandlingoffish,especially ); avoid overstocking/high 3 >18°C ). kg/m 3

cause thedisease. A Flavobacterium, Pseudomonad, belongingby to thebacteria the periods. M transport procedures and between harvest loading andinappropriate quarantine D of rough handling, over‑crowding, low peduncle andusuallyoccurs asaresult ofthecaudal caudal finanddistalpart byis characterised necrosis ofthe and grow‑out farms. The disease fromare hatcheries transported to quarantine tanks, orwhenfingerlings from ponds andtransported harvested to late are summerwhenfingerlings in juvenile silver perch. I relatively disease common bacterial Tail rot syndrome orfin rot, isa ‘T eromonad bacterial groupseromonad bacterial mostlikely O ail , high temperatures, high organic organic high temperatures, high ,

rot

syndrome ixed infections t occurs mid ’ V ibrio oribrio diagnosis, inhabitants offishmucus. are natural often these bacteria (e.g. Signs Aeromonas Flavobacterium P Source: Phil Read tailrotEarly onthedistalendofacaudalfin. Figure 76 most freshwaters; polar flagellum,ubiquitous found in motilerodslong, by asingle short, 0.8 to 1.0 • • • • • athogen trea transport following harvest/ Chronic mortality facing current orairstones L fry/fingerings colour,Dark sometimesblotchy Necrotic tissueoncaudalpeduncle Eroded tailfin ethargic, often near tank surface orethargic, neartanksurface often P. fluorescens tmen µm diameter and1.0to 3.5 & spp. (e.g. tionpreven of spp. asfor columnaris; ); similarto Pseudomonas A. hydrophila

the diseases of Aeromonas spp. ), ), –

the australian

µm ; exposing ( skeletalstructure to peduncle, ulcerated tissueoften more advanced cases, caudalfineroded appearance withfocal haemorrhages; caudal pedunclehaving pale, mucoid early stages( early edges andreddened caudalfinin Gross appearance; fishwithfrayed Diagnosis Source: Stuart Rowland Source: Stuart Silver perch withtailrot. fingerlings Figure 77 resolves. regrow finray thesoft tissueifinfection having mildcasescancompletely enter system. circulatory bacteria Fish M cultures andisolation ofbacteria. Definitive diagnosis by fishnecropsy, fungalinfectioncommon.secondary ortality increases significantly onceortality freshwa ter Fig. 76 fish silver ); skin ofthedistal); skin h perc (b Fig. 77 idyanus bidyanus ); ); )

p|41 • diseases and pathogens p|42 • diseases and pathogens Tanks: Treatment • • • environment ofapond. once restocked into thelow‑stress good water quality restock into recently‑filled pondwith advanced cases. fishpromptly,moribund particularly fungal infection; may assistinrecovery by preventing salt (NaCl)2 antibiotic usage, plus recommended to ensure appropriate cultures results andsensitivity are this antibiotic; however, laboratory this syndrome responds often to to ‘dilute’ loadandre‑treat; bacterial levels, goodaeration; water exchange 10 20–30° at days 7 ingredient, oxytetracycline bath, 20 days at <20°C;maintain low light g/L continuous bath – remove infected, – fish canrecover mg/L active C or or clean water andaeration. (2–5 provide toprior saltbath transport; and 4–5daysfingerlings postharvest Quarantine(pond andfishtransporter). proceduresoxygen harvest during avoid over‑crowding; always usebottled when water ispoorandDOlow; quality hotweather,avoid during harvesting procedures; nets; useonlyknotless M P revention inimise stress harvest during g/L) for 24–48 hrs post‑harvest, ornamental goldfish( on acommercial that farm alsoproduced involving pond silver perch inanearthen outbreakhas beenonlyonereported common ( carp and systemic infections are probably and/orfinulcersexpresses itselfasskin without showing symptoms. The disease bypathogen infected canbecarried fish The typical strainThe ofthisbacterium, typical Aeromonas salmonicida Source: Stuart Rowland Source: Stuart G Figure 78 A. salmonicida salmonicida Aeromonas salmonicida nova importation ofinfected goldfish( importation probably introduced into furunculosis, insalmonids. GUDwas A (‘Goldfish Aeromonas Ulceration oldfish (Carassius auratus) with GUD. n atypical strainn atypical ofthebacterium, causesthisulcerative disease. There , causes the serious disease,, causestheserious Ulcer hasbeenidentified in

caused Cyprinus carpio salmonicida

Carassius auratus disease , thesubspecies subspecies

by A ustralia by the

) andthe ’, GUD)

no Fig. 78 v a ). ). ; ). ). Aeromonas salmonicidanova P asymptomatic carriers. resistance to GUD, as butmay act are usuallylow. M infectionsin theabsence ofsecondary rateslikely late intheepizootic; mortality Source: Stuart Rowland Source: Stuart Silver perch withGUD, Aeromonas causedby thebacterium salmonicidasubspeciesnova Figure 79 Signs survive long periods offthehostfish. longperiods survive and circular colonies; pathogen may on agarmediaare grey, typically small gram‑negative isolates grown bacterium; • • • athogen ‘pale’ halo( pale orred centres withaperipheral lesions to crater‑like ulcers, may have ranging reddened from superficial, L L Chronic fishmorbidity/mortality esions and ulcers on skin andfins,esions andulcers onskin ethargic swimmingandinappetence Fig. 79 urray cod have shown ) ; non‑motile, diagnosis, Tanks: Treatment ulcers.superficial is more revealing thansampling and spleen)insystemic infections from internalof bacteria organs (kidney isolation;culture isolation andbacteria examination ofinfected fish;necropsy, Definitive diagnosis requires laboratory Diagnosis • • • trea Fluids (ascites) inabdominalcavity laboratory sensitivity testing sensitivity laboratory antibiotic choice shouldbebasedon daily; re‑treat exchange to ‘dilute’ loadand bacterial light levels, goodaeration; water or 10days at <20°C;maintain low ingredient,active 7days, at 20–30°C oxytetracycline (pure), bath, 20 tmen & tionpreven of

the diseases of . mg/L

the australian

and limepondswithC reduce stresses; regularly dry quality; water supplies;maintain goodwater be eliminated from ponds, drains and possible sources ofinfectionandshould are goldfishandcarp water supply; Ponds: A. salmonicida Prevention requires elimination of P (calcium hydroxide orcalciumoxide). • revention prior toprior saleoffish. veterinarian; and prescription ofaregistered be usedunderthesupervision for 10 oxytetracycline, 75 testing; sensitivity by laboratory appropriate antibiotic, determined prompt oral administration of freshwa days; antibiotics canonly ter from andits thefarm fish W silver ithdrawal timesapply mg/kg fish a( h perc OH) (b 2 orC idyanus bidyanus aO

)

p|43 • diseases and pathogens p|44 • diseases and pathogens (‘pop‑eye’) ( clinically fishmay exhibit exophthalmia takes theform ofsepticaemia,and bass.and striped The diseasetypically eels, channelcatfish, tilapia,yellowtail fish worldwide, includingrainbow trout, responsible for diseaseinmany cultured Silver perch reared were inRAS infected recorded inpopulations ofwildfish. conditions. Natural epizootics have been epithelium orby stressful environmental tois likelyto beenhanced by injury thought to bemainlyby and contact Transmission of andintestineabdominal cavity (ascites). The bacterium, The bacterium, Source: Matt Landos note exophthalmia. Silver perch infected by Streptococcosis iniae; Figure 80 were significant. although lossesinthefew outbreaks The diseasehasbeenrarely reported, causes streptococcosis insilver perch. Streptococcosis Fig. 80 Streptococcus iniae Streptococcus Streptococcus ) orfluidinthe

spp. is spp. are , epizootic. mayfactors have contributed to the (18 to 11°Cover 12 following water fluctuating quality Signs range (10–45°C anaerobically, inawidetemperature β rarely form chainsininfected fish; cocci; immotile;single orpaired but Gram‑positive, ovoid to elongate P • • • • • athogen -haemolytic; many speciescangrow behaviour L pond edges L distension Exophthalmia andabdominal Fish pigmented darkly Chronic fishmortality/morbidity oss ofappetite andnervous andat fishnearthesurface ethargy; ). h); however, other

Source: Phil Read indicate systemic infections. bacterial fromHaemorrhaging thevent cansometimes Figure 81 Tanks: Treatment at 48hours onbloodagarmedia. raised androunded, 1to 2 produces dull, yellowish/grey, slightly positive, culturekidney); bacterial organs (spleen,liver, brain, eye and isolation from ofBacterial avariety Diagnosis • • • results fish can be started onresults fishcanbestarted sensitivity. testing as sensitivitybased onlaboratory ofantibiotic shouldbeselection inside of abdominal cavity ( inside ofabdominalcavity andoperculum, baseoffinsandskin, aroundDiffuse haemorrhages deformity (scoliosis) may developSurvivors spinal S. iniae W hilst awaiting culture hasvariable mm colonies Fig. 81 ) Ponds: chloride (1,000 chloride (500 and equipment, sodiumhypochlorite disinfecttanks, floorsponds regularly; should beremoved; andlime dry infected periods; fishorcarcassescritical handlingduringold feed orunnecessary over‑crowding, over‑feeding, feeding A P • revention void stress dueto poorwater quality, 10 oxytetracycline, 75 oral administration viafeed: to ‘dilute’ loadandre‑treat. bacterial levels, goodaeration; water exchange 10 20–30° at days 7 ingredient, oxytetracycline, 20 mg/L for 2mins),benzalkonium days. days at <20°C;maintain low light mg/L for 20mins). mg/kg fishfor mg/L active C or or diagnosis, most frequently isolated include fish worldwide. The common strains andfreshwater150 speciesofmarine disease hasbeenrecorded inover Mycobacterium marinum Source: Phil Read ( onabarramundiUlceration ofskin Figure 82 aquarium fish( aquarium used for barramundi, M recirculating systems suchasthose disease that canbepersistent in M particularly thespleen;approximatelyparticularly nodules (granulomas) ontheviscera, mycobacteriosis exhibitedwhite typical present. Large silver perch (500 a significant at threat to theindustry silver perch; however, thediseaseisn’t has beenrecorded inpond‑reared worldwide M distribution. isolated from infected fish;allhave a environmental strains have been and Mycobacteriosis Lates calcarifer) caused by mycobacteriosis. ycobacteriosis isachronic bacterial trea M. fortuitum tmen & tionpreven of Figs. 82 althoughother and

the urray cod and , M. chelonae ycobacteriosis diseases of 83

). The g) with

the australian

Source: Phil Read note finerosion. Barramundi (Lates calcarifer) withmycobacteriosis; Figure 83 to culture. 10 are slowunevenly; to grow (upto positive, staining acid‑fast;often rods, 0.4 S P of infection. topical disinfectant to minimisetherisk be rapidly cleanedandtreated witha spike wounds andabrasions should having any diseases. bacterial C ofwhen handlingfishsuspected gloves islow; shouldbewornthe risk can infecthumans(zoonotic); however, 60% over 8 increasing from approximately 20%to propagated inthepondwithprevalence a 2 was recorded over20% mortality traight immotile orslightly curved, athogen weeks required) andcanbedifficult month period. The infection freshwa × 1.0 to 4.0 weeks. ter fish silver Mycobacterium µm long;gram h perc (b idyanus bidyanus uts, spp. )

p|45 • diseases and pathogens p|46 • diseases and pathogens Signs Source: Matt Landos organ dueto mycobacterial granulomas. Silver perch spleen;note irregular margins of Figure 84 • • • • • • • • • heart), 1to 4 heart), Granulomas in viscera (kidney, spleen, Fin erosion Shallow to deepulcers A Emaciation andpoorgrowth L edges andsurface I Chronic fishmortality/morbidity swelling (ascites) Exophthalmia andabdominal rregular swimming, fishat pond oss ofappetite bnormal dark colour dark ofskin bnormal mm diameter ( Fig. 84 ) inflammatory cells.inflammatory include peripheral, lighter coloured, for granulomas; thelatter may andspleentissuemounts ofkidney examination, 200×,ofwet, squashed Tanks: control oreradicate. Once established, canbedifficultto Treatment granulomas ( oftissuesmears; histological sections staining (Ziehl‑N diagnosed by acid‑fastandgram cultureLaboratory ofbacterium; Diagnosis Source: www.fishdisease.net bluefish. by mycobacteria ofanA inthe kidney ofagranulomaHistological caused section Figure 85 • required mycobacteria). to kill (10,000 using sodiumhypochlorite equipment; disinfectequipment contaminated tanks, pipes and remove infected fish;clean chlorine reported level reported mg/L chlorine Fig. 85 ielson stained)of ); microscopic merican superficial infections. superficial minimise damageto fishto prevent practices; water andhusbandry quality infected anddeadfish;maintain good utilise UVand/orozone units;remove Mycobacterium P Ponds: C between crops; limepondswithC and ‘bullying’ ponds ofinfected fish;dry ulcers from infectedof bacteria skin transmission probably viatheshedding strains are natural soilorganisms; intheenvironmentperiods andmany • revention a( de‑silt andlimepond.de‑silt remove infected batch offish;dry, OH) 2 ; disinfecttanksandequipment; spp. long cansurvive aO or base of the pectoral fins( base ofthepectoral peduncle, top ofthehead, flanksand areas onthecaudal oftheepidermis ofsigns begin asde‑pigmentation purging systems are increased. Clinical densitiesin whenstocking particularly summer (causing ‘summer spots’) late during and spring post‑harvest The diseaseinsilver perch isobserved hydrophila Source: Phil Read of low harvest. periods DOduring MAIEarly infection(‘summer spots’) causedby Figure 86 untreated, ‘spots’ candevelop into more species infectingfishare material asanutrientsource. The main rivers andbottom mud, utilisingorganic and found inmostfreshwater ponds, A susceptible, includingsilver perch. of freshwater fish.M diseasesthe mostcommon bacterial A Aeromonad Aeromonad eromonad bacteria areeromonad ubiquitous bacteria eromonad infectionsare oneof , A. sobria

Infection dermatitis , and any speciesare A. caviae Aeromonas Fig. 86 , MAI) (Motile ). I . f left diagnosis,

polar flagellum. 0.9 gram‑negative, motilerod; 0.8to short, Signs Aeromonas hydrophila P if soldwholeorlive. render fishunsightly andunmarketable insilver perch, butcanmortalities The diseasehasnotcausedsignificant associated withlive transportation. around theaffected area from stress significant scale loss and haemorrhaging M advanced, red, lesions. necrotic skin • • • • athogen ild lesionscanprogress rapidly, with trea flanks, fins, headorabdomen(early) areas on de‑pigmented Superficial, L L L µm ×1.5to 3.5 oss ofequilibrium ethargy oss ofappetite tmen & tionpreven of µm; motile, singular and

the diseases of A. sobria ;

the australian Tanks: Treatment histopathology examination. identification withaccompanying culture,fish; bacterial isolation and necropsyLaboratory ofdiseased Diagnosis • • • • • (antibiotic‑resistance iscommon). display aregular pattern ofsensitivity doesnotresults asthisbacterium antibiotic sensitivitylaboratory treatment shouldbebasedonthe haemorrhagic, swollen intestine/vent Distended abdomen,clearfluids; Exophthalmia, opaquenessofeyes infection L (advanced)haemorrhaging Ulcerated lesions, margins whitishor esions may fungal have secondary freshwa ter fish silver h perc (b idyanus bidyanus )

p|47 • diseases and pathogens p|48 • diseases and pathogens Ponds: • • • • can complicate thehealingprocess. a problem. 10 oxytetracycline, 75 administration viafeed; appropriate antibiotic; oral 18°C assuper‑infection of when water temperatures are under lesions result inspontaneous resolution of returning fishto the pondwilloften or 10 salt (NaCl)2 loadandre‑treat;bacterial aeration; water exchange to ‘dilute’ maintain low light levels, good ingredient, 7days, continuous bath; oxytetracycline 20 days; resistance to anti‑microbials hourly bathsg/L hourly daily. – this shouldnotbedone g/L prolonged immersion mg/L active mg/kg fishfor Saprolegnia

use UV/ozone andsalt;water exchange. filters;clean pipesandtanks;backwash ammonia andovercrowding; regularly water;purge avoid ingoodquality high withbottomcontact muds/organics; conditions, highsuspendedsolidsand harvesting, avoid overcrowding, hypoxic MAI isastress‑borne disease. P revention W hen of distinct transparentof distinct capsules. The gill hypertrophy andtheformation organism affectsmainlygills, causing environments.and marine The fish ofseveral speciesinbothfresh injuvenileconsiderable mortalities high concentrations ithascaused benign andnon‑pathogenic, but in conditions. isusually Epitheliocystis insignificant undercommercial pond the diseaseremains relatively however, heldinaquaria; fingerlings I probably Chlamydia‑like organism. is anintracellular most bacterium, fish. and marine The causative agent diseaseaffectingfreshwaterbacterial isawidespread chronicEpitheliocystis Epitheliocystis t hasbeenrecorded insilver perch juveniles ( filaments affected insilver perch membrane;trilaminar upto 96%gill peripheral10–87 µmdiameter; round to oval shaped; (transparentcysts to yellow capsules) gill microscopy; under scanningelectron coccoid rod‑shaped; visible bacterium; I P the diseaseresolving withouttreatment. developingimmunity insome species, evidence of gills respiratorycapacity; leadingtostructure impairmentofthe gills swell andlosetheirlamellae Source: Dr BarbaraSource: Dr Nowak, Prof. Assoc ofAquaculture, School UTAS middle lamella: [h note swellingof afishwith epitheliocystis; ofthe micrographElectron showing gill filament cells Figure 87 ntracellular, non‑motile, gram negative, athogen Figs. 87 ] hypertrophied [arrows]] hypertrophied cell. , h 88 and

89 ). ). diagnosis, displaying round to oval shaped, cells; cells hypertrophied ingill filament epithelialof gill tissue;caninfectskin I Diagnosis Signs Source: Robert Tennent,Source: Robert Assoc. Lect., ofMedicine, UTAS School blood space. pathogens: [c micrographElectron containing ofcyst Figure 88 nitially, microscopic examination, 200× • • • • • • trea G bodyconditionDeclining respiration Distended opercular cover; rapid S L M ethargy wimming nearthesurface aping mouth(mortalities) oribund fish,mortalities oribund tmen e & ] cyst; [e ] cyst; tionpreven of ] epithelial cells; [bs] c

the diseases of bs

the australian and quarantine No known treatment, except disinfection Treatment Source: Dr BarbaraSource: Dr Nowak, Prof. Assoc of Aquaculture, Dept UTAS inclusions. showing [arrows]with epitheliocystis basophilic ofagill ofasilverHistological section perch Figure 89 recommended. isolation ofinfected batches offish is of UVirradiation onintake water and M available free chlorine, for 60 baths,using chlorine 1 and disinfectgeartanksregularly culture appliances; maintain cleanliness contamination ofnetsandotherfish disease possiblytransmitted by abouttheorganism;Little known P within cysts. required coccoid to observe bodies transparent microscopy electron cysts; revention aintain minimalstress infish.U freshwa ter fish silver h perc mL/ 10–12% (b idyanus bidyanus mins. se )

p|49 • diseases and pathogens p|50 • diseases and pathogens perch culture. is potentially threat aserious to silver under experimental conditions and has beenshown to affectthespecies epizootic haematopoietic necrosis, under culture conditions. Onedisease, viral diseasesaffectingsilver perch economic losses. There are noknown andseverecause highmortalities species inwhichthediseasescan are from economically‑important fish virusesthat have beenreported is relatively new, of andamajority The studyofviral diseases infish cells inotherorganisms to replicate. by protein. comprised ofDNAorRNAsurrounded V Viral iruses are extremelysmallagents Diseases V iruses mustinvade living

perch ( ( native fishsilver perch, M exposure to affectsthe EHNVseriously the laboratory, ithasbeenshown that 4%. Underexperimental conditions in introut are usuallylessthanmortalities south‑eastern A south‑eastern The virusisgeographically limited to haematopoietic necrosis virusEH NV caused by theiridovirus epizootic EHN isahighlyinfectiousdisease ( trout ( I common outcome following exposure. ato thevirus, with100%mortalities juveniles inboth species. The disease 12°C inspring/summer, involving often when water temperatures are above in redfin andtrout occur typically necrosis Epiz t is known to alsoaffectrainbowt isknown Macquaria australasica Perca fluviatilis ootic Oncorhynchus mykiss Macquaria ambigua (EHN)

haematopoietic ) are very sensitive) are very ustralia. R ) andgolden acquarie perch edfin perch ). O ) although utbreaks

. Signs (inredfin andtrout) and genus V P 150–170 may besusceptible. hence many fishspecieshost specificity; I oramphibians.possibly utilisinginsects sediments for prolonged periods, degradation, likelyto remain in is highlyresistant to environmental decomposing carcasses. The virus viabodyfluidsandfromviral particles in water, withinfected fishshedding redfin perch, that EHNVisreadily spread agencies. I to diseasesurveillancebe reported is internationally notifiableandmust ridoviruses arefor known theirlackof • • athogen irus amemberoftheI Slow orrapid spiralling to thesurface M ortalities nm indiameter. t is known fromt isknown studieson Ranavirus ; polyhedral virus, ridoviridae familyridoviridae electron microscopyelectron and/orother tests. polymerase (PCR), chainreaction immuno‑fluorescent staining, ELISA followed by histopathology, tissue for virusisolation; cell culture; andspleensamples;fixingofkidney C Diagnosis • • • • • • ollection offresh andfixedollection liver, in liver Peritoneal fluid;white foci ofnecrosis S stages, redfin) C L above thebottom W discolourationErosion offins;skin oss ofappetite welling ofspleenandliver utaneous haemorrhages (terminalutaneous haemorrhages eak swimming; ‘head‑standing’ diagnosis, piscivorous birds. exclusionand disinfectionofgear; of trout); regular cleaning(particularly levels; maintain goodwater quality source; instocking reduction ponds, drains andthefarm’s water redfin perch fromfish, particularly Exclusion ofwildfishandornamental P hypochlorite for 2 disinfection (200 to prevent spread; cleaningand treatment; quarantineNo known strict Treatment disposal. revention trea tmen & tionpreven of mg/L sodium h); proper carcass

the diseases of

the australian cause stress, reduce feeding andfeed hypoxic conditions (<3 fishto prolongedSubjecting chronic when DOdecreases to 2 silver perch ‘gasp’ at thesurface copper sulfate inponds. G chemical treatment usingformalin or summer), ‘crashes’ ofalgalblooms, and during or failedaeration (particularly DO have occurred following inadequate associated withlow concentrations of systems.transport Fish mortalities as well astanksandinpurging and perch following acute hypoxia inponds, have beensignificant lossesofsilver is closelylinkedto fishhealth. There variable inintensive aquaculture, and DO isthemostlimitingwater quality Miscellaneous H conditions diseases y po freshwa xia (low , ter disorders

fish

dO) silver

non‑infectious h perc mg/L DO mg/L orless.

and enerally, (b idyanus bidyanus

) will

)

p|51 • diseases and pathogens p|52 • diseases and pathogens Signs or weeks. infectionsinsubsequent daysbacterial necrosis andsecondary cause skin (minutes) periods oflow DOcanshort infections. E opportunistic Chronic hypoxia canpredispose fishto assimilation, andresult inpoorgrowth. Source: Phil Read lack ofpigmentation. note adrainsuspended solidsduring harvest; silverDead perch causedby low DOandhigh Figure 90 • • • • • and blotchy ( skin fishhavingDead paleappearance A Largest fishdyingfirst near edges Fish congregating at water inletsor morning early particularly Fish ‘gasping’ at water surface, cute mortality Figs. 90 ven relatively , 91 and 92 ) power‑take‑off aerator) power‑take‑off aeration (2ndaerator and/ortractor higher DOlevels) andsupplemental (including from otherpondshaving Provide water emergency exchange Treatment meter. calibrated usingahighquality morning) R R Diagnosis Source: Phil Read death by hypoxia. Open mouthandflared operculum –signs of Figure 91 • • • outine dailymonitoring ofDO(early offishandponds.egular observation Open mouthandflared opercular (tanks) andinactivity ofskin Darkening tanks) (particularly R apid declineoffeeding response .in RAS procedures andharvest andtransport (>28°C ofhighwaterperiods temperature wasteful feeding; reduce feeding during excessive densitiesand stocking treatments; avoid over‑crowding, 24 temperature andprovide continuous algacide treatments above 25°Cwater power back‑up; avoid formalin or >4 Provide adequate aeration (maintain DO P Source: Phil Read of hypoxia ortransport. harvest during De Figure 92 revention -pigmentation ofsilver perch tails–asign h aeration for 4–5days following early morning) andemergency morning) mg/L early ); provide oxygen (bottled)during

procedures ( of bottom sedimentsharvest during aerated pondsfollowing thedisturbance Problems have occurred inpoorly death with few, ifany, diagnostic signs. <0.003 concentrations (e.g. levels shouldbe and tanks, where H ofsilver perch inpondsmortalities have beenseveral casesofhigh andpungentdistinctive smell. There ‘rotten egggas’ dueto itsstrong, I bacteria. breakdown oforganic matter by anaerobic the during produced is been suspected. H H of bore water are naturally highin been lyingstagnant and/ortheuse Hydrogen sulphide(H Source: Stuart Rowland Source: Stuart anaerobic mudonthebottomBlack, ofapond. Figure 93 H 2 ydrogen S. The useofbore water that has mg/L) andcancauserapid t is commonly known ast iscommonly known Fig. 93

sulphide 2 2 S istoxic at low ). S S poisoninghas 2 ome sources S) isagasthat poisoning diagnosis, mechanisms causinghypoxia. indicative ofaproblem. Smell of ‘rotten egggas’ may be Diagnosis Signs and sodiumhydroxide (to >pH following withzincacetate preservation sample canberefrigerated andstored and testing by aqualifiedlaboratory; (2litres,collection sealedunderwater) H intanks.have alsocausedfishmortality lines flushedwaterof poorly delivery • • • • • 2 S interferes withfishrespiratory trea R S and death R Erratic swimmingaround pondedges disturbance orwater exchange A chooling at water inflows edness infinsandtails apid breathing, thenlistlessness cute mortality following sedimentcute mortality tmen & tionpreven of

the W ater sample diseases of 9)

the australian

Ponds: Treatment pumps well above bottom sediments. water linesandposition footvalves of and till ponds to oxidise sediments; flush regularlypoor water dry, flow; de‑silt ponds that causesediment build‑upand (e.g.objects rocks, tyres, cages)from reduce stagnant areas ofwater; remove both oxygen andcreate currents will regimes; useofaerators that provide appropriate aerators and aeration M P Tanks: • • revention aintain aerobic conditions using H potassium permanganate to oxidise water exchange; theadditionof aerators; type rapid surface‑spray vigorous aeration ofwater using pH willdecrease H lowering temperature andincreasing use packedcolumn degassers; 2 S freshwa . ter fish silver 2 S toxicity. h perc (b idyanus bidyanus )

p|53 • diseases and pathogens p|54 • diseases and pathogens weather conditions. at high water temperatures andstill DO through excessive photosynthesis may result insupersaturated levels of of macrophytes inpondssummer unicellular algaeorextensive growth silver perch ( of gasemboliinthetailsandgills of have been associated with the formation super‑saturated levels ofDO(160%) disease associated withnitrogen, but ofgasbubbleno confirmed reports in thesilver perch industry. There are does notrepresent asignificant problem losses dueto gassupersaturation, butit There have beenseveral of reports Source: IanCharles G Figure 94 (Gas Gas as emboli[arrows] inthe tailofsilver perch.

supersaturation Bubble Fig. 94 Disease) ). Large bloomsof

Ponds: Treatment gas emboli( examination ofgill, 100×;presence of microscopicfish isheldunderwater; whilethegas bubblesfrom theskin to squeezegas emboliinfins;ability M Diagnosis Signs Source: Phil Read (this level usually asymptomatic) (×100 mag.). G Figure 95 • • • • • • as emboli[arrows] inthe gills ofasilver perch acroscopic examination offish; several aerators days using surface aeration ofpondfor >1 placed inwater Formation ofbubbles onobjects Exophthalmia (‘pop‑eye’) O G inshallow water) (particularly thendivingFish surfacing as emboliinfinsand/oreyes edema of secondary gill lamellae edema ofsecondary Fig. 95 ). h eachday for Tanks: tanks around 100%oxygen. excessstrip gas;maintain fishtransport leaks; usepackedcolumn degassersto pumps andassociated plumbinghave no an algacide(e.g. copper sulfate). Ensure diluted usingwater exchange oruseof algal bloomsinsmallerpondscanbe aerators; insmallerponds, troublesome splashing paddlewheel orothersurface M P • revention aintain dailyaeration using using apackedcolumn degasser. pumps; excess gascanbestripped ingress of air under pressure via faulty caused by saturation ofbore water or most likelynitrogen gas(notoxygen) water exchange. to equilibrate withtheatmosphere; (e.g. paddlewheels)willallow thegas temperatures were at acceptable levels variables,quality except high thevery tanks within36–48hours. O fish that were recovered harvested in schooling at inflowing water andthose rain. Fish displayed erratic behaviour, temperatures (>30°C was preceded by extremepondwater circinalis bloom containing the blue‑green algaebloom containing theblue‑green following the ‘crash’ ofalarge algal silver perch suffered 100%mortality algal blooms. I have beenassociatedmortalities with perch farms, butsomeunexplained fish lossesonsilvernot causedserious systems.marine Noxious algaehave ofproblems in occurring the majority worldwide withimplicated infishkills Noxious phytoplankton hasbeen Source: Phil Read fins.pectoral aroundhaemorrhaging themouth,pelvic and algaepoisoning ofsilverSuspected perch; Figure 96 flos‑aquae Microcystis be potentially toxic ( No xious ; bothspeciesareto known

algae n oneinstance, large Fig. 96 ) followed by heavy and Anabaena ). The crash ther water diagnosis, limited. under aquaculture conditions remains andalgaltoxins fish morbidity/mortality decay. However, theevidence linking the algaereleased toxins death and after throughout theevent. I or following inL preservation identification (examination within24 (2 frozentransported andawater sample fishneedto bea toxicology laboratory; Definitive diagnosis canonlybedoneat Diagnosis Signs • • • • litres) for shouldbecollected algae trea kin andfinrednessSkin A movements, swimmingincircles) jerky Erratic swimming(jumping, Fish swimmingaround pondedges cute mortality tmen & tionpreven of

t ispossiblethat the diseases of ugol’s

the australian hrs 2 to 3years). clean pondsonaregular basis(every Source: Phil Read a silver perch pond. blue Thick, Figure 97 algae ( of blue‑green water temperatures blooms andheavy reduce feeding high during quality; oxygen depletion;maintain goodwater ponds, butcare mustbetakento avoid A P thought to beimminent. whenlossesare harvest emergency undertake aeration immediately; Provide water exchange and24 Treatment of algaetoxicosis. diagnosis to support necessary quality) (parasites, viral bacterial, andwater elimination ofanotheraetiology iodine solutionandrefrigeration); revention lgacides canreduce noxious algaein freshwa - green algae scum on the surface ofgreen algae scumonthesurface ter fish silver Fig. 97 h perc (b ); dry and ); dry idyanus bidyanus h )

p|55 • diseases and pathogens p|56 • diseases and pathogens stress. Transporting fish,even for short with excessive densitiesand stocking significant differences inpH)associated of fishbetween waters having (low DO;highsolids,quality movement bins, andpoorwaternets andharvest abrasive, rough handling, crowding in cause ismostlikelyacombination of theaetiology ofthediseaseisunknown; waters having highorganic load. The (>20°C prevalent at warmerwater temperatures containers. The problem ismore orconfinement intransport harvesting and purging systems following in silver perch intank‑based quarantine poor husbandry techniques ( poor husbandry are usuallytheresultfins (andskin) of Cloudy eyes ofthe andhaemorrhaging ‘Cloudy Source: Phil Read E Figure 98 and ye damagecausedby poorhandling. 99 ) andwhenfishare confined in ). The problem manifests often ’ eyes

and

red

tails Figs. 98

Signs Source: Phil Read handling stress andpoorwater quality. anddamagedtailfincaused byHaemorrhaging Figure 99 densities. DO conditions (cleanwater; highsanitary perch willrecover in3–5days ifheldin plastics orothersimilarmaterials. Silver netsusingcoarse nettingormakeshift problem isexacerbated whenusing hand netshascausedeye damage. The or binsandtheover loadingoffishin periods, insmallvessels suchasbuckets • • • • the lateral line R S caudal fin offinsparticularly Haemorrhaging Opaqueness ofoneorbotheyes ), usingsaltandatstocking normal cale loss edness of skin, particularly below particularly edness ofskin, Tanks: Treatment handlingprocedures.or soonafter oftheclinicalsigns duringobservation Presumptive diagnosis isbasedon Diagnosis • lesions resolve spontaneously. andhygienehusbandry willhelp improvement inwater quality, good antibiotic treatment butgenerally infectionsmay requirebacterial baths at 10 severe cases:asabove withdailysalt high aeration (DO>4 2–3 days; maintain cleanwater and and retreat 24 saltevery salt (NaCl)at 2 stocking densities<30 stocking mild clinicalsigns: holdfishat g/L for 1 indefinitely; flushg/L indefinitely; hour; secondary hour; mg/L). M kg/m hrs for first 3 ; provide ore indicated; use knotless nets.indicated; useknotless disorders harvest unlessemergency compromised by diseaseornutritional avoidand transporters; handlingfish avoid over‑crowding bags inharvest from ponds; transportation post‑harvest ceramica highquality airstone during fish; provide bottledoxygen through touse anaestheticprior handnetting and at hightemperatures (>28°C A P revention void harvesting inpoorwatervoid quality harvesting ); diagnosis, Source: Phil Read Poorly developed ‘paintbrush’ tail. Figure 100 Source: Phil Read permanently exposing thegill lamellae. Poorly developed operculum [arrow] Figure 101 heads called ‘axeheads’ or ‘snub‑nosed’, (scoliosis andlordosis), deformed ofthespinecommon beingcurvature over thelast5years, withthemost increased inthesilver perch industry The incidence has ofabnormalities Physical trea tmen &

abnormalities tionpreven of

the diseases of

the australian uncertain, but most areuncertain, probably a result The are causesoftheabnormalities have onsomefarms. alsobeenreported 102 Source: Phil Read A juvenile fishwithadeformed (‘axehead’) skull. Figure 103 Source: Guy Jeff A Figure 102 ‘paintbrush’ caudalfins( reduced ormissingpelvicfins, and deformities oftheopercula bones, bnormality of the skull (‘snub oftheskull bnormality , 103 freshwa , 104 ter and fish silver 105 ). Jaw deformities h perc Figs. 100 -nosed’). (b idyanus bidyanus , 101 , )

p|57 • diseases and pathogens p|58 • diseases and pathogens Signs vitaminsandminerals. particularly contain theappropriate ingredients, andjuvenilesfor should post‑larvae overstocked dietsused andany artificial metals. E be free ofpathogens andany heavy be well filtered andoxygenated, and waterand optimumnutrition; should waterand maintain thehighestquality great care to minimisephysical damage, shouldbehandledwith eggs andlarvae phase, broodfish, thehatchery During rearing stages.hatching andlarvae eggincubation, during poor husbandry including inbreeding andtheuseof of inappropriate practices hatchery Source: Phil Read A juvenile fishwithadeformed (‘axehead’) skull. Figure 104 • • • • Jaw andheadanomalies Deformed fins Deformed ormissingopercula Spinal curvature ggs and larvae shouldnotbe ggs andlarvae abnormal fry prior to prior stocking. fry abnormal feeds. artificial C use highquality breeding matings, performance, etc); records (weight, offishperformance culture; tagallbroodfish andkeep to besuitableforknown intensive deleterious genes;usegeneticstrains replace broodfish ofcarrying suspected origin (e.g. caughtdams); infarm being closelyrelated orwithunknown do notusebroodfish of suspected recommended breeding programs; rearing techniques; followlarval U P possible causes. accomplishedoften by rulingoutother anomalies; determining geneticlink M Diagnosis Source: Phil Read [arrows] around the caudalpeduncle region. Fish showing (lordosis) curvature ofthespine Figure 105 revention se recommended and hatchery any possiblecausesfor developmental ull all the swelling iscaused by fluidsorgas. problem (organs andif orbodycavity) to determinebe dissected thesite ofthe exhibiting abdominalswelling should malformation fish and/ordysfunction; in otherspeciescausedby swimbladder A to water issuesorfeed quality availability. feeding was terminated for 1–3days due recommencement offeeding after S feeds oringestionofnoxious algae. infection, ingestionofcontaminated causes may includesystemic bacterial and thecauseremainsPossible unknown. been relatively low (<1% fishaffected) pond, inthefew‑recorded outbreaks has The prevalence ofthediseasewithin mosteventually die. normally; function andare unableto feedsurface or abdomen, float inverted onthepond syndrome have agreatly distended the abdominalcavity. Fish withthis silver perch affected withgasesin There have beenseveral of reports Abdominal ome episodeshave followed the bdominal distension hasbeenrecorded

swelling (‘ bloat ’) distension behaviour. andabnormal abdominal oftypical Observation Diagnosis Signs Source: Unknown stomach. Silver perch (≈ fingerlings Figure 106 withaeration.quality maintainlow goodwater humidity); mould‑free stored andcorrectly (cool, A P Unknown. Treatment • • • revention etiology unknown; ensureetiology unknown; feed isfresh, inability to swimnormally inability Fish inverted at pondsurface, gases orfluids Organs inflated orbodycavity with Distended abdomen( 70 g) withagas‑filled Fig. 106 ) diagnosis, Source: Phil Read stress.showing harvest Silver perch suffering and poornutrition Figure 107 lead to healthproblems suchaspoor The useofinappropriate dietscan minerals are essential for growth. levels ofproteins, andvitamins energy thanomnivorous fish.A fish require higherlevels ofprotein and andhealth,carnivorousperformance or speciesgroups, e.g. for optimal diets are formulated for specificspecies increased to susceptibility disease. M and poorperformance nutrition, sized pelletsresults ininadequate orfeeding thewrongand underfeeding low DOandhighammonia,particular can leadto water problems quality in effects onfishhealth.O feedquality canhave detrimental the feeding ofcontaminated orpoor unsuitable orunpalatable dietsand pelletsizes,incorrect theuseof overfeeding, feeding underfeeding, Poor feeding suchas practices Nutritional trea tmen & tionpreven of

disorders

the verfeeding fishverfeeding diseases of dequate

the australian ost ( (see Ergasilids) orskeletaldeformities necrosis oftheliver, parasitic diseases excessiveperformance, fat deposition, Source: Phil Read bladder. S Figure 108 where natural feed may beavailable. atthose farmed lower densities stocking problems, ofnutritional risk particularly Fishmanufacture). inpondsare at less oldfeedfeeding (>12months very since inassociation withalso beenobserved aflatoxin.suspected S food contaminated withmouldsand systems following thefeeding of of native fishinrecirculating tank have ofhighmortalities beenreports degeneration andulceration. There immune depression, deformity, hepatic and rancid food ingestioncancause and shelf‑life. affecting mineral and vitamin availability in fat can oxidise andbecome rancid Figs. 107 tarved silver perchtarved withanenlarged gall freshwa , 108 ter V fish and itamin CandEdeficiency silver 109 evere diseasehas h perc ). Feeds high (b idyanus bidyanus )

p|59 • diseases and pathogens p|60 • diseases and pathogens Signs Source: Phil Read Feeds highinfat can causeexcessively ‘fatty’ fish. Figure 109 • • • • • • • bacterial orfungalinfections bacterial C procedures Poor response to handling normal Fatty liver Fin erosion feeding ofcontaminated feed A Skeletal abnormalities Poor growth, emaciation, starvation oncomitant diseasesuchas cute mortality following thecute mortality

manufactured. months feeding. Ensure feed isrecently enough feed for approximately 3–4 and temperatures <14°C;onlyorder feed inrooms having low humidity and silver perch diets;handleand store U P help diagnose problem. anutritional of feeding, canprovide information to dates, andstorage, delivery andrecords events, includingfeed manufacture C by orbiochemists. qualifiednutritionists deficiencies inthedietrequire analyses or formulation offeeds. Suspected practices, orinappropriate storage are usuallytheresult ofpoorfeeding well requirements definednutritional Problems inspecieshaving arising Diagnosis revention ollection ofanaccurate ofollection history se recommended feeding regimes and fraying finrays ofthesoft ( damageandnecrosis,fish causingskin (mainly caudal)andflanksofsubmissive fish. A involving aggressive andsubordinate to theestablishment ofhierarchies butisprobablyis unknown, linked densities. The causeofthebehaviour bacterial andfungalinfectionsarebacterial become anddie. moribund S not feed, grow andeventually poorly of thetanksandcages;thesefishdo onthesidesnear thewater surface Submissive fishpositionthemselves Source: Phil Read trauma and aggression. andtail findamagedue tode‑pigmentation Silver perch showing fingerling skin Figure 110 m moderate densities(25–50 stocking in smallercagesandtankshaving has shown theproblem more prevalent display aggressive behaviour. R Silver perch insmallcagesandtankscan A ggression 3 ) rather thanlower andhigher ggressive silver perch nipfins econdary Fig. 110 esearch fish/ ). ). Signs m densities(>25 and at higherstocking systems (<14 days) periods for shorter common. Silver perch heldinpurging held insmallcagesortanks(e.g. infish between individualsparticularly ofaggressiveObservation behaviour Diagnosis supportive diseasediagnosis.supportive clinical signs intheabsence ofother of densities;observation stocking at moderate, rather thanlight orheavy • • • • 3 ) behave normally. Sporadic commotion intanks/cages appearance necrosis,Skin scaleloss, blotchy and corners ofcages/tanks I tanks andcages M ndividual fish stationary near surface nearsurface ndividual fishstationary oribund fish and/or mortality in fishand/ormortality oribund 1m 3 diagnosis, ) kg/ densities (>100fish/m stock fishat low (<15fish/m tanks/cages over (months); longperiods A P scale loss,infections. fungalorbacterial salt and/oranti‑microbial onfishhaving cages canexacerbate theproblem. U offishintanks/ densities. Underfeeding fish; lowering orincreasing stocking cages; cullingofaggressive individual R Treatment feeds andusefeeding incages. rings Feed fishto satiation usingsemi‑floating broodfish incages(upto 8 revention emoval ofaffected fishto othertanks/ void containment offishinsmall trea tmen & tionpreven of 3 , grow

the diseases of fish/m 3 ) orhigh - out); hold 3 ). ).

the australian se freshwa ter fish silver h perc (b idyanus bidyanus )

p|61 • diseases and pathogens p|62 • diseasep roblems inp urging systems harvest; (iii) the use of poorly designed (iii)theuseofpoorly harvest; havepractices the beenusedduring (ii)whenpoorhusbandry harvesting; inthefirst24hoursafter particularly is minimalorzero water exchange, following conditions: (i)where there in recirculating systems underthe disease problems are more prevalent a combination ofthetwo. G using tanks, filtration andUVunits;(iii) exchange; (ii)arecirculating system system usingperiodic, ‘batch,’ water options are generally used:(i)astatic well‑aerated water. Three management in tanksfor upto 7days inclean, requires fishto beheld harvested for product quality Purging themarket. from fish,ensures auniform, high Program), ortheremoval ofoff‑flavours in theSilver Perch A Quality industry. Purging (called ‘conditioning’ and tanksystems in thesilver perch Diseases are common inpurging disease problems ssurance enerally, swimming into currents andlethargy. head andcaudalpeduncle, skin, dark haemorrhaging, white patches onthe frayedpost‑harvest) fins, blotchy skin, (5–10 fish/day, 2–3days starting Clinical signs includechronic mortality Signs tanks isstrongly recommended. all parasites before pondsand stocking infested. Treatment offishto eliminate in purging tanks, theycanbereadily recognise thatare whenfingerlings held other chemicals. I resistance oftheeggstageto saltand are difficultto eradicate dueto the also common inpurging systems and infestationsHeavy ofgill flukesare fungal diseasesare themostcommon. and fish.Bacterial numbers ofharvested oflargenitrite causedby thestocking sudden increases inammoniaand has notbeen ‘conditioned’ to assimilate purging systems; (iv)where thesystem

in purging t is important tot isimportant

systems systems P • • • • • • revention ofdiseaseinpurging harvest, and then periodically (>30%; andthenperiodically harvest, (in static systems) theday after then~ harvest, during Exchange water intanksconstantly well‑aerated water post‑harvest. S andpurging system).transport measure water inpond, quality and anaestheticsintransport; (use oxygen, densities low stocking I and highammoniapost‑harvest). (preventsto harvest fouling ofwater notfeedDo fishfor 2–3days prior poor water quality. fishfrom pondswith notharvest Do diseasedfish. notharvest Do mplement good harvest proceduresmplement goodharvest tock fishat rates <30kg/m 80% ofwater 3 inclean, • • • • • nitrification bacteria). (desiccation ofthesystem willkill through units bio‑filtration L including pipes, tanksandbio‑filters. R system. notfeedDo fishinthepurging (daily); DO M 2–5 water exchange to ensure alevel of followingnitrite poisoning;re‑salt infections, reduce stress andprevent of 2–5 Hold fishincontinuous bath (>48 and flushammonia. organic matter, loads dilute bacterial 2ndto 3rdevery day) to remove eave water circulating permanently egularly clean/scouregularly purging system easure water regularly quality g/L ismaintained. g/L saltto prevent fungal , pH, salinity andammonia. , pH,salinity

diagnosis, h) h) quality (e.g.quality addingsalt).N any othersuddenalterations to water fish (andsubsequently ammonia)and introduction oflarge biomassesof severely compromised following the ammonia to nitrite thennitrate), is potential (theprocess ofchanging units; however, thefilter’s nitrification or keepaloadonthebio‑filtration recirculating systems willhelp ‘condition’ Holding somefishpermanentlyin pre‑biofilter filtrationpre‑biofilter or water exchange. suspended solids)dueto inadequate matter (mucus, scales, grass, and has beencontaminated withorganic the ammoniaload, and/orthebio‑filter undersized andisunableto assimilate bio‑filter’s area (SSA specificsurface compromised whentheis further • trea trichlorfon to lowertrichlorfon flukelevels. Periodically treat purging system with tmen & tionpreven of

the diseases of itrification

the australian ) is freshwa ter fish silver h perc (b idyanus bidyanus )

p|63 • diseasep roblems inp urging systems p|64 • aquatic plants and fish health ( following ways. treatment andcontrol ofdiseaseinthe maintenance offishhealthandthe can have asignificant effectonthe of pondsinafew days. M plants and covering entire surfaces rapid propagation, buddingfrom adult (L duckweed S deeper sections. colonising theentire pondincluding and water thyme are capableof submerged speciessuchasribbonweed torestricted shallow areas ofponds, ponds. been problematic insomesilver perch ( ( milfoil ( is undesirable. Plant speciesincluding (macrophytes) inaquaculture ponds The presence oflarge, aquatic plants Source: Phil Read The cumbungi plant colonising pondedges. Figure 111 a • Hydrilla Vallisneria Typha feeding. I quatic nterfere withpondmanagement and sp.) ( W Myriophyllum spp.) ( hile someplant speciesare sp.) andwater thyme Fig.111 emnaceae) are capableof Figs.112 ome speciesof ), ribbonweed plants sp.), cumbungi and acrophytes 113 ) have

and Source: Phil Read Hydrilla sp. ‘choking’ asilver perch pond. Figure 112 • • • • • • • • harvesting. orpreventHinder samplingand evapotranspiration. C decompose. high T C which may remain untreated. Provide havens for fishandparasites load. concentrations dueto highorganic I concentrations. andchemical distribution R transfer, ecto‑parasites. particularly C levels). nutrients, highpH causeabnormally compete withphytoplankton for I nterfere withchemical onwater (clearwater,mpact quality estrict water flow and therapeutic therapeutic and flow water estrict ontribute to water lossthrough ontribute to oxygen depletionand rowd thefishandenhance disease

AN levels whenthey fish

health

Management Source: Phil Read algae; note the water clarity. Extensive growth ofHydrilla sp. and filamentous Figure 113 A P onto theproperty. and ponds;quarantine allfishcoming suppliesprevent into surface run‑off from ponds;usebore orwell waters and birds; exclude stock farm suchascattle water); dissuadeaquatictransportation introduced from other locations (e.g. fish • • • • revention void contamination from waters S U and/or application offertiliser. through feeding correct regimes I seeding. tothey appearespeciallyprior their problem weedsHarvest assoon 1–2 years. ponds every and de‑silt Dry ncrease phytoplankton turbidity ervice for advice).ervice se a herbicide (contact Extension (contact se aherbicide chemical use and legislation (january 2007)

Chemicals play an important role in Fish farmers need to familiarise The APVMA may allow the use of aquaculture in the management of fish themselves with the rules and unregistered chemicals, or registered diseases, the improvement of water regulations of these Acts in order to use chemicals off‑label, under a minor use quality and the control of aquatic chemicals legally. permit (MUP). MUPs are a ‘temporary’ vegetation. approval system for the use of chemicals Few chemicals are registered in Australia when no alternative treatment is In Australia, the Australian Pesticides for aquaculture use. To be approved registered. The APVMA still carries out a and Veterinary Medicines Authority for use in food animals a drug must risk assessment before issuing an MUP. (APVMA) regulates the supply of generally undergo rigorous testing of chemicals used in agriculture, including its efficacy for treating specific diseases It is important to verify with the APVMA aquaculture. In NSW other relevant in each species at specific dosages and the applicability and validity of any legislation relative to chemical use routes of administration. Data must be MUP (this can be done using their web includes the Stock Medicine Act 1989, the obtained on residue dynamics, safety site) and/or to verify with NSW DPI Pesticides Act 1999 and the Food Act 2003. for the operator and consumer, and under what conditions a chemical can Several agencies [e.g. NSW DPI, NSW effects on the environment. This can be used. Some chemicals registered for Food Authority, and Food Standards require years of experimental trials and use on other food‑producing animals Australia New Zealand (FSANZ)] work high costs. At the end of the process (e.g. chickens, sheep or cattle) may be closely with the APVMA administering registered drugs must be used only in able to be used off‑label with written

issues dealing with chemical evaluation accordance with the label to treat the veterinary directions (prescription). 2007) and chemical residues in food. species on the label at the directed dose Some chemicals used only for water y rates. treatment and with no residue concerns Further information can be obtained at are exempt from registration (see some www.apvma.gov.au,

specific examples in Table 1). ( j anuar t ion www.foodstandards.gov.au and www.dpi.nsw.gov.au. legisla emical use an d use c h emical •

65 | p Table 1. Status of chemicals in the aquaculture industry (Nov 2005)

Registered Minor Use Permitsa Exempt AQUI‑S (Isoeugenol) Formalin Zeolite Buserelin (GRH) Benzocaine Calcium carbonate Chorulon (Chorionic Gonadotrophin) Hormones (Ovaprim, OvaRH, LHRHa) Calcium hydroxide Anguillvac C – (Vibriosis C vaccine) Oxytetracycline Inorganic fertilisers Copper sulfate Organic fertilisers Trichlorfon Propionic acid Sodium chloride Registered chemicals and MUPs must Potassium permanganate be used according to label instructions. a Check with the APVMA for expiry dates Before using any chemical to treat aquatic animals confirm that it is approved for use with the APVMA or your NSW DPI advisor to avoid illegal 2007) y use and possible residue contamination. ion ( j anuar t ion legisla emical use an d use c h emical •

66 | p Table 2.I preparedness mustbeinplace ( features, strategies andadegree of maintain fishhealth,specificdesign To keepfishlossesto aminimumand (DO waterSuperior meters andkits quality in eachpond/tank fishsize,Known numbersandbiomass Chemicals stored onsite specific water levels tankandpondvolumesKnown at NO Information im diagnose 3 , T , formalin, copper ) AN, pH,alkalinity, salinity, N0 p nformation to berecorded andessential design to criteria assistintheprevention, diagnosis, treatment andcontrol ofsilver perch diseases. ortant /Design , treat

information Table 2 2 , ). ).

fewer stock lossesandcosts. operatepractices efficiently andhave Silver perch adoptingthese farms and

control • • • • • • • • C

omment formalin orcopper treatment. during Need to accurately determine andmaintain concentrations of S meters advisable. problems intanks andpurging systems; possessionoftwo DO possible aetiological agents; diagnosis ofwater quality process indiseasediagnosis and/orelimination ofother A pellet size). viaaccurateOptimum nutrition feeding schedules (rations, medicated feeds basedon%bodyweight (biomass). S rate).(prevalence, mortality A overcapable ofrapid spread 2–3days. andhighmortalities Prompt diseasetreatment; white spotandchilodonellosis to stockhealth; ability eggsandfishat densities. correct disease control; prevention ofoverdosing, dangerous to fish of underdosingcausingineffective treatment andpoor A re ystemic diseasecontrol through theapplication of afe useofC ccurate records facilitate confident interpretations; integral ssists indiseasediagnosis; recording ofdiseaseevent history pplication ofaccurate chemicalconcentrations; prevention q uired uSO

disease 4 dependent upon alkalinity levels. dependent uponalkalinity

to p re v ent ,

p|67 • important information require dto prevent, diagnose,t reat and controld isease p|68 • important information require dto prevent, diagnose,t reat and controld isease lines flushing ofbores, andwater bio‑filters exchange intanks/ponds;daily A and ponds oftanksmonitoring; dailyobservation R A surface water surface W Bottled oxygen,Bottled linesandairstones equipment M Information egular water anddisease quality eration bility to providebility rapid water ater source – bore orscreened icroscope, samplinganddissection /Design • • • • • • • • • • • • • • • C omment DO following chemicaluse(formalin, C A of diseaseandpoorwater quality. O prevention diseasedueto oflow periods DO ofbacterial M aeration intanks.Emergency introduction oftrash fishpotentially disease. harbouring water (rivers,Surface dams)filtered to <500 Bore water ispathogen-free. Flushing ofhighlevels ofammonia/nitrite andH R episodesofpoorwaterduring quality. Essential emergencies during to secure stock particularly growth anddisease. Discouragement ofbird predation; stress canleadto poor colour. ofbehavioural irregularities orchangesinwaterObservation detection/treatmentEarly andprevention ofmajorlosses. Essential for diseasediagnosis, treatment andcontrol. ‘collapse’ ofthebio‑filter. Prevention andpoornitrificationor oforganics inbio‑filters additional paddles;PT Failsafe measures are mandatory hotweather orovercastdie‑offs, conditions. apid dilutionofchemicals(over‑dosing). bility to providebility additionalaeration episodesoflow during xygen is essential for fish health particularly during periods during isessential forxygen fishhealthparticularly aintenance of fish health during harvest andtransportation;aintenance harvest offishhealthduring O aeration – back‑up generators; uSO 4 ), phytoplankton µm willprevent 2 S. . Knowledge ofOH&SandzoonosesKnowledge withstaff/family sharing Knowledge contacts Extension V numbers Significant andtank tankcapacity generator Power generation; testing of weekly Information eterinarian, A eterinarian, ssociation and /Design diagnosis, trea tmen & tionpreven of • • • • • • • C omment poor water intanksandponds. quality A safety ofstaff Provide training andappropriate equipment for healthand procedures, power emergency configuration. standard operating procedures, volumes, treatment W stock by inventory more known thanoneperson. Farm operational procedures, water reticulation planand submissions; additionaltesting ofwater quality. diagnose andtreat disease;avenues for sample laboratory I introduction to andbetween pondsonthefarm. thefarm Essential for quarantine andprevention ofdisease harvests emergency To provide to hold/treat thecapacity fishfollowing nformation to andpermits obtainchemicals, investigate, utomated during ‘mains’ failure; prevents majorlossesdueto ritten andreadily accessible healthstrategy planoutlining

the diseases of

the australian freshwa ter fish silver h perc (b idyanus bidyanus )

p|69 • important information require dto prevent, diagnose,t reat and controld isease calculations, treatments and dose rates

Treatments can be of great value when used properly but when incorrectly applied, can cause large losses of fish. In order to properly apply chemicals to the water or feed, it is important to accurately determine the dosage and the best application methods.

volume conversions 1,000 mL (millilitres) = 1 L (litre) 1,000 L = 1 m3 (cubic metre) 1,000,000 L = 1 ML (megalitre) Volume of water (round tank) = 3.142 × r2 (radius) × d (depth) Volume of water (square tank) = l (length) × w (width) × d (depth) Volume of pond = length (m) × width (m) × mean depth (m) weight conversions 1,000 µg (micrograms) = 1 mg (milligram) 1,000 mg = 1 g (gram) = 1 mL (millilitre) of water t es 1,000 g = 1 kg (kilogram) = 1 L (litre) of water 1,000 kg = 1 t (tonne) = 1 m3 of water ose ra d ose

length conversions s an d s 1,000 µm (microns) = 1 mm (millimetre) t men 10 mm = 1 cm (centimetre) t rea 1,000 mm = 100 cm = 1 m (metre)

ions, t ions, area conversions 1 ha (hectare) = 10,000 m2 = 2.5 acres

calcula 2 • 1 acre = 0.4 ha = 4,000 m (e.g. a pond measuring 50 × 80 metres) 70 | p diagnosis, treatment & prevention of the diseases of the australian freshwater fish silver perch (bidyanus bidyanus)

concentrations ppm = part per million, ppt = part per thousand liquid chemical forms solid chemical forms 1 ppm = 1 L (litre) in 1,000,000 L = 1 mL in 1,000 L 1 ppm = 1 mg in 1 L = 1 g in 1,000 L 20 ppm = 20 L in 1,000,000 L = 20 mL in 1,000 L 20 ppm = 20 mg in 1,000 L 1 ppt = 1 mL in 1 L 1 ppt = 20 g in 1 L 5 ppt = 5 kg in 1,000 L active ingredient (a.i.) Treatment rates unless otherwise stated are based on the active ingredient (a.i.) only. Dose (g or mL) = Volume (m3) × Concentration of Therapy (ppm) × 100 ÷ % a.i. example calculation A pond (3.2 ML) is to be treated at 0.5 ppm with a liquid chemical having 40% a.i.

3

Dose (mL) = 3,200 m × 0.5 × 100 ÷ 40 = 4,000 mL = 4 L t es

Formalin Precautionary measures when using • Paraformaldehyde ose ra d ose formalin. Formaldehyde solution, also known Formalin should be stored in the as formalin, contains 37% to 40% • Oxygen dark and above 4°C to inhibit an d s dissolved formaldehyde gas; however, paraformaldehyde formation, a toxic Each 5 mg/L of formalin added to a t men for application it is used as if it was white precipitate; if present, decant and

pond can remove 1 mg/L of DO from t rea a 100% pure compound. Formalin is use clear liquid only. the water at temperatures over about depleted rapidly in ponds and the rate

20°C. Formalin kills some algae and • Water quality t ions, can vary according to factors such as micro‑organisms, which then decay temperature, aeration, fish biomass Formalin is more toxic in soft, acid water using oxygen. and organic matter. In general, formalin and at high temperatures. Formalin calcula • reaches ineffective concentrations • Aeration undergoes a series of chemical reactions 71 | and breaks down quickly in pond water p within 48 hours and most of the Ponds and tanks must be continually (within 4 days). formalin is lost within 4 days of aerated during formalin treatment. application to ponds. To prevent under Oxygen levels must be regularly • Fish or over‑dosing and to maintain effective monitored. Additional aeration may be Some fish are more sensitive to formalin concentrations, a formaldehyde test kit needed during formalin treatment. should be used to accurately monitor than others. formalin concentrations. p|72 • calculations,t reatments and dose rates will ensure antibiotic thecorrect isselected. that contains anantibiotic. A M well‑ventilated areas. Protective clothingshouldbeworn handling. during Formalin isvolatile andcancauserespiratoryproblems. Handleandusein additional feed that isgiven shouldbenon‑medicated. the bodyweight perday becausesick fishgenerally have reduced appetites. A I Medicated n practice thefeedingn practice rate whenusingmedicated feed be0.5%or1%of willoften • much antibiotic mustbeaddedto thefeed to provide dosage? thecorrect level for the antibiotic is75 fish are feeding at 1%oftheirbodyweight perday. The recommended treatment diet. The commercial premix contains 5% of the active ingredient (antibiotic). The A pondof2,000fish,meanweight 350 Ex 4. 3. 2. A 1. A any diseasesoffishcanbesuccessfully bacterial treated withmedicated feed Human health The dailyration oftreated feed =7kg = 10.5 The premix ingredient has5%active therefore 525g÷0.05 = 525g = 525,000 = 75 = 70 ample t 1%bodyweight feed rate, 700 ntibiotic treatment rate is75 mg ×700kg10days kg in10 kg ofantibiotic premix isto beaddedto the feed. /

calculation 70 kgfeed Feed mg days.

– Oral mg active ingredientmg active ccurate diagnosis ofthecausative agent ofthedisease

mg/kg fishperday

kg fishrequire 7 medication g (700 / day kg offish)isto befed medicated / kg offishfor 10days. How

kg feed / day

ny veterinary diagnostic laboratory.veterinary testingand antibiotic at sensitivity a of thediseaseneedsidentification used inthefeed, thecausative agent To ensure antibiotic thecorrect is and become inactivated. appropriate asthechemicalsbreakdown daily. S be madeupasfresh aspossible place.cool, M dry M fish when being challenged by a disease. feed andisusefulto assistrecovery of increase theacceptance ofmedicated W likely to result inworse outcomes. dosing are equallyunproductive andare resistance. O prevent thedevelopment ofantibiotic dosing andduration oftreatment help appear to have recovered. A days recommended, even ifthefish should befed for thetotal numberof maximum recommended doseand Treatments shouldalways beto the medicated feed. points whenusingImportant • • • • edicated feed shouldbestored ina ithholding food for 12to 24hoursmay Diagnosis Storage Fasting Treatment torage beyond 10days isnot

verdosing andunder

edicated feed should ppropriate – ideally ingested by thefish. antibiotic into thewater, to prior being the feed. This assistsinavoiding lossof U medicated feeds. handling antibiotic premixes and including gloves andaface maskwhen A control parasites, fungusorviruses. A drug coating. only longenoughto ensure aneven To avoid pelletbreakage, stirgently and cement mixer. byto handorusinga thepellets stirring mixtureSlowly addthedrug‑gelatine dissolved. S 2.8 Slowly dissolve 125 M Gelatine (P Homemade • • • tir theantibiotic into the gelatine until lways wear protective clothing ntibiotic medicated feeds donot se gelatine to bindtheantibiotic to akes 45 iper etal. 1982) Gelatine Human safety Target diseases litres ofhotwater. kg offeed for large fish.

medicated

g ofgelatine in

feeds

diagnosis, neutral. the pellets. Pour over mixture orspray thedrug‑oil warm oil. mixthedrugevenly intoQuickly the Heat soybean oilto ~ feed. 100 parts U Soy oil and C copper hydroxide complexes ( most abundant at low pH,whilethe hydroxide complexes; ionis cupric of copper are ionandcopper cupric are toxic to silver perch. The toxic forms concentrations of0.25 e.g. salmonidsare highlysensitive, and species are equally tolerant to copper, (see ‘ figure whendetermining thedosage calculations shouldbebasedonthis approximately 24.5%copper and value. C ashavingreported somebactericidal hexastichaChilodonella . I as Ichthyophthirius multifiliis and diseases causedby protozoans such filamentous algae, orto control to pondsto control algae, including C sulfate Alk opper (ascopper sulfate) isapplied se a wt:wt ratio of 2 to 3 parts oil: se awt:wtratio of2to 3parts trea alinity Active ingredient tmen u ( opper sulfate contains OH) (C & 2 tionpreven of u predominate at pH’s above

SO and 4 )

copper ’ above). Notallfish 40°C. mg/l andhigher

the t isalso diseases of

C uOH

the australian lime (aslimestone, C can beincreased withtheadditionof should be>50 to copper sulfate application and should beaccurately measured prior the diseaseiscontrolled. A the level between 0.1–0.2 followed by dailytreatments to maintain 0.2 to treat diseasesinsilver perch is treatment regime whenusingcopper of 80–100 silver perch even at highalkalinities of 0.25 skin colour.skin C swimming at pondedges, anddark silver perch includeinappetence, fish clinical signs ofcopper toxicity in and disruptthefish’s ionregulation; levels ofcopper cancausegill damage higher presence ofthetoxic forms. Toxic applying copper sulfate becauseofthe special care mustbetakenwhen compounds. I with thecopper to form lesstoxic reduce toxicity by combining chemically bases, associated withhigheralkalinity recommended levels. The increased remained belowwhen alkalinity reduce copper toxicity insomespecies of calciumhardness can andsalinity research hasshown specificlevels however,modifier ofcopper toxicity; A lkalinity isregarded asthemainlkalinity (active ingredient)mg/L (active initially, freshwa mg/L andabove are toxic to mg/L. The recommended ter oncentrations ofcopper n waters oflow alkalinity, fish mg/L asC silver aCO h perc aCO 3 ; dolomite, mg/L until lkalinity lkalinity (b 3 idyanus bidyanus ; alkalinity ; alkalinity )

p|73 • calculations,t reatments and dose rates p|74 • calculations,t reatments and dose rates food source. arefingerlings reliant onplankton asa andsmallused inpondswhere larvae pond zooplankton andshouldnotbe corrosion. C steel, shouldbewell to rinsed prevent containers holding copper, particularly water treated withcopper and (sheep, cattle etc) shouldnotdrink agriculturalcause irritation; stock andeyes maycompounds withskin the treatment. C aeration shouldbeprovided during algae; additionalandcontinuous low levels following thedeath ofthe concentrations to drop to dangerously containing algae, may causeoxygen sulfate. C whenusingcopperbe observed S the treatment andDOmeasured daily. be maintainedtheduration during of copper concentration. A used dailyto measure theponds/tank spots’. Areliable instrument shouldbe pond area to avoid thecreation of ‘hot to dispersethecopper over theentire (or tanks)andcare shouldbetaken dissolved before applyingto ponds copper sulfate shouldbethoroughly can beincreased usinggypsum. The C (NaHCO ome precautionary measures shouldome precautionary aMg ( CO 3 ); calciumhardness andsalinity opper treatments inponds 3 ) 2 ) orsodiumbicarbonate opper isalsotoxic to most ontact ofcopperontact eration should and ‘ as known ‘permanganate ofpotash’ Potassium permanganate (KM manganese dioxide (M the permanganate ionisreduced to culture water ishigh.Once applied, required iftheorganic content ofthe chemical; higherconcentrations are immersion inat least2 Effective treatments require aprolonged and dissolved organic compounds). of organic matter (e.g. algae, detritus, from solutiondueto theoxidisation tanks. The chemicalmay berapidly lost both safe andeffective inpondsand to achieve treatment regimes whichare requires andeffort careful observation The useofpotassiumpermanganate sulphide from water. used to remove iron andhydrogen Potassium permanganate canalsobe diseasesinsilver perch.bacterial proven beneficialincontrolling some tanks following offishhas harvest dissolved inwater. I powder thatis acrystalline iseasily by protozoans andmonogeneans. I fish diseases, includingthosecaused compound that cancontrol some the chemical inactive; thewaterthe chemicalinactive; colour (KM Potassium nO C ondy’s crystals’, isachemical 4 ) permanganate ts application to nO mg/L ofactive 2 ) rendering nO

4 ) also t recirculating aquaculture systems). (RAS permanganate (andotherchemicals)to approach when applying potassium I treatment. needed for apotassiumpermanganate 2.5 to calculate theconcentration (mg/ L) concentration ismultipliedbyof afactor remains isconsidered theendpoint. This concentration inwhichthepinkhue for 15 and observed concentrations of1,2,3,4and6 having 1 containers (orclearplasticbags)each done. The chemicalisaddedto five glass simple 15minute demandtest canbe potassium permanganate needed, a a pond. To determine theamount of permanganate shouldbeaddedto more than6to 8 is restored. I of 2 should bere‑treated usingincrements has changedcolour within8hours clear glasscontainer. thewater inathe airorobserving regularly by splashingwater into water colour shouldbeinspected whether are‑treatmentisrequired, water inponds. quality To determine to differences inorganic content and tan. dueThe rate reduction canvary changing from apinkhueto alight t isadvisableto adoptaprecautionary mg/L until the light pinkcolour litre ofculture water to achieve t isrecommended not mg/L total potassium minutes. The lowest W ater which mg/L, be dissolved ina separate container and 15–30 mins. A then dissolves slowly over thefollowing S adverse environmental effects. of thelarge quantities required and should notbeusedinpondsbecause prevent nitrite toxicity. S inRAS of fishintanks. I andpreventtransport, fungalinfections relieve stress handlingand during treat infestations ofsome ectoparasites, S acids. combustible materials includingstrong sunlight andaway from flammableand area, outofdirectin acool dry be stored inatightly closedcontainer, gloves).dust mask, The chemicalshould itshandling(protectiveduring clothing, with formalin andcare shouldbetaken permanganate shouldnotbemixed dioxide onthegills. Potassium deposition ofinsolublemanganese to fishinwater having highpHdueto toxic be may permanganate Potassium operation. ofeachRAS withthedesign andthe effectsmay vary effectsonnitrification,butinhibitory Potassium permanganate canhave Salt alt can be added directly toalt canbeaddeddirectly tanks; it (NaCl)isusedtoalt orsodiumchloride (N aCl) lternatively, thesaltcan t canalsobeusedto alt diagnosis, C and caneasilybedecanted. however, this is usuallyofnoconcern foam oftanks; to form at thesurface deteriorates. S flushed andre‑treated ifwater quality salt treatments andtanksshouldbe nitrite) shouldbemonitored during parameters (DO salt shouldbeused. Noniodizedadded slowly to thetank. low water temperatures). S eradicated (may beupto 4weeks at a bath of2 ichthyophthiriosis (white spot)requires repeated 24 after 10 chilodonellosis is effectively treated with static baths (i.e. noflow). For example, (1 with short‑term I following handlingandtransporting. stress andprevent fungalinfections recommended to relieve osmotic 0.2–0.5%; 2,000–5,000 nitrite; therefore 2 willprotect fishfromchloride 1part adding salt. G purging systems canbecontrolled by (‘brown blood’ and disease)inRAS (e.g. higher dosagesfor effective control parasites (e.g. gill flukes)may require nfestations ofectoparasites are treated oncentrations of2–5 trea g/L for 1 15 tmen g/L, 1 & g/L until the pathogen is h (thetreatment shouldbe tionpreven of h bath). N enerally 5 to 6 parts ofenerally 5to 6parts alt treatments cancause , T h), whereas control of , salinity andAN, salinity g/L shouldprevent h) orlong‑term, W g/L (2–5ppt; mg/L) are ater quality

itrite toxicity the diseases of ome larger

the australian dichlorvos; the chemical reaction is thechemicalreaction dichlorvos; toxic more the to degrades trichlorfon of theparasites. system an essential enzyme nervous withcholinesterase, by interfering acts flukes andanchorworms. The chemical crustacean ectoparasites suchasgill infestations ofmonogeneanand that canbeusedto treatinsecticide Trichlorfon isanorganophosphate of saltlevels inthefarm’s water system. store salinewater to prevent abuildup should have aspecificeffluent pondto difficult to handleanddissolve. Farms causes thesaltto cakerendering itmore likely to have ‘sweated’ whichoften R surfaces. andawaylow humidity from metal areaand shouldbestored with inadry S recirculation. water normal toflushed prior re‑joining at recommended saltrates andthen isolated from thebiofilter, treated to adjust. A few days)every to allow thebiofilter be addedinsmallincrements (<2 saltshould decrease biofilter efficiency; R nitrite toxicity problems insilver perch. Trichlorfon alt isusuallypurchased in25 apid additionofsaltto can RAS freshwa ecently‑packed saltisless lternatively, tankscanbe ter fish W silver hen addedto water, h perc (b idyanus bidyanus kg bags g/L

)

p|75 • calculations,t reatments and dose rates p|76 • calculations,t reatments and dose rates trichlorfon and/or dichlorvos toxicity. and/ordichlorvos trichlorfon Fish gasping, indicate rolling orshaking allow 2–3weeks between treatments. between treatments. I should bewell aerated andflushed and/or resistance problems. Tanks treatments totrichlorfon avoid toxicity is required whenusingrepeated thereforetrichlorfon; somecaution persistent, degrading more slowly than ismoredichlorvos, toxic andcanbe or cages. The majorbreakdown product, whentreating smalltanksparticularly mixed withwater to prior application To avoid ‘hotspots’, thedoseshouldbe to applytheappropriate concentration. need to beprecisely calculated inorder system. Pond andtankwater volumes and adversely affectthefish’s immune Trichlorfon canbehighlytoxic to fish, as longpossible. maintain aneffective concentration for be treated soasto morning intheearly temperatures should intheafternoon Ponds withhighpH(>8.5)and aeration, andhighpHtemperature. accelerated bysuchaslight, factors t isadvisableto trichlorfon treatment areas.trichlorfon it isadvisableto stay upwind from other organophosphate pesticides, and otherhighlytoxic fumes. A andtherelease ofdichlorvos trichlorfon Heat may causethe decomposition of kept well place. packedinacool, dry strong oxidizing agents. I andisincompatibleof alkalis, with will alsodecompose inthepresence handling thechemical. Trichlorfon and overalls mustbeworn when clothing includingrespirator, gloves Protective throughabsorbed theskin. organophosphates, isreadily trichlorfon A and storing trichlorfon. C perch andponds. and reduce adverse effectsonsilver prevent thedevelopment ofresistance to treat infestations ofgill flukesmay andformalinof alternating trichlorfon Astrategywith long‑term useonafarm. may become resistant to trichlorfon crustaceans andzooplankton. Gillflukes Trichlorfon isalsotoxic to some are mustbetakenwhenhandling t shouldbe s withall s with sufficient. your have withholdingperiods been R regarding withdrawal periods. A good ruleofthumbis600- times are notgiven for achemical, a 500 (25 treatment, thedegree days would be 20 mean temperature were 25°Cfor the number ofdays measured. Thus ifthe daily water temperatures for thetotal are calculated by addingthemean required withdrawal time. Degree‑days has beenadvocated for estimating the ofthis,Because theterm ‘degree days’ conditions, especiallytemperature. greatly withenvironmentalcan vary consumption. The excretion ofadrug present in food for fish harvested human tofarmer ensure illegalresidues are not prescribing thetreatment andthe I Withdrawal t isthelegalresponsibility oftheperson esidue tests are available to ensure lways seekadvice from aveterinarian days immediately stopping after the × 20). W hen specificwithdrawal

Periods

degree days. diagnosis, treatment & prevention of the diseases of the australian freshwater fish silver perch (bidyanus bidyanus) NOTIFIABLE FISH DISEASES

Within Australia, lists of notifiable or greatly assists in the understanding reportable fish diseases are defined by and management of diseases and helps each state. The lists include all relevant protect other aquaculture industries. Office International des Epizooties (OIE) Two of these diseases, Epizootic listed notifiable diseases that represent Ulcerative Syndrome (EUS) caused by Australia’s international surveillance, the fungal pathogen Aphanomyces monitoring, notification and reporting invadans, and Goldfish Ulcer Disease obligations. These diseases are (GUD) caused by the bacterium considered important for social, Aeromonas salmonicida nova have been economic, international trade and public reported in silver perch. health reasons. The current NSW Notifiable Diseases list In NSW declared diseases are listed in and other relevant information can be the Fisheries Management (Aquaculture) viewed at www.legislation.nsw.gov.au under Regulation 2007. the Fisheries Management (Aquaculture) In NSW it is a condition of the Regulation 2007. Aquaculture Permit that all significant disease outbreaks are reported to a Fisheries Officer. This will lead to an accurate diagnosis of the disease and the implementation of any control and/or containment measures that may be required. This information H D ISEASES F IS H T I F IA B LE NO

•

77 | p p|78 • glossary of crustaceans The combined headandthorax region C fin isattached The regionto which thecaudal ofbody C Protozoan peripheral bearing cilia C ciliated protozoa Hairlike locomotor organelles of C grow to theoriginalform whicheachdaughterdivide after cell Asexual reproduction where cells fission Binary dye thatcanproducts stainedby be abasic to acell,Applied itscomponents, or Basophilic of adiseasecondition Showing nosymptoms; novisiblesigns A serous cavity fluidintheabdominal effusionandaccumulationAn of A of disease The science thatdeals withthecause A wash carbol‑fuchsin (red dye), heatandalcohol stainingtechniqueA laboratory using A glossary ephalothorax audal peduncle iliate ilia etiology cid fast symptomatic scites internal body surfaces internal body The cellular covering and ofexternal Epithelium a sample. presence oranantigenin ofanantibody mainly inimmunology to the detect isabiochemicalAssay technique used ImmunoSorbent The Enzyme‑Linked ELISA together withnoharmto either living surface; host’s the on Organisms E attachment or reference of point the from Away Distal within thecell membrane ofcellPart outsideofthenucleus and C recurring rate;gradual also orconsistent mortality overOccurring oftime, alongperiod with Chronic eye from the orbit Abnormal protrusion ofthe oftheglobe Exophthalmos addition ofnutrients of waterThe enrichmentofabody by the E Wasting ofthebody Emaciation apopulation A diseaseaffecting Epizootic utrophication cto‑commensal ytoplasm Foci locomotion ofsomeprotozoans for used is that organelle Whiplike Flagella activity Rapid andabnormal increased respiratory Hyperventilating normal cells intissueoranorgan Abnormal increase inthenumber of Hyperplasia excessAn part inabody ofblood Hyperaemia parasites Tissue to invading; usually pertaining Histozoic changes indiseasedtissue The studyofmicroscopically visible Histopathology The escape from ofblood vessels Haemorrhage cells) (phagocytic aggregationsnodular ofmacrophages response withA chronic inflammatory Granuloma onthecelldependent walls constituents Staining characteristics ofbacteria Gram negative ( to, oremanatingfrom afocus pertaining to atissueaslimited to asmallarea, The size ordistributionofchanges Gram positive) In adyingstate M withoutknowncauseOccurring Idiopathic ofoxygen Deficiency Hypoxia comparedthe body to theenvironment High concentration ofsalts/compounds in Hyper‑osmotic Bony covering ofthegill Operculum tissue spaces The excessive accumulation offluidsin O environment only inaparticular Characterised to bysurvive theability Obligate body living a within cells or tissues of death The Necrosis death involving dissection after fish the of examination medical A Necropsy to fungi Pertaining M organisms The science oftheform andstructureof M edema oribund orphology ycotic diagnosis, Pyriform orprotection from disease Defending Prophylactic with thetemperature oftheenvironment temperatureHaving abody thatvaries Poikilothermic water surface offishgulpingorgaspingattheThe act Piping andothercells foreignbacteria, particles ingesting of capable cell inflammatory An Phagocyte organs cavityAbdominal whichcontains various Peritoneal cavity mother’s body Egg laying, withhatching outsidethe O facilitate normalcellular function Control ofionicconcentrations to Osmoregulatory Attached, not mobile S Lateral, abnormalcurvature ofthespine S toxin bacterial often with pathogenic organisms or their toxins; Systemic associated diseaseintheblood S Pear‑shaped essile coliosis epticemia viparous trea tmen & tionpreven of

the diseases of

the australian un‑ionised andionisedammonia Total Nitrogen; thesumof Ammonia TAN orgills) skin affecting asawhole(versus thebody Affecting only S transmitted to humans A diseaseofanimalsthatcan be Zoonosis dead tissue;can haemorrhagic be or tissuecaused by damageandlossof A localofanorgan onthesurface defect Ulcer oraforeignpathogen body response to aa chronic inflammatory orraisedSmall nodule area onasurface, Tubercles epithelium and skin The feedingstageofI.multifiliisundergill Trophont stageinI.multifiliis from thecyst The smallciliated stagethatisreleased Tomite I. multifiliis The free‑swimming, infestive stageof Theront ystemic freshwa ter fish silver h perc (b idyanus bidyanus

)

p|79 • glossary p|80 • references an dfurther reading Brown, L.(E New S pp. ofA 154‑180. Department February 1983.(E Culture Hoffman, G.L(1999). C American Freshwater Fishes, University of Hoffman, G.L(1967).Parasites ofNorth First Freshwater Aquaculture Workshop pitheliocystis insilver perch,(1997). Epitheliocystis Frances, J., Tennent, B.F. R.andNowak, Bay, A pp. 67‑75.A Diseases ofsilver perch. I C C Bidyanus bidyanus (2002) Aquaculture andAquatic Health Animal Fish Diseases American Freshwater Fishes in fishculture. I A University ofS Foundation in 2002, Published by Post Graduate Veterinarians references ornell University Press.ornell alifornia Press, Berkeley. pp486. allinan, R.B. andR shburner, L.D. (1983).Diseaseproblems ustralia. , Proceedings 347,17‑19A outh (E ds S.J. R W ditor) (1993). ustasia A

. Pergamon Press L 20 ales, S ydney. V n, , 453‑457. eterinary S eterinary owland andC.Bryant), ditor L.F. R (M Proceedings ofthe owland S.J. (1995). ydney. quaculture, S itchell). Parasites ofNorth n, Aquaculture for , 2nded, cience, Silver Perch eynolds),

Journal ofJournal griculture and td. pril, andy ,

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