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N S W D P I

Phil Read Matthew Landos Stuart J. Rowland Charlie Mifsud

DIAGNOSIS, TR EATMENT &

PREVENTION OF THE DISEASES OF THE

AUSTRALIAN FRESHWATER FISH

SILVER PERCH Bidyanus bidyanus

Fisheries Research andDevelopment Corporation



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DIAGNOSIS, TREATMENT AND PREVENTION OF THEDISEASES OF THE AUSTRALIAN FRESHWATER FISH

SILVER PERCH Bidyanus bidyanus

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



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DISCLAIMER

The information contained in this publication isbased on knowledge and understanding at the timeof writing (April 2007). However, because of advances

in knowledge, users are reminded of the need toensure that information upon which they rely is upto date and to check currency of the informationwith the appropriate officer of New South WalesDepartment of Primary Industries or the usersindependent adviser..

CHEMICAL USE

ALWAYS READ THE LABEL

Users of agricultural (or veterinary) chemicalproducts must always read the label and any Permit,before using the product, and strictly comply withthe directions on the label and the conditions of anyPermit. Users are not absolved from compliance withthe directions on the label or the conditions of thePermit by reason of any statement made or not madein this publication.

State of New South Wales through NSWDepartment of Primary I ndustries (April 2007). Youmay copy, distribute and otherwise freely deal withthis publication for any purpose, provided that youattribute NSW Department of Primary Industries asthe owner.

ISBN 978 0 7347 1792 4

JOB NUMBER 5938

FOR FURTHER INFORMATION

GRAFTON AQUACULTURE CENTRE

PMB2, Grafton NSW 2460Ph 02 6640 1690, or

PORT STEPHENS FISHERIES CENTRE

Locked Bag 1, Nelson Bay NSW 2316Ph 02 4982 1232


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DIAGNOS IS , TREATMENT & PREVENTION OF THE DIS EAS ES OF THE AUS TRALIAN FRES HWATER FIS H S ILVER PERCH Bid y an u s b id y an u s

ACKNOWLEDGEMENTS 3

INTRODUCTION 4

ANATOMY OF SILVER PERCH 6

DIAGNOSTIC TECHNIQUES 9

DISEASES AND PATHOGENS 16

ECTOPARASITIC PROTOZOANS 16

Chilodonellosis Chilodonella hexasticha

Ichthyophthiriosis (white spot, ich) Ichthyophthirius multifiliis

Ichthyobodosis Ichthyobodo necator

Trichodinosis Trichodinasp.Tetrahymenosis Tetrahymenasp.

MYXOZOAN INFECTIONS 24

Henneguyaspp.

ECTOCOMMENSAL CILIATES 26

Ambiph yraspp.

MONOGENEANS 27

Lepidotrema bidyana

COPEPODS 29

Anchor worm Lernaeaspp.

Ergasilusspp.

CESTODES AND NEMATODES 32

TABLE OF CON TENTS

FUNGAL DISEASES 34

Saprolegniosis Saprolegnia parasitica

Epizootic Ulcerative Syndrome (EUS, Red SpotDisease) Aphano myces in vadans

BACTERIAL DISEASES 39

Columnaris Flavobacterium columnare

Tail rot syndrome

Goldfish ulcer disease Aerom onas s almon icida nova

Streptococcosis Streptococcus iniae

Mycobacteriosis Mycobacteriumspp.

Aeromonad dermatitis Aeromo nasspp.

Epitheliocystis

VIRAL DISEASES 50

Epizootic haematopoietic necrosis (EHN)

MISCELLANEOUS NONINFECTIOUSDISEASES, DISORDERS AND

CONDITIONS 51

Hypoxia

Hydrogen sulphide poisoning

Gas supersaturation (Gas bubble disease) Noxious algae

Cloudy eyes and red tails

Physical abnormalities

Abdominal swelling (bloat)

Nutritional disorders

Aggression

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ABLEOF

CONTENTS

DISEASE PROBLEMS IN PURGING

SYSTEMS 62

AQUATIC PLAN TS AND FI SH HEALTH 64

CHEMICAL USE AND LEGISL ATION

JANUARY 2007 65

INFORMATION REQUIRED TO PREVENT,

DIAGNOSE, TREAT AND CONTROLDISEASE 67

CALCULATIONS, TREATMENTS AND

DOSE RATES 70

Formalin

Medicated feed

Alkalinity and copper sulfate Potassium permanganate

Salt

Trichlorfon

Withdrawal periods

NOTIFIABLE FISH DISEASES 77

GLOSSARY 78

REFERENCES AND FURTHER READING 80


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The authors would like to thank andacknowledge the members of the native

fish hatchery and silver perch industriesfor their input and information over theyears, in particular Mark Scifleet and IanCharles.

We also thank the following whoallowed access to their facilities andshared their knowledge of fish diseases;Paul Trevethan, Alan and John Hambly,

Noel Penfold, Calvin and Lisa Terry, BruceMalcolm, Ray Partridge, Roger Munzel,Trevor Pontifex, Andrew Yazbek, Craigand Parry Anderson, Nic Arena, SteveGrammer, Nick Lambert, Grantley Blake,Jim Cliffe, Lindsay Fraser, Ainsley Pope,Lindy Trudgeon, Marcia Thompson,Ron and Peter Randall, Bruce Rhoades,Graham Bailey, Steve Wood, Gar y Webb,Dennis Bressan, Dennis Cole, AlbertCooke, Nathan David, Colin Dickson,Michael Gilbert, Bob Hamilton, JohnHeslin, Roger Kershaw, Mat Kilham, ChrisLawson, Rob McCormack, Peter Moore,Gay Passfield, Ross Thompson, Laurie

Tomlin, Steve Vidler, Roger Camm, TrevorWalshe, Gary Webb, Bob Overguard,

Charles Faulkner, Mike Beveridge, SamClift, Jeff Guy, Ric Mailler, Andrew Pratt,Grant Webster, Tom Sole, Geoff andBen Pope, Ian Brunton, Rob Bartley,Ross Burton, Brian Taylor, Stan Moore,Michael Hickey, Bruce Sambell, WarwickReakes and Mike Murphy.

We thank Dr Gordon Beakes (UK),

Professor Iva Dykova (Czech Republic),Dr Craig Hayward (University ofQueensland) and Dr Brett Ingram(Department of Primary Industries,Victoria) for their work and contributionon specific diseases and parasites, andPatrick Tully (NSW DPI) for his efforts andcontributions to photographic editing,sketches and diagrams.

The authors acknowledge the effort andinput of staff at the Narrandera FisheriesCentre, Wollongbar Agricultural Instituteand the Grafton Aquaculture Centre.In particular, we thank Dr RichardCallinan, Stephen Thurstan, Mark Nixon,

Peter Selosse, Ken Bock, Les Rava, PaulRobertson, Matthew Hollis, Kevin Clark,

Peter Boyd, David Glendenning, NathanFerrie, Todd Rowland, Leo Cameron,Luke Ferguson, Joanne Murray, RalfJahrling, James Lang, Peter Dickson,Matt Parker, Brendan Palmer, Nat Sewell,Joel Crispin, Daniel Kratz, Andrew Ford,Tony McClymont and Steve Pepper.

This disease manual was prepared as

part of a project that was funded bythe former NSW Fisheries, including theAquaculture Initiative, the current NSWDepartment of Primary Industries, andthe Fisheries Research and DevelopmentCorporation (FRDC). We thank BillTalbot, Dr Nick Rayns, Dr Geoff Allanand Ian Lyall for their support andencouragement. We acknowledge andare grateful for the support of the silverperch industry by FRDC.

ACKNOWLEDGEMENTS

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CKNOWL

EDGEMENTS


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Silver perch (Bidyanusbidyanus) isan Australian native freshwater fish

endemic to the inland Murray-DarlingRiver System (Fig. 1). Hatcherytechniques were developed at theNarrandera Fisheries Centre (formerlythe Inland Fisheries Research Station)in the late 1970s, and transferred to anew commercial industry in 1982. Theroutine production of fingerlings bygovernment and private hatcheries over

the past 27 years has provided a solidfoundation for the development of agrow-out industry.

Research at the Grafton AquacultureCentre in the early 1990s demonstratedthat silver perch is an excellent speciesfor pond culture with high survival, fastgrowth and high production rates. Anindustry has been developing since the

mid 1990s and is based primarily onaerated, earthen ponds. There is some

production in recirculating aquaculturesystems (RAS) and cages, and theseintensive systems have potential forsignificant production in the future.Some silver perch farms have achievedhigh survival and production undercommercial conditions; however, forsuccess, farms must have a good supplyof high quality water, a reliable power

supply for aeration and pumps, begeographically located in a region thatenables fast growth and good health,and be well managed.

Diseases of silver perch under cultureconditions have been previouslydescribed by Ashburner (1983), Rowland(1983), Rowland and Ingram (1991)and Callinan and Rowland (1995). The

expansion of the silver perch grow-outindustry since the mid 1990s has seen a

corresponding increase in the incidenceof diseases, plus several new diseasesand pathogens including a winterfungal disease, gill flukes, and varioussyndromes and conditions. The commondiseases of silver perch are caused byprotozoans, monogeneans, fungi andbacteria. Diseases have had a significantimpact on commercial production

through induced stress on fish, loss ofgrowth and production, death of stockand high costs of treatments.

In 2001 2005, a project entitledDevelopment of a Health ManagementStrategy for the Silver Perch AquacultureIndustry was undertaken to study thediseases and health management ofsilver perch. Major outcomes were:identification of new and importantdiseases; development of control andpreventative methods for most diseases;and a health management strategy forthe industry based on three separate

Figure 1

Silver Perch (Bidyanus bidyanus).Source: Patrick Tully

INT RODUCT ION

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NTRODUC

TION


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publications, Health ManagementPlan for Silver Perch Culture, HatcheryQuality Assurance Program for MurrayCod (Maccullochella peelii peelii),Golden Perch (Macquaria ambigua)and Silver Perch (Bidyanus bidyanus)and the manual Diagnosis, Treatmentand Prevention of the Diseases ofthe Australian Freshwater Fish SilverPerch (Bidyanus bidyanus). This manualhas been prepared as an easy-to-usepublication with numerous photographs

of diseased fish and pathogens thatwill facilitate the prompt diagnosis andappropriate treatment of silver perchdiseases. Its use in conjunction with thehealth management plan, should reducethe incidence and severity of diseaseoutbreaks, leading to improved survivaland performance of fish, and increased

production, efficiency and profitabilityof silver perch farms.

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NTRODUCTION


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NATOMY

OFSILVERPERCH

Silver perch (Bidyanus bidyanus) belongsto the Class Osteichthyes or bony fishes.Teleosts are the highest bony fishesin evolutionary terms, and constitutethe largest group within Osteichthyes.Teleosts can loosely be divided intotwo main groups, the soft-rayed andspiny-rayed fish. The latter group, whichincludes silver perch, is more advancedand typically possess bony spines insome fins, ctenoid scales and a swim

bladder which lacks a connection withthe oesophagus. Most of the organsystems (heart, liver, kidney, etc) ofteleosts are similar to those found inmammals, with differences reflectingadaptation to an aquatic life. Thecardiovascular system consists of asingle circuit, with blood being pumped

by the heart to the gills from whereit passes under low pressure to thebody and then back to the heart. Silverperch also have lymphatic, nervous,reproductive and endocrine systems.Some organs, like the pancreas aredifficult to locate and are sited in

Figure 2

External features of silver perch.Source: Patrick Tully

Figure 3

Gross anatomy of the viscera of silver perch.Source: Patrick Tully and Phil Read

mesenteric fat between the pyloriccaecae (Figs. 2and 3). Silver perchare poikilothermic (cold blooded)

animals, i.e. their body temperatureis determined by the environmentaltemperature. Fins are median (dorsal,

ANATOMY OF SILVER PERC H

heartspleen

liverpyloric caeca

gall bladder

intestines

swim bladder

kidney

gonad

caudal muscle

trunk musclestomach

gill rakers

gill lamellae

nostril

operculum

pectoral fin

pelvic fin

urogenital aperture

anus

anal fin

caudal fin

caudal peduncle

dorsal fin (soft)

dorsal fin (spinous)

lateral line

nape


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NATOMY

OFSILVERPERCH

caudal and anal) or paired (pectoraland pelvic). The skeleton (Fig. 4) ismade up of the skull, vertebral columnand the fin skeleton. The skull has acomplex arrangement of bony plates(neurocranium) which still allowflexibility and surrounds the olfactory,optic and otic areas. The lower sectionof the skull (branchocranium) consistsof bones associated with the jaw,operculum and gill arches.

EXTERNAL FEATURES

Opercula bony cover which servesto protect the gills and assist withrespiration.

Lateral line pressure sensory organhaving epidermal pores; runs bilaterallyfrom head to caudal fin.

Fins bony/spiny and soft-rayed; assistwith locomotion, positioning andaggressive behaviour.

Figure 4

Main skeletal features of silver perch.Source: Patrick Tully and Phil Read

Figure 5

Diagrammatic representation of a section through fish sk in.Source: Phil Read (adapted from Storer et al. 1972)

Epidermis cellular-epidermal material,sloughed cells, and mucus secreted tothe surface; immuno-active properties;assist in osmoregulation and swimming;protects against abrasion; primary

protection against the environment;sensory receptors; excretory, somerespiratory functions; dermis containsmany pigment cells containing melanin(Fig. 5).

scaleopening of lateral line canal

epidermis sensory organ scale

dermis

lateral nerve muscle

pterygiophores

skull

ribsvertabrae

caudal vertabrae


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NATOMY

OFSILVERPERCH

Scales calcified, flexible plates withgrowth rings; covered by an epidermallayer of cells; assists in osmotic control;physical protection (Fig. 6).

RESPIRATION

Gills main respiratory organ; largesurface area; uptake of oxygen andexcretion of nitrogenous wastes andcarbon dioxide; maintenance of osmoticand ionic balance (absorption of water,

excretion of salts) (Fig. 7).

INTERNAL FEATURES

Swim bladder (gas bladder) thin-walledsac filled with gases; detects waterpressure changes; assists with bodybuoyancy and positioning; sound

production and perception.

Kidney excretion of water to maintainblood osmolarity balance; protein andion resorption; removal of nitrogenouswastes from the blood; anterior andposterior kidney.

Heart two chambered (atrium andventricle); posterior to gills in separatethoracic cavity; distributes blood viaarteries to the gills, organs and body.

Spleen flat, strap-like, dark,red-coloured organ located near the

stomach within the abdominal fat;circulatory system filter; capable ofgenerating new blood cells.

Liver large, pale tan to red in colour;produces enzymes to assist digestion;stores carbohydrates and fats; processesnutrient and toxins absorbed from gut;blood cell destruction and regulation;

nitrogen excretion.

Gall bladder dark, mottled green; bileproduction to assist in lipid digestion.

Stomach firm, sac-like organ attermination of oesophagus; digestion;secretes mucus, enzymes and acid.

Pyloric caecae finger-like pouches;digestion.

Blood hyper-osmotic; transfer ofnutrients, gases and wastes; immuneresponse.

Intestine digestion; osmoregulatorycontrol; lipid and protein regulation.

Gonads sex organs; paired; suspendedfrom the dorsal abdominal wall; testeswhite/cream coloured, flattened/angular; ovaries pink/cream coloured,rounded.

Musculoskeletal system skeleton oftrue bone, skull, vertebral column, ribspectoral girdle, accessory bones; red and

white muscle utilised for aerobic activityand short anaerobic bursts of power.

Figure 6

Ctenoid scales from the flank of a mature silver perch and the caudal peduncle of a juvenile fish.Source: Phil Read

Figure 7

Silver perch gills (100 mag.).Source: Phil Read

adult ju ven ile


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IAGNOS

TICTECHNIQUES

OBSERVATION

Ponds, cages and tanks should be

checked daily, in particular those withthe following features.

Recently (within 2 weeks) stocked orpartially harvested;

High stocking densities (particularlyfingerling ponds);

High feeding rates (>60 kg/ha;

summer temperatures);Poor water quality or suddenvariations e.g.

Crash of algal bloom

Low dissolved oxygen (DO) (30C)

Sudden decreases in temperature

(>4C in 24 hrs)High ammonia and high pH

Heavy surface scum, blue-green algae

blooms

Recent water exchange;

Bird predation;

Valuable broodfish.

SIGNS

Diseased fish display many physical andbehavioural signs, and these can varybetween diseases, levels of infestation orinfection, size, age and condition of fish,culture facility and season. In general,

any unusual signs in fish or unexpectedchanges in the water could be indicativeof disease or pending disease. Some ofthe more common and important signsdisplayed by fish are:

Loss of appetite reduced feedingactivity by some, many or all fish;

Fish congregating near the surface,

edges, aerators (Fig. 8);

Fish swimming or acting abnormally,e.g. flashing;

DIAGNOSTIC TOOLS

The following equipment is needed to

perform on-farm, disease diagnosis.Binocular compound microscopewith powered light source, moveablestage, 10 ocular with 4, 10, 20and 40 lens magnification (finalmagnification, 40, 100, 200 and400).

Dissection kit including forceps,sharp-pointed scissors, scalpeland blades, microscope slides andcoverslips, cutting board and killingknife or pithing spike.

Cast net, seine net and hand nets;buckets, airstones and airpump.

Figure 8

Diseased silver perch schooling in incoming water.Source: Phil Read

DIAGNOSTIC TECHNIQUES


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IAGNOSTICTECHNIQUES

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IAGNOSTICTECHNIQUES

Fish with unusual colouring; may bepale or dark, eroded patches of skin,bulging eyes, red brains or enlargedand discoloured organs;

Moribund or dead fish;

Increasing numbers of moribund ordead fish.

Presence or absence of feed in gut.

WATER QUALITY MONITORING

The first action after the observation ofunusual signs is to immediately monitorwater quality with calibrated meters.Ensure:

DO (>3 mg/L), ammonia(


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IAGNO

STICTECHNIQUES


EXAMINATION OF GILL AND SKIN

TISSUE

Live, preferably moribund fish collected

for necropsy should be held incontainers having aerated pond water(use water from pond). Microscopicexamination should commenceimmediately following euthanasia(severing of spinal cord immediatelybehind head or pithing brain) as someparasites are prone to detaching and/orimmobilisation soon after death of fish.Using anaesthetics for euthanasia is notrecommended as some ecto-parasitesmay be killed or detach rapidly fromthe fish and will therefore be unseenduring the examination. The followingprocedures are used to diagnoseecto-parasitic and some fungal andbacterial diseases.

Gill examination large fish:

lift the opercular cover and usingscissors, sever the white, cartilaginous

gill arch (2 cuts) and remove >10 mm ofgill (Figs. 10and 11);

place on a slide and using a scalpel,sever the cartilaginous gill arch fromthe primary gill lamellae (Fig. 12);

discard the gill arch and add 23 dropsof distilled water to the gill lamellae (donot use chlorinated tap water or pond

water);

lay a coverslip over the material andapply light pressure to encourage thelamellae to spread (Fig. 13);

examine the tissue at low (40), thenhigher magnification (100).

Gill examination small fish (


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IAGNO

STICTECHNIQUES

Skin examination:

position the caudal fin on a slide;

using a scalpel and light pressure,

scrape along the side of the bodyfacing upwards (Fig. 14);

remove skin/mucus from the scalpelto the slide;

add 23 drops water, coverslip andexamine as described for gill tissue.

Fin clip examination:remove a small piece of caudal fin (orany portion of fins that demonstrateabnormalities such as ragged edges)and prepare it as described for skinscraping.

LABORATORY SUBMISSION OF

FISH FOR DISEASE DIAGNOSIS

When the disease cannot be diagnosed

on-farm, samples of fish should bedelivered to a fish disease diagnosticlaboratory. Moribund fish are the mostsuitable and reliable for diagnosis.If delivery of live specimens is notpossible, freshly euthanased specimensshould be kept on wet ice and sentunfrozen provided they will arrive at thelaboratory within 3 hours. If the delayis greater than 3 hours, the specimensshould be sent preserved in 10% neutralbuffered formalin. Tissue should notexceed 7 mm in thickness. In all casesthe sample (organs or whole fish) shouldbe representative of the population andideally include moribund specimens.

Live specimens:

package 4 to 6 fish in strong plasticbags; pond water, pure oxygen;

air-tight seal; watertight container;preferably overnight transport ordeliver samples personally;

do not feed fish prior to transport

Iced specimens:

wrap fish in a damp cloth or towel;

place the sample in a plastic bag andcover with ice;

place in a watertight container anddeliver within 3 hrs.

Figure 14

Scraping the skin to obtain a sample.Source: Jeff Guy


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IAGNO

STICTECHNIQUES


Preserved specimens small fish

(


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IAGNO

STICTECHNIQUES

recent husbandry (past 2 weeks)e.g. harvesting; grading; waterexchange; fish delivery

system changes e.g. new tanks;

changes in diet; chemical treatments

environmental changes; weatherconditions.

LABORATORY PROCEDURES

Specimens received at the laboratory

will be processed and further examined.Histopathology fixed or fresh tissuesdecalcified and individual tissues cutin to assess single cel l depth sect ions;stained; microscopically examined forpathogens and changes in tissue.

Bacteriology bacterial culture onspecific media; targeted organs kidney, spleen, brain, peritonealfluids; also skin lesions; fresh tissue

only (do not submit fixed tissuefor bacterial culture); identificationof bacteria; screening of bacterialcolonies for antibiotic susceptibility(Fig. 15).

Virology viral culture on variousfish cell lines; molecular diagnosticsincluding PCR, sequencing andimmunological tests to identifyviruses.

LEARNING TO RECOGNISE THE

SIGNS AND DIAGNOSE DISEASE

Daily observation of fish, ponds and

tanks, regular monitoring of waterquality and a concise evaluation ofskin and gill biopsies are the firststeps used to investigate fish diseases.To the new or inexperienced fishfarmer, interpreting physical signs andmicroscopic images is challenging.However, the regular sampling ofhealthy and diseased fish will facilitatethe recognition of normal and abnormaltissues, help in identification of thecommon pathogens, and develop theskills required to accurately diagnosedisease. Most disease outbreaks insilver perch culture involve the commondiseases and pathogens during theearly stages of an investigation look for

the obvious!

Figure 16

Histological section of normal gill structure.Source: Matt Landos

Figure 15

Bacterial colonies growing on a blood agar plate.Source: Matt Landos

Figure 17

Histological section showing hyperblastic [arrows]silver perch gills.Source: Matt Landos


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IAGNOSTICTECHNIQUES


Changes in the appearance of bothskin and gill tissue are common duringa disease event; however, determiningthe aetiological agent(s), or causes, is

occasionally difficult due secondaryinvasion of pathogens or otherorganisms, or the manifestation ofovert signs caused by systemic disease.Changes in skin can include hyperaemia,haemorrhaging, ulceration, erosion,changes in pigment or thickening of theepithelium. Diseased gill tissue often

shows hyperplasia and hypertrophy,causing cell growth and fusion betweenthe secondary lamellae. Skin and gilltissue can have parasites and bacteriapresent without causing clinical disease;the interpretation of their significancewill depend upon other clinical findings(Figs. 16, 17, 18, 19, 20, 21 and 22).

Maintaining water quality is critical inpreventing disease; however, it is notalways controllable. Water quality (DO,temperature, pH and TAN) should be

monitored on a regular basis usinghigh-quality meters. Sudden changesin water quality e.g. an algae crash(pond water turning tea colour), largetemperature fluctuations (>5C over

24 hrs), high TANs and periods oflow DO (


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PATHOGENS

ECTOPARASITIC PROTOZOANS

Protozoans are usually single celled

organisms that reproduce by binaryfission and have specialised organellessuch as cilia or flagella for locomotion.When present in large numbers,they greatly impair the epithelium,particularly of gill tissue. Someprotozoans feed on the cells andmucus, while others cause physicalinjury, and some may produce toxins.Protozoans cause more diseases in silverperch culture than any other group oforganisms.

CHILODONELLOSIS

Infestations of the protozoan

Chilodonella hexastichacause thedisease chilodonellosis in silver perchin ponds, cages and tanks. The diseaseusually progresses rapidly; however, theparasite may exist in low numbers (e.g.12 organisms on 5 fish) over a period ofmonths before predisposing conditionscause a rapid increase in parasitenumbers. The parasite can causeserious losses of silver perch, especiallyfingerlings. Outbreaks in all seasons,particularly autumn, winter and earlyspring, and over the temperature rangeof 1030C. Needs to be diagnosed andtreated quickly to avoid large losses.May have a cyst stage.

Pathogen

Chilodonella hexastichais a ciliate

protozoan; ovoid to kidney shaped;dorso-ventrally flattened; 5070 m inlength, 2040 m wide.

Signs

Chronic to acute morbidity and/ormortality rates

Loss of appetite

Flashing

Lethargy, swimming slowly, head-upposition, often near surface andedges

Ragged fins

Emaciation

Skin may have mottled and/or greyappearance

DISE ASES AND PATHOGE NS


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ESAND

PATHOGENS


Diagnosis

Microscopic examination at 100magnification. Found mainly on gillsbut also skin (Figs. 23and 24). Infestedfish may have heavy or light parasiticloads (Fig. 25); large variation betweenindividual fish can sometimes makediagnosis difficult in the early stagesof an outbreak; important to examineat least 4 fish from pond. The organismcan quickly become immotile or detachrendering detection more difficult;

prompt examination required followingslide preparation. Cytoplasm oftenappears granular; cilia noticeable athigher magnification. Characteristicgliding motion; often slow or littlemovement at low temperatures; groupsof individuals often clumped on gill tips.

Treatment

Tanks:

10 g/L salt (NaCl) for 60 min, flush and

repeat following day.5 g/L salt continuous (includingpurging) and/or formalin 25 mg/Lcontinuous bath for at least 8 h, flushand repeat the following day; aeratewell; no feeding.

formalin 150 mg/L for 60 minutes(not larvae or fry); observe during

treatment; aerate well (oxygen, ifneeded); flush well on completion.

Ponds/cages:

formalin 2530 mg/L, maintain 24 haeration for 45 days; one treatmentusually sufficient; re-examinepond fish to gauge treatment

effectiveness; may need to re-treatponds after 34 weeks.

prophylactic for broodfish: formalin2530 mg/L winter/early spring(e.g. June then again in August)

Prevention

Quarantine and treat all fishprophylactically (25 g/L salt), includingfingerlings prior to stocking, newarrivals to the farm, and fish beingmoved between ponds. Maintain goodwater quality and nutrition. Do notoverstock. If possible, use source water

having no trash fish and prevent birdactivity on ponds.

Figure 25

Heavy infestation of Chilodonella hexastichaon[arrows] primary gill lamellae (100 mag.).Source: Phil Read

Figure 23

Chilodonella hexastichain skin mucus [arrows](100 mag.).Source: Stuart Rowland

100 mFigure 24

Chilodonella hexastichagrazing [arrow] gi lllamellae (200mag.).Source: Phil Read

100 m


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ISEASESAND

PATHOGENS

ICHTHYOPHTHIRIOSIS

WHITE SPOT, ICH

One of the most common and serious

diseases of silver perch. Infestations ofthe ciliate protozoan,Ichthyophthiriusmultifiliis , cause the disease known aswhite spot or ich. Occurs in silver perchin ponds, tanks and cages. Diseasecan progress rapidly and cause 100%mortality. Affects fish of all sizes. Thereis some evidence in other species offreshwater fish that survivors of white

spot develop immunity against futureinfestation. Occurs year round; decreasein water temperatures to/below 15Cin autumn associated with outbreaks.Needs to be quickly diagnosed andtreated. Has a complex life cycle(Fig. 26) involving attached, encystedand free-swimming stages; stages of

life-cycle temperature-dependent, less

than 4 days, >24C; more than 5weeks,


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PATHOGENS


Diagnosis

Microscopic examination of skin andgill tissue. Parasites readily seen at40 100 magnification. Trophontsusually embedded under gill andskin epithelium (Figs. 31and 32); canbe present only on gills; cytoplasmusually dark granular with slowswirling motion; horseshoe-shapedmacronucleus sometimes visible inmature trophonts, spherical nucleusin immature individuals; body with

uniform cilia; theronts ciliated, usuallyclearer cytoplasm than trophonts.

Treatment

Tanks:

salt (NaCl) 25 g/L salt continuous

until disease controlled, may be forup to 20 days; aerate well; no feeding;

temperature manipulation todecrease length of life cycleraise to30C for 10 days.

Ponds/cages:

formalin 30 mg/L initially (when

water temperature 50 mg/L (see chapter Calculations,Treatments and Dose Rates). Caution:copper sulfate is an algacide, thedecay of algae can cause dangerously

low DO.

Prevention

Quarantine and treat all fishprophylactically (25 g/L salt), especiallyfingerlings and new fish on farm prior tostocking. Maintain good water quality.Quarantine infected ponds including

Figure 31

Heavy infestation of Ichthyophthirius multifiliison silver perch gills; note horse-shoe shapedmacronucleus in some parasites [arrow] (100 mag.).Source: Phil Read

Figure 29

Silver perch infested with white spot about toflash on a submerged pipe.Source: Phil Read

Figure 30

Silver perch flashing.Source: Phil Read


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ISEASESAND

PATHOGENS

equipment, vehicles, water; preventaquatic birds spreading disease. Nilwater exchange when source waterknown to hold diseased fish. Closely

observe/monitor fish in all ponds andtanks when white spot is diagnosed inany pond or tank. It is common for morethan one pond or tank to be affectedsimultaneously by this parasite. Dry andde-silt ponds between crops.

ICHTHYOBODOSIS

ORIGINALLY CALLED COSTIOSIS

Ichthyobodo necator(previously

known as Costia necatrix) is a flagellateprotozoan that causes the diseaseichthyobodosis. It is one of the smallestparasites and is often overlooked duringmonitoring. Ichthyobodo necatorisparticularly dangerous for fingerlingsand larger fish held at high stockingdensities in tanks and cages. Outbreakshave been common in recirculating

aquaculture systems (Fig. 33).Ichthyobodo necatorexists in a detached,mobile form or an attached form; thelatter usually feeding on gill tissue(Fig. 34). Ichthyobodo necatorcausesdisease over a wide temperature range.Epizootics have been uncommon duringgrow-out of silver perch in ponds.

Figure 32

Ichthyophthirius multifiliistrophonts [arrows] inskin mucus and scales (100 mag.).Source: Phil Read

100 m

Pathogen

Ichthyobodo necatorfree-swimmingform, kidney-shaped, dorso-ventrallyflattened, 1020 m in size. Two flagellaattached to ventral part of body;attached form, pear-shaped (Fig. 35).Some evidence in other fishes of saltresistance in I. necator.

Signs

Chronic morbidity and/or mortality

Mucus secretion and epidermal

sloughing

Fish may have a bluish sheen to theskin

Flashing

Ragged fins

Hyper-ventilation

Lethargy and loss of appetite

Figure 34

Ichthyobodo necator [arrow] attached to gill tissue(400 mag.).Source: Phil Read

Figure 33

Disease caused by the protozoan,Ichthyobodo necator, can be common in tanksystems with poor water quality.Source: Phil Read

DIAGNOS IS TREATMENT & PREVENTION OF THE DIS EAS ES OF THE AUS TRALIAN FRES HWATER FIS H S ILVER PERCH Bid y an u s b id y an u s


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Figure 35

Diagram of Ichthyobodo necator.Source: Phil Read (redrawn from Hoffman, 1967)

Figure 36

Ichthyobodo necator [arrows], a flagellatedprotozoan (1000 mag.).Source: Stuart Rowland

Diagnosis

Microscopic examination of gill andskin; parasites often detach from host prompt examination of fresh tissue.Free-swimming form may exhibit aflicking motion; often rapid swimmingaround tissue sample; flagella difficultto see; attached pear-shaped parasitesseen at 100400 magnification ongill epithelium (Figs. 34 and36); gillhyperplasia, particularly betweensecondary lamellae.

Treatment

Tanks:

salt (NaCl) 1013 g/L for 60 min, flushand repeat following day; and/or

formalin 25 mg/L, continuous bath,flush and repeat after 1 or 2 days;

aerate water well; no feeding.

formalin 150 mg/L for 60 minutes(not larvae or fry); observe duringtreatment; aerate well (oxygen ifneeded); flush well on completion

Ponds/cages:

formalin 2530 mg/L, may need torepeat after 1 or 2 days; maintain 24 haeration for 45 days; one treatmentusually sufficient in ponds; repeatedtreatments may be required in RAS.

PreventionQuarantine and treat all fishprophylatically, especially fingerlingsprior to stocking. Maintain good waterquality and nutrition in cages andtanks. Reduce stress and overcrowding.Regularly sample, examine and monitorstock.

50 m

TRICHODINOSIS

Trichodinosis is a relatively innocuousdisease caused by infestations of theciliated protozoans, Trichodinaspp.Trichodinaspp. are widely distributed,but seldom cause mortalities in large(>100 g) silver perch. Trichodinacaninfect silver perch larvae and fingerlingsin large numbers, but rarely causehigh level mortality in the short-term.Trichodinosis is often associated withpoor water quality and high organic

loadings, and is commonly found onjuvenile fish that are overcrowded,debilitated with other diseases or in poorcondition. Common on post-larvae andfry in larval rearing ponds.


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Pathogen

Trichodinaspp. are circular,saucer-shaped, 25100 m in diameterwith a fringe of cilia around theperimeter; circular arrangement oftooth-like structures within the body;browses over skin and gill surface oftenwith a spinning motion (Figs. 37and 38).

Signs


Emaciation

Excess mucus production

Frayed fins, skin erosion, dark skin

Flashing and flaring of opercula

Lethargy

Head-up, swimming near surface

Diagnosis

Microscopic examination of skin and gill;easily recognised at 100 magnificationand common on skin and fin tissue(Fig. 39); observation of low numbers(e.g. 13 parasite/field of view) isinconsequential. Increasing levels ofinfestations to above 20 parasites/fieldof view may require treatment.

Treatment

Tanks:

salt (NaCl) 10 g/L for 60 min;

formalin 25 mg/L, continuous bath forat least 8 h; aerate water; no feeding.

Ponds/cages:

formalin 1520 mg/L, maintain 24 haeration for 45 days, one treatmentusually sufficient for ponds; or

copper (as copper sulfate, CuSO 4)0.2 mg/L, alkalinity must be>50 mg/L, continuous aeration duringtreatment, one treatment should besufficient; monitor water quality for45 days after treatment.

Prevention

Quarantine and treat all fishprophylactically (25 g/L salt), especiallyfingerlings prior to stocking. Eliminatepoor water quality by reducing feeding,maintaining or increasing aeration, andimplementing water exchange. Maintainwell-fed larvae and fry, and reduceovercrowding.

Figure 38

Scanning electron micrograph (SEM) ofTrichodinasp.Source: courtesy of www.fishdisease.net

Figure 39

Trichodinasp. a parasitic ciliated protozoan(100 mag.).Source: Stuart Rowland

100 mFigure 37

Trichodinasp. showing [arrows] cilia [c] anddenticles [d].Source: courtesy of www.fishdisease.net

WCS

30 m

d

c



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, y y

Figure 40

Tetrahymenasp. diagram with keycharacteristics [arrows]; cilia [c], caudal cilium [cc].Source: Phil Read

Figure 41

Tetrahymenasp., a ciliated protozoan (200 mag.).Source: Stuart Rowland

TETRAHYMENOSIS

Tetrahymenaspp. are free-livingsaprophytic ciliates that cause thedisease tetrahymenosis in silver perch;however, it is rarely a problem onfarms. Tetrahymenaspp. are similar inappearance to Chilodonella hexastichabut are usually more pear-shaped andoften larger (up 100 m in length)(Fig. 40). Severe losses have occurredin silver perch fry associated witha high organic load in the water. In

advanced cases in other fish speciessuch as carp, catfish, and salmon, theparasite can penetrate muscle tissue andorgans causing swelling, necrosis andulceration.

Pathogen

Tetrahymenais pyriform or radiallysymmetrical, ovoid body 3060 m wide,50100 m long; evenly-distributed cilia;movement is often spiralling comparedto the gliding of C. hexasticha. Granularappearance of cytoplasm (Fig. 41).May be confused with nonpathogenicciliates.

Signs


Excess mucus production

Epithelial damage, e.g. localisedswelling, ulceration, and necrosis

Loss of appetite and lethargy

White patches or spots on skin

Emaciation

Diagnosis

Microscopic examination of skin andgill tissue; parasite recognisable at 100magnification; relatively fast glidingmovement; penetration of Tetrahymenainto muscle or organ tissues possible;however, few cases reported for silverperch.

Treatment

Tanks:

formalin 25 mg/L, continuous bath forat least 8 h; aerate water; no feeding.

Ponds/cages:

formalin 1520 mg/L; maintain 24 haeration for 45 days; one treatmentusually sufficient for ponds; systemicinfections may be difficult to treat.

PreventionImprove water quality; reduce stress andovercrowding.

300 m

c

cc


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MYXOZOAN INFECTION S

Many species of myxosporidians arefound worldwide in a variety of fishhosts. They are obligate parasites withdifferent life stages and intermediatehosts. There have been few records ofmyxosporidians causing disease in silverperch and light infections usually donot cause mortalities or affect growth.However in one epizootic, a highinfection rate (>90% of fish affected)of Henneguyasp. on silver perch

(300450 g) resulted in chronic mortality(40/day) over two weeks before thedisease was controlled. Gill function wasseverely compromised; most secondarylamellae were invaded by multiplespore-producing, histozoic plasmodia.There is evidence Henneguyaspp. utilise

annelids (worms) as an intermediatehost in their lifecycle. The lifecycle ofthe species infecting silver perch it notknown. Most infestations have occurred

at temperatures >20C.

Pathogen

Myxosporidian (Henneguyaspp.), sporesize can vary, 8 to15 m 4 to10 m, tail40 to 50 m; two polar capsules and twocaudal appendages (Figs. 42, 43and 44).

SignsChronic fish mortality

Fish listless at pond surface;individual or small groups

Loss of appetite

Gills grossly thickened with nodules

Poor growth and emaciation

Diagnosis

Grossly thickened gill lamellar tissuewith mildly nodular appearance(Fig. 45).

Microscopic examination of gills, 100magnification; dark brown/tan encystedplasmodium (Fig. 46); intra-lamellar,~ 80150 m in diameter, ovoid to roundin shape, inflammatory response markedin resolving plasmodia; squashedpreparation of plasmodium, sporesas per description above (Fig. 47);plasmodium could be confused withIch. No moti lity of spores or encystedplasmodia.

Figure 43

High magnification of Henneguyaspores.Source: Prof.Iva Dykova, Institute of Parasitology, Czech Republic

Figure 42

Silver perch gills severely compromised byHenneguyasp. histological section showing thespore-producing histozoic plasmodia.Source: Matt Landos

10 m500 m

Figure 44

Histological section of Henneguya plasmodiashowing internal spores [arrow] each with twopolar capsules [pc].Source: Prof.Iva Dykova, Institute of Parasitology, Czech Republic

50 m

pc



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Treatment

Ponds/cages:

Treatments not well defined;

formalin, 25 mg/L may controloutbreaks by targetingfree-swimming spore stages; re-treatafter 23 days; aerate 24 h for severaldays.

Prevention

Quarantine fish before stocking,

examine a sub-sample microscopically.Maintain good water quality andappropriate stocking densities; dryand de-silt ponds regularly (every 1 to2 years); control intermediate hosts.Disinfect tank systems and equipmenton a regular base.

Figure 46

Henneguya plasmodia on silver perch gills(100 mag.).Source: Phil Read

Figure 45

Silver perch gills; grossly visible changes causedby the myxosporidian, Henneguyasp.Source: Phil Read

Figure 47

Wet mount of Henneguyaspores (400 mag.).Source: Phil Read

100 m


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ECTOCOMMENSAL CILIATE

INFESTATIONS

Species of sessile, ecto-commensalciliates have rarely been recorded onsilver perch; to date all cases have beenidentified as Ambip hyraspp. Parasitesattach to skin or gill tissue by a holdfast(scopula) often in colonies (Fig. 48).The parasites feed on bacteria andorganic matter in the water and use thehost primarily for attachment. Therehave been no reports of problems

with this parasite in the silver perchindustry. Large numbers on the gillscould potentially impede gas exchange,metabolic function and/or offer a site forbacterial and fungal infection (Fig. 49).

Pathogen

Bell or goblet-shaped, elongated ciliates;attached either by stalk or scopula;spiral of cilia at posterior end (Fig. 50);

some species having ciliary girdlemid-body; most range 40100 m inlength; some species solitary; somecolonial. No obvious motility.

Signs

Hyperventilation (heavy infestations)

Emaciation

Flashing

Figure 49

Ambiphrya sp., a ciliated, ecto-commensalparasite on silver perch gills (100 mag.).Source: Unknown

Figure 48

Diagram of key characteristics of Ambiphrya sp.Source: Phil Read (redrawn from Noga, 2000 & Hoffman, 1967)

Diagnosis

Microscopic examination of gill (mainly),fin and skin tissue; easily recognisableat 100 magnification; identification to

species not needed; treatment the samefor all species

Treatment

Tanks:

formalin 25 mg/L, retreat after23 days; aerate water; no feeding.

salt 10 g/L (NaCl) for 60 min orprolonged immersion at 5 g/L; somespecies may be resistant.

Figure 50

Ambiphrya sp., showing [arrows] scopula [s]and oral cilia [c] (200 mag.).Source: Brett Ingram

c

s



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Ponds/cages:

formalin 1520 mg/L, maintain24 h aeration for 45 days, repeattreatment after 23 days if necessary.

Prevention

Presence is indicative oforganically-polluted water that couldhave a high concentration of bacteria;improve water quality (aeration andexchange) to alleviate the problem andminimise the risk of recurrence.

MONOGENEANS

Monogeneans (skin and gill flukes),in particular Lepidotremabidyana(Dactylogyridae) are commonly foundon silver perch in ponds, cages andtanks. They have become widelydistributed in the industry over thelast 10 years, and the parasites nowoccur on most farms. This rapid spreaddemonstrates the risk of movingpathogens with live fish and the needfor stringent on-farm quarantine

measures to be implemented to avoidthe transfer of pathogens betweenfarms and onto farms from wild fish.Gill flukes attach using their posterior,haptor organ to gills (adult flukes) andto skin (juveniles). Heavy infestations

(>15 parasites per field of view) offlukes have not caused mortalities insilver perch; however, the parasite maycause stress, poor feeding response and

growth, tissue damage and interferencewith gill function, predisposing the fishto fungal and bacterial diseases (Fig. 51).Eradication of L. bidyanafrom ponds andtanks is difficult with current therapeuticagents. Infestations of a similar parasiticgroup in the family Gyrodactylidaehave also been recorded on silver perch

(Fig. 52).

Figure 51

Histological section of gill showing themonogenean Lepidotrema bidyana[arrows].Source: Prof. Iva Dykova, Institute of Parasitology, Czech Republic

100 m

Figure 52

Gyrodactylussp. showing [arrows] haptors [h] onthe adult and the internal larva (100 mag.).Source: Stuart Rowland

h


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Pathogen

Worm-like parasite, adults up to600 m in length; attached posteriorly;oviparous, producing eggs which are

released to the aquatic environment;eggs hatch as a free-swimming infestivestage (oncomiracidium); juveniles candevelop into gravid adults within 7 days;eyespots and head organs obvious; lownumbers of parasites may be presentwithout causing problems or stress.

SignsFlashing

Excessive mucus production onskin and gills

Gill hyperplasia

Loss of appetite

Emaciation (heavy, prolonged

infestations)

Diagnosis

Easily identified; microscopicexamination of gill at 40100magnification (Fig. 53); both adults (gill)

and juveniles (skin) show characteristicstretch and recoiling motion.

Treatment

Monogeneans can re-infest silverperch between 5 and 30 days aftertreatment with formalin or trichlorfon(an organophosphate), depending

on water temperatures and degreeof pond contamination with eggs.Up to three treatments, 21 days apartmay be required to eradicate orreduce monogenean numbers to aninsignificant level.

Tanks:

formalin 30 mg/L, aerate water, no

feeding; or

formalin 150 mg/L, 30 minute bath; or

trichlorfon 0.25 mg/L activeingredient indefinite bath; or

salt 15 g/L, 1 h bath, repeatfollowing day; or

Ponds/cages:

trichlorfon 0.5 mg/L active ingredient,indefinite bath;

formalin 30 mg/L (when water


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Figure 54

An anchor worm head showing organs use toattach below the epidermis.Source: Phil Read

Figure 55

Lernaeasp. [arrow] attached to the soft tissue ofa silver perch dorsal fin.Source: Parri & Craig Anderson

COPEPODS

Copepods are crustaceans with acomplex life cycle, developing throughegg, nauplii and copepodid larvalstages before attaching and maturingas adults on the host. The freshwater,parasitic copepods, Lernaeaspp. andErgasilusspp. have been recorded onsilver perch.

LERNAEASPP. ANCHOR WORM

Anchor worms possess anchor-likeprocesses for securing themselves tothe host (Fig. 54). Silver perch farms inthe Murray-Darling Basin may have ahigh incidence of anchor worm becausecommon carp (Cyprinus carpio) are oftencarriers of the parasite. However theparasite has also been recorded on silverperch (and other freshwater species) inthe eastern drainage. Parasites can infestindividual fish in high numbers (100s)

without causing mortality; however,poor feeding response and growth hasbeen recorded. Attachment sites areoften areas for secondary bacterial orfungal infections. Numbers of parasitesmay increase in slow-flowing or staticwater sources when carp and nativefish become concentrated. Anchor

worm is more common in summer,but the parasite can occur year round.Marketability of fish infested withLernaeais compromised due to the

presence of small, red lesions.

Pathogen

Anterior end of adult female buried inflesh of fish (Fig. 55); body cylindrical,wormlike; cephalic segment withtwo to four soft horns; adult femaleup to 20 mm in length; paired egg

sacs greenish, conical or ovoid atposterior end (Fig. 56); eggs hatch13 days, nauplius metamorphose intocopepodids 416 days, completion ofseveral developmental stages priorto copulation, female attaches; maledisappears, presumably dying; life cycletemperature dependant.


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Figure 56

Lernaeasp., a parasitic copepod withegg sacs [es] [arrow].Source: Phil Read

Figure 57

Haemorrhaging caused by the copepod Lernaeasp.Source: Ian Charles

Signs

Anchor worms clearly visible tonaked eye

Haemorrhaging and red lesions at

site of attachment (Fig. 57)

Emaciation and poor growth

Flashing

Diagnosis

Macroscopic examination of externalfeatures of fish; gravid females easilyrecognisable by eye attached to gills andskin, often on areas having softer scalecover such as soft ray tissue, mouth andnares; Microscopic and macroscopicexamination of gills; small immaturestages, such as copepodids may not begrossly visible.

Treatment

Tanks:

removal of individual parasites withforceps;

trichlorfon 0.25 mg/L activeingredient, indefinite bath;

salt 10 g/L, 1 h bath, repeat daily.

Ponds/cages:

trichlorfon 0.5 mg/L active ingredient,indefinite bath; repeat every 7 days

for 28 days.repeated treatments required toprevent re-infestation by emerginglarval stages of Lernaea.

Prevention

Quarantine and prophylactic treatmentprior to stocking; lowering of stockingdensity; improvement in water quality;

ensure water source and storagereservoir free of carp and other fish.

es



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ERGASILUS S P.

Infestations of the copepod,Ergasilussp., have rarely been recordedon silver perch farms. Ergasilids areoften described as gill maggots dueto the appearance of white egg sacsattached to the adult females. Theparasites clasping attachment causessevere gill damage and interferencewith gill function (Fig. 58). In one case,pond-reared, silver perch (>500 g)suffered a heavy ergasilid infestation

(species unknown). Fish werenutritionally challenged, displayedlong periods of inappetence, recordedrelatively poor growth and were easilystressed during harvest. Parasites wereattached to the gills. No mortalitieswere recorded in ponds. Damage to gilltissue caused by ergasilids can lead to

secondary bacterial or fungal infections.

Pathogen

Distinct cephalothorax and abdomen,1 mm length; large, paired, claw-likeantennae (used for locomotion), length,

1 mm; female having posteriorlyattached white egg sacs, length,12 mm;eggs ~100/sac, 0.05 mm diameter,colour darkens on maturity (Fig. 59). Lifecycle, egg hatching to free-swimmingnauplius; several copepodiddevelopmental stages via moulting;copulation at free-swimming stage;

females enter gill cavity and attach torakers and gills.

Signs

Flashing

Loss of appetite

Poor growth

Haemorrhaging of fins

Patchy/blotchy, dark skin

Stress following handling

Strong reaction to light anaesthesia

Gill hyperplasia

Diagnosis

Macroscopic examination of gills, gillmaggots; easily recognisable on gilltissue at 40 magnification; immatureforms may not be grossly visible.

Figure 59

Ergasilidsp. showing body with grasping antennae,head, thorax, abdomen and egg sacs [es arrow].Source: courtesy of www.fishdisease.net

Figure 58

Ergasilidsp. [arrow] attached to gills.Source: courtesy of www.fishdisease.net

1 m

es


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Figure 60

Large (~ 40 cm) cestode (species unknown) foundin the intestine of silver perch.Source: Phil Read

Figure 61

Intestinal (~ 2 cm) nematode (species unknown).Source: Phil Read

Treatment

Tanks:

trichlorfon 0.25 mg/L activeingredient; or

salt (NaCl), 10 g/L continuous for3 days.

Ponds/cages:

trichlorfon 0.5 mg/L activeingredient, prolonged immersion.

Prevention

Quarantine and prophylactic treatmentprior to stocking; lowering of stockingdensity; improvement in water quality;use of high quality feeds.

CESTODES AND NEMATODES

Cestodes and nematodes (tapewormsand roundworms respectively) areendoparasites inhabiting the intestine

of many vertebrates including fish.Both parasites have similar life cycleswith at least one intermediate host(e.g. copepod, insect nymphs, worms).The final host can be piscivorous birdsor predatory fish. Some cestode andnematode larval stages (plerocercoids)are commonly found in the viscera or

musculature of some fish. Long, white,ribbon-like cestodes (species unknown)have been reported protruding fromthe anus of silver perch held in purgingsystems (Fig. 60). Comparatively,nematodes are characterised by aslender and cylindrical body having

tapered ends and no true segmentation.Nematodes (species unknown) havebeen found in the digestive tract ofsilver perch and a species of the genus

Camallanus, has parasitised the gutof Barcoo grunter (Scortumbarcoo)(Figs. 61and 62). Normal behaviour andgrowth was reported for silver perchparasitised by cestodes and nematodes.

Pathogen

Cestodes: up to 40 cm; body long,

ribbon-like; white to cream colour;scolex (head) not pronounced havingadhesive grooves (bothria). Nematodes:slender, cylindrical body, covered withcuticle; up to 10 mm length; red incolour.



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Signs

Worms protruding from vent ( Fig. 63)

Swollen abdomen

Diagnosis

Large worms identified grossly; wetmounts of faecal matter may be usefulin determining the presence of eggsor larvae. Microscopic examination ofphysiological features (scolex, shape,size, and segmentation) required toidentify species. Samples should be sentto a reference laboratory for definitiveidentification.

Treatment

There are currently no treatmentswhich are registered, or the subject ofan Australian Pesticides and Veterinary

Medicines Authority (APVMA) permit.Chemicals which have registrationin other food producing species ofanimals (non-fish) may be used under anoff-label prescription from a registeredVeterinary Surgeon.

Prevention

Regularly dry, de-silt and disinfect pondsusing calcium hydroxide or calciumoxide. Minimise access of animals thatcould be carrying parasites, includingbirds and turtles.

Figure 63

Nematode (species unknown) protruding fromthe anus of a silver perch.Source: Matt Landos

Figure 62

Histological section of the intestine of Barcoogrunter (Scortum barcoo) showing the nematodeCamallanus sp. [arrow] attached to the gut wall.Source: Matt Landos

200 m


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FUNGAL DISEASES

Fungi or water moulds belong to theClass Oomycetes and are ubiquitous infreshwaters. They form a large group

of saprophytic organisms that feedopportunistically on dead organicmatter. Fungi are important pathogensof fish. They are generally considered tobe secondary pathogens, with infectionsoften induced by stress, physicaldamage and/or immuno-suppression.Fungal infections are inherently difficult

to treat because of the complex biologyof aquatic fungi.

SAPROLEGNIOSIS

The fungus, Saprolegnia parasitica,causes the disease saprolegniosisin silver perch. Fungal infections in

silver perch are common after roughhandling, removal of mucus anddamage to the epidermis. A new,important disease in silver perch, wintersaprolegniosis, usually affects larger(>250 g) fish (Fig. 64) and is prevalent attemperatures


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Signs

Abnormal swimming and behaviour(fish at pond edges, in currents, onsurface, isolated)

Focal areas of pale skin (early stages)

Haemorrhaging on underside ofabdomen (early stages) (Fig. 69)

Light fungal growth on caudal fin(early stages)

White cotton wool-like patches on

skin or gills (advanced stages)Fungal plaques attached to thesoft tissue on the distal end of theopercula (early stages)

Diagnosis

Macroscopic examination of skin andgills; pale and/or haemorrhagic areas,white to green-brown coloured fungal

growth. Microscopic examination ofskin and gills; fungal hyphae of variablewidths (1030 m); sporangium oftenwith zoospores; easily diagnosed at100 magnification; fungal growth(mycelium) not so obvious in earlystages.

TreatmentTreatment difficult, many fungalinfections show resistance tochemotherapy; recovery related tothe amount of skin and gill infectedby fungus; gill infections are usuallyterminal.

Tanks:

salt (NaCl) 25 g/L preventativetreatment, continuous, indefinitebath (adults, juveniles, larvae);

elevated temperature may assist,maintain >20C;

eggs, larvae, salt 2 g/L preventativetreatment, continuous, indefinitebath;

eggs, formalin 1,000 mg/L for 15 minsdaily (used to control saprolegniosis

on Murray cod eggs).

Figure 67

Electron micrograph of Saprolegnia parasiticaspores.Source: Dr Gordon Beakes (University of Newcastle upon Tyne, UK)

Figure 66

Saprolegniosis of the gill tissue; myceliumcontaminated with organic matter.Source: Phil Read


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Figure 69

Mild haemorrhaging on the lower abdomenof silver perch early stages of the diseasesaprolegniosis.Source: Phil Read

Figure 70

Saprolegnia parasiticagrowing [arrow] on fish feed.Source: Matt Landos

Ponds/cages:

emergency harvest is often theonly way to avoid a major loss fromsaprolegniosis. Fish need to be dip

bathed in a high concentration offormalin 100 mg/L for 30 minutes,prior to being held in a very cleanrecirculation system with at least25 g/L salt.

formalin 30 mg/L initially (whenwater temperature 50 mg/L. Copper may provide somedegree of prevention if used regularlyup to and throughout the high riskperiod of winter.

Prevention

Salt bath (25 g/L) prevents or slowsrate of infection in tanks. Eliminateor reduce predisposing stressorslate summer/autumn when watertemperatures start to fall < 18C; ensurefish free of ecto-parasites; treat parasiticdiseases; reduce feeding; reduce high

organic load in ponds (dead fish andorganic matter, including feed arefertile substrates for colonisation ofthe fungus) (Fig. 70); reduce biomass

especially large (>500 g) fish; maintaingood water quality, especially followingcrashes of algal blooms; avoid handlingand skin damage; on farms where wintersaprolegniosis is a problem, weeklyapplications of formalin or copper maybe beneficial after temperatures declineto 16C in late autumn/winter; removedaily any dead fish (or eggs); dry andclean ponds between crops.

Figure 68

Saprolegnia parasiticaoogonium.Source: Matt Landos


f


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EPIZOOTIC ULCERATIVE SYNDROME

EUS, RED SPOT DISEASE

The aquatic fungus, Aphano mycesinvadans, causes EUS on silver perch

farms located in coastal regions innorth-eastern NSW and south-easternQueensland. The fungus is known tocause serious losses of farmed fish inAsia and estuarine fish in Australia;the latter usually following periods ofhigh rainfall and subsequent decline ofwater quality (low salinity, low pH, high

organic load). The disease can occurperiodically on silver perch farms thathave a surface water supply. Epizooticscan cause high morbidity, particularlyin juvenile (


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Diagnosis

Initially, macroscopic examination; palepatches of skin, small, single scale-sizedred lesions, small ulcers to large, deep

(exposing skeletal muscle) necroticulcers in advanced cases. Microscopicexamination (x100 mag.) of squashedmuscle tissue underlying ulcers;presence of fungal hyphae, 1218 m indiameter, amongst muscle fibre (Fig. 73).

Treatment

No known treatment of infected fish.Recovery has been recorded in largesilver perch after improvement in water

quality.The following assist in reducing newinfections through killing the infectiouszoospore stage.

Tanks:

formalin, 25 mg/L continuous bathand 50 mg/L, 1 h bath; or

salt (NaCl) 10 g/L 1 h bath, then5 g/L indefinite bath.

transfer of fish to clean tank,lower stocking density (chlorinatede-stocked tank).

Ponds:

emergency harvest, treatment (asabove) and re-stocking to newponds proven beneficial in recoveryof advanced cases in fingerlings;

re-stocking of large fish having earlysigns (small lesions to medium sizedulcers) has helped fish heal naturally;improve water quality.

Prevention

Avoid excessively high stockingdensities and high biomasses.Outbreaks known to occur underone or combinations of the followingpredisposing conditions; infestationsof ecto-parasites, poor water quality,

especially high or low pH, high organicmatter, days of extreme hot weather,high rainfall leading to a fresh insource water. Do not pump water fromrivers and creeks with a fresh, in floodor containing infected fish. Maintaingood water quality; dry ponds regularly.Spelling surface water in a fish-freeenvironment for 710 days is likely tobe sufficient to eliminate infectiouszoospore stages of the fungus.

Figure 73

Diagrammatic representation ofAphanomycesinvadanszoosporangia.Source: Phil Read


BACTERIAL DISEASES COLUMNARIS Pathogen


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BACTERIAL DISEASES

Bacteria form a large, diverse groupof small, ubiquitous organisms thatplay a key role in nature. Bacterial cells

are simple, do not contain complexorganelles and can divide rapidly. Somebacteria cause common and damagingdiseases in fish. Most bacterial diseasesresult directly from environmentalstress such as poor water quality and/orrough handling. To date, seven bacterialdiseases have been reported in silver

perch. However, other than conditionsrelated to poor handling, silver perchappear to be robust and largely resistantto bacterial infections. Systemicinfections are very uncommon in silverperch.

COLUMNARIS

The bacterium, Flavobacteriumcolumnare, causes the diseasecolumnaris. Flavobacterium columnare

has a worldwide distribution, iscommon in the pond environment andcan rapidly infect fish causing highmortalities. The disease is not commonin silver perch, although it has causedmortalities in fingerling and maturesilver perch, but usually followingstressful precursors such as physical

injury, other disease and crowdedconditions associated with low DOand high organic loads. Flavobacteriumcolumnarecan be invasive onceestablished, through production of arange of tissue toxins; pathogenicity isusually higher at temperatures >20C.

Pathogen

Slender, filamentous gram negativerod; 0.4 m diameter, 4 to 10 m length;lacking flagella, motile by gliding

mechanism; preference for aerobicconditions colonising gills and skin;prevalent at temperatures >20C.

Signs

Chronic to acute fish morbidity ormortality

Erosive and necrotic skin lesions onhead and caudal regions (Figs. 74and75)

Lesions whitish colour, with inf lamed,red periphery

Frayed and eroded fins

Gill infection, eroded lamellae withyellow to white necrotic edge

Ulcers with yellowish pigmentation

Figure 74

Columnarisbacterial infection in silver perch fry.Source: Phil Read

1 cm

Diagnosis salt (NaCl) 2 g/L continuous bath Prevention


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Figure 75

Deep ulceration on the caudal peduncle of silverperch caused by the bacterium, Flavobacteriumcolumnare.Source: Phil Read

Diagnosis

Microscopic examination of wetmounts of lesions (skin and gill); 1,000magnification; bacteria as slender rods

having characteristic gliding motion;bacteria usually congregate intocolonies giving a haystack appearancehence the name columnare; lesions mayhave secondary fungal infection.

Treatment

Tanks:

oxytetracycline 20 mg/L activeingredient, 7 days at 2030C or10 days at 50 mg/L; continuous aerationduring treatment.

Prevention

Avoid poor handling of fish, especiallyexposure to any periods of low DO;avoid harvesting at high temperatures

(>28C); avoid overstocking/highorganic loading during harvestprocedures; maintain good waterquality. Ensure rapid solids removal intank systems and maintain appropriatestocking levels (e.g. up to 40 kg/m318C).


TAIL ROT SYNDROME Pathogen Diagnosis


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TAIL ROT SYNDROME

Tail rot syndrome or fin rot, is arelatively common bacterial diseasein juvenile silver perch. It occurs mid

to late summer when fingerlings areharvested and transported from pondsto quarantine tanks, or when fingerlingsare transported from hatcheriesand grow-out farms. The diseaseis characterised by necrosis of thecaudal fin and distal part of the caudalpeduncle and usually occurs as a result

of rough handling, over-crowding, lowDO, high temperatures, high organicloading and inappropriate quarantineprocedures between harvest andtransport periods. Mixed infectionsby the bacteria belonging to theFlavobacterium, Pseudomonad, Vibrio orAeromonad bacterial groups most likelycause the disease.

Pathogen

Flavobacteriumspp. as for columnaris;Aeromonasspp. (e.g. A. hydrophila),0.8 to 1.0 m diameter and 1.0 to 3.5 m

long, short, motile rods by a singlepolar flagellum, ubiquitous found inmost freshwaters; Pseudomonasspp.(e.g. P. fluorescens); similar to Aeromonas;these bacteria are often naturalinhabitants of fish mucus.

Signs

Eroded tail fin

Necrotic tissue on caudal peduncle

Dark colour, sometimes blotchy fry/fingerings

Lethargic, often near tank surface orfacing current or airstones

Chronic mortality following harvest/transport

Diagnosis

Gross appearance; fish with frayededges and reddened caudal fin inearly stages (Fig. 76); skin of the distal

caudal peduncle having pale, mucoidappearance with focal haemorrhages;more advanced cases, caudal fin erodedto peduncle, ulcerated tissue oftenexposing skeletal structure (Fig. 77);secondary fungal infection common.Definitive diagnosis by fish necropsy,cultures and isolation of bacteria.

Mortality increases significantly oncebacteria enter circulatory system. Fishhaving mild cases can completelyregrow the soft fin ray tissue if infectionresolves.

Figure 77

Silver perch fingerlings with tail rot.Source: Stuart Rowland

Figure 76

Early tail rot on the distal end of a caudal fin.Source: Phil Read

Treatment Prevention ULCERATION CAUSED BY


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Figure 78

Goldfish (Carassius auratus) with GUD.Source: Stuart Rowland

Tanks:

oxytetracycline bath, 20 mg/L activeingredient, 7 days at 2030C or

10 days at


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y p yin the absence of secondary infectionsare usually low. Murray cod have shownresistance to GUD, but may act as

asymptomatic carriers.Pathogen

Aeromonas salmonicida nova; non-motile,gram-negative bacterium; isolates grownon agar media are typically grey, smalland circular colonies; pathogen maysurvive long periods off the host fish.

Signs

Chronic fish morbidity/mortality

Lethargic swimming and inappetence

Lesions and ulcers on skin and fins,ranging from superficial, reddenedlesions to crater-like ulcers, may havepale or red centres with a peripheralpale halo (Fig. 79)

y

Diagnosis

Definitive diagnosis requires laboratory

examination of infected fish; necropsy,culture and bacteria isolation; isolationof bacteria from internal organs (kidneyand spleen) in systemic infectionsis more revealing than samplingsuperficial ulcers.

Treatment

Tanks:oxytetracycline (pure), bath, 20 mg/Lactive ingredient, 7 days, at 2030Cor 10 days at


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The bacterium, Streptococcus iniae,causes streptococcosis in silver perch.The disease has been rarely reported,

although losses in the few outbreakswere significant. Streptococcusspp. areresponsible for disease in many culturedfish worldwide, including rainbow trout,eels, channel catfish, tilapia, yellowtailand striped bass. The disease typicallytakes the form of septicaemia, andclinically fish may exhibit exophthalmia

(pop-eye) (Fig. 80) or fluid in theabdominal cavity and intestine (ascites).Transmission of Streptococcusspp. isthought to be mainly by contact andis likely to be enhanced by injury toepithelium or by stressful environmentalconditions. Natural epizootics have beenrecorded in populations of wild fish.Silver perch reared in RAS were infected

(18 to 11C over 12 h); however, otherfactors may have contributed to theepizootic.

Pathogen

Gram-positive, ovoid to elongatecocci; immotile; single or paired butrarely form chains in infected fish;-haemolytic; many species can growanaerobically, in a wide temperaturerange (1045C).

Signs

Chronic fish mortality/morbidity

Fish darkly pigmented

Exophthalmia and abdominaldistension

Lethargy; fish near the surface and atpond edges

Loss of appetite and nervousbehaviour

operculum, base of fins and skin, andinside of abdominal cavity (Fig. 81)

Survivors may develop spinal

deformity (scoliosis)

Diagnosis

Bacterial isolation from a variety oforgans (spleen, liver, brain, eye andkidney); positive, bacterial cultureproduces dull, yellowish/grey, slightlyraised and rounded, 1 to 2 mm colonies

at 48 hours on blood agar media.

Treatment

Tanks:

selection of antibiotic should bebased on laboratory sensitivitytesting as S. iniaehas variablesensitivity. Whilst awaiting culture

results fish can be started on

Figure 80

Silver perch infected by Streptococcosis iniae;note exophthalmia.Source: Matt Landos

Figure 81

Haemorrhaging from the vent can sometimesindicate systemic bacterial infections.Source: Phil Read


oxytetracycline, 20 mg/L active MYCOBACTERIOSIS 20% mortality was recorded over


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ingredient, 7 days at 2030C or10 days at


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Chronic fish mortality/morbidity

Irregular swimming, fish at pondedges and surface

Loss of appetite

Emaciation and poor growth

Abnormal dark colour of skin

Shallow to deep ulcers

Fin erosion

Granulomas in viscera (kidney, spleen,

heart), 1 to 4 mm diameter (Fig. 84)

Exophthalmia and abdominalswelling (ascites)

Laboratory culture of bacterium;diagnosed by acid-fast and gramstaining (Ziehl-Nielson stained) of

smears; histological sections of tissuegranulomas (Fig. 85); microscopicexamination, 200, of wet, squashedmounts of kidney and spleen tissuefor granulomas; the latter mayinclude peripheral, lighter coloured,inflammatory cells.

Treatment

Once established, can be difficult tocontrol or eradicate.

Tanks:

remove infected fish; cleancontaminated tanks, pipes andequipment; disinfect equipmentusing sodium hypochlorite

(10,000 mg/L chlorine reported levelrequired to kill mycobacteria).

remove infected batch of fish; dry,de-silt and lime pond.

PreventionMycobacteriumspp. can survive longperiods in the environment and manystrains are natural soil organisms;transmission probably via the sheddingof bacteria from infected skin ulcersand bullying of infected fish; dry pondsbetween crops; lime ponds with CaO or

Ca(OH)2; disinfect tanks and equipment;utilise UV and/or ozone units; removeinfected and dead fish; maintain goodwater quality and husbandry practices;minimise damage to fish to preventsuperficial infections.

Figure 85

Histological section of a granuloma causedby mycobacteria in the kidney of an Americanbluefish.Source: www.fishdisease.net

Figure 84

Silver perch spleen; note irregular margins oforgan due to mycobacterial granulomas.Source: Matt Landos


AEROMONAD DERMATITIS MOTILE

AEROMONAD INFECTION MAI

advanced, red, necrotic skin lesions.Mild lesions can progress rapidly with

Ulcerated lesions, margins whitish orhaemorrhaging (advanced)


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AEROMONAD INFECTION, MAI

Aeromonad infections are one ofthe most common bacterial diseases

of freshwater fish. Many species aresusceptible, including silver perch.Aeromonad bacteria are ubiquitousand found in most f reshwater ponds,rivers and bottom mud, utilising organicmaterial as a nutrient source. The mainspecies infecting fish are Aeromonashydrophila, A. sobria , and A. caviae.

The disease in silver perch is observedpost-harvest during late spring andsummer (causing summer spots)particularly when stocking densities inpurging systems are increased. Clinicalsigns begin as de-pigmentation ofareas of the epidermis on the caudalpeduncle, top of the head, flanks andbase of the pectoral fins (Fig. 86). If leftuntreated, spots can develop into more

Mild lesions can progress rapidly, withsignificant scale loss and haemorrhagingaround the affected area from stress

associated with live transportation.The disease has not caused significantmortalities in silver perch, but canrender fish unsightly and unmarketableif sold whole or live.

Pathogen

Aeromonas hydrophila and A. sobria ;gram-negative, short, motile rod; 0.8 to0.9 m 1.5 to 3.5 m; motile, singularpolar flagellum.

Signs

Loss of appetite

Lethargy

Loss of equilibrium

Superficial, de-pigmented areas onflanks, fins, head or abdomen (early)

haemorrhaging (advanced)

Lesions may have secondary fungalinfection

Exophthalmia, opaqueness of eyes

Distended abdomen, clear fluids;haemorrhagic, swollen intestine/vent

Diagnosis

Laboratory necropsy of diseasedfish; bacterial culture, isolation and

identification with accompanyinghistopathology examination.

Treatment

Tanks:

treatment should be based on thelaboratory antibiotic sensitivityresults as this bacterium does not

display a regular pattern of sensitivity(antibiotic-resistance is common).

Figure 86

Early MAI infection (summer spots) caused byperiods of low DO during harvest.Source: Phil Read

oxytetracycline 20 mg/L activeingredient 7 days continuous bath;

Prevention EPITHELIOCYSTIS


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ingredient, 7 days, continuous bath;maintain low light levels, goodaeration; water exchange to dilutebacterial load and re-treat;

salt (NaCl) 2 g/L prolonged immersionor 10 g/L hourly baths daily.

returning fish to the pond will oftenresult in spontaneous resolution oflesions this should not be donewhen water temperatures are under18C as super-infection of Saprolegnia

can complicate the healing process.

Ponds:

appropriate antibiotic; oraladministration via feed;oxytetracycline, 75 mg/kg fish for10 days; resistance to anti-microbialsa problem.

MAI is a stress-borne disease. Whenharvesting, avoid overcrowding, hypoxicconditions, high suspended solids and

contact with bottom muds/organics;purge in good quality water; avoid highammonia and overcrowding; regularlyclean pipes and tanks; backwash filters;use UV/ozone and salt; water exchange.

Epitheliocystis is a widespread chronicbacterial disease affecting freshwaterand marine fish. The causative agent

is an intracellular bacterium, mostprobably Chlamydia-like organism.It has been recorded in silver perchfingerlings held in aquaria; however,the disease remains relativelyinsignificant under commercial pondconditions. Epitheliocystis is usuallybenign and non-pathogenic, but in

high concentrations it has causedconsiderable mortalities in juvenilefish of several species in both freshand marine environments. Theorganism affects mainly gills, causinggill hypertrophy and the formationof distinct transparent capsules. The


gills swell and lose their lamellaestructure leading to impairment of the

Signs

M ib d fi h t liti

transparent cysts; electron microscopyrequired to observe coccoid bodies


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structure leading to impairment of thegills respiratory capacity; evidence ofimmunity developing in some species,the disease resolving without treatment.

Pathogen

Intracellular, non-motile, gram negative,coccoid bacterium; rod-shaped; visibleunder scanning electron microscopy; gillcysts (transparent to yellow capsules)round to oval shaped;1087 m diameter; peripheraltrilaminar membrane; up to 96% gillfilaments affected in silver perchjuveniles (Figs. 87, 88and 89).

Moribund fish, mortalities

Lethargy

Swimming near the surface

Distended opercular cover; rapidrespiration

Declining body condition

Gaping mouth (mortalities)

Diagnosis

Initially, microscopic examination, 200of gill tissue; can infect skin epithelialcells; hypertrophied cells in gill filamentdisplaying round to oval shaped,

required to observe coccoid bodieswithin cysts.

Treatment

No known treatment, except disinfectionand quarantine

Prevention

Little known about the organism;disease possibly transmitted bycontamination of nets and other fish

culture appliances; maintain cleanlinessand disinfect gear and tanks regularlyusing chlorine baths, 1 mL/L 1012%available free chlorine, for 60 mins.Maintain minimal stress in fish. Useof UV irradiation on intake water andisolation of infected batches of fish isrecommended.

Figure 88

Electron micrograph of cyst containingpathogens: [c] cyst; [e] epithelial cells; [bs]blood space.Source: Robert Tennent, Assoc. Lect., School of Medicine, UTAS

Figure 87

Electron micrograph showing gill filament cellsof a fish with epitheliocystis; note swelling of themiddle lamella: [h] hypertrophied [arrows] cell.Source: Dr Barbara Nowak, Assoc Prof. School of Aquaculture, UTAS

Figure 89

Histological section of a gill of a silver perchwith epitheliocystis showing [arrows] basophilicinclusions.Source: Dr Barbara Nowak, Assoc Prof. Dept of Aquaculture, UTAS

h

bs

e

c

VIRAL DISEASES

Vi t l ll t

EPIZOOTIC HAEMATOPOIETIC

NECROSIS EHN

is internationally notifiable and mustbe reported to disease surveillance


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Viruses are extremely small agentscomprised of DNA or RNA surroundedby protein. Viruses must invade living

cells in other organisms to replicate.The study of viral diseases in fishis relatively new, and a majority offish viruses that have been reportedare from economically-importantspecies in which the diseases cancause high mortalities and severeeconomic losses. There are no known

viral diseases affecting silver perchunder culture conditions. One disease,epizootic haematopoietic necrosis,has been shown to affect the speciesunder experimental conditions andis potentially a serious threat to silverperch culture.

NECROSIS EHN

EHN is a highly infectious diseasecaused by the iridovirus epizootic

haematopoietic necrosis virus EHNV.The virus is geographically limited tosouth-eastern Australia. Redfin perch(Perca fluviatilis) are very sensitiveto the virus, with 100% mortalities acommon outcome following exposure.It is known to also affect rainbowtrout (Oncorhynchus mykiss) although

mortalities in trout are usually less than4%. Under experimental conditions inthe laboratory, it has been shown thatexposure to EHNV seriously affects thenative fish silver perch, Macquarie perch(Macquaria australasica) and goldenperch (Macquaria ambigua). Outbreaksin redfin and trout typically occurwhen water temperatures are above12C in spring/summer, often involvingjuveniles in both species. The disease

be reported to disease surveillanceagencies. It is known from studies onredfin perch, that EHNV is readily spreadin water, with infected fish sheddingviral particles via body fluids and fromdecomposing carcasses. The virusis highly resistant to environmentaldegradation, likely to remain insediments for prolonged periods,possibly utilising insects or amphibians.Iridoviruses are known for their lack ofhost specificity; hence many fish species

may be susceptible.

Pathogen

Virus a member of the Iridoviridae familyand genus Ranavirus; polyhedral virus,150170 nm in diameter.

Signs (in redfin and trout)

Mortalities

Slow or rapid spiralling to the surface


Erosion of fins; skin discolouration

Weak swimming; head standing

Treatment

No known treatment; strict quarantine

MISCELLANEOUS NONINFECTIOUS

DISEASES, DISORDERS AND


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Weak swimming; head-standingabove the bottom

Loss of appetite

Cutaneous haemorrhages (terminalstages, redfin)

Swelling of spleen and liver

Peritoneal fluid; white foci of necrosisin liver

Diagnosis

Collection of fresh and fixed liver,kidney and spleen samples; fixing oftissue for virus isolation; cell culture;ELISA followed by histopathology,immuno-fluorescent staining,polymerase chain reaction (PCR),electron microscopy and/or other tests.

No known treatment; strict quarantineto prevent spread; cleaning anddisinfection (200 mg/L sodium

hypochlorite for 2 h); proper carcassdisposal.

Prevention

Exclusion of wild fish and ornamentalfish, particularly redfin perch fromponds, drains and the farms watersource; reduction in s

enfermedades peces

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