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Home , Haliotis rufescens, Mya truncata, Ostrea edulis

OTHER DISEASES, OTHER MOLLUSCS

Hemic Neoplasia of Bivalve Molluscs

The disease known as hemic, hematopoietic, or hemocytic neoplasia HCN! is also referred to as hemic proliferative disease, leukocytic neoplasia, sarcomatous neoplasia, sarcomataidproliferative disorder, disseminated sarcoma, and atypical hemocyte condition. As a neoplasia, it is considered ta be a form of cancer of similar to leukemia in higher and man in the way it affects the host. It should be emphasized, however, that this is a cancer of shellfish, not of humans, and that consuming shellfish with this condition poses na known health threat ta humans. Soine research has suggested that the disease is caused by a virus, but this is not yet confirmedor generally accepted. However, it has been shawn in some cases to be highly contagiousfrom one individual shellfish to another. The disease occurs throughout the warld in a variety af bivalve molluscs and appears to causesignificant mortality in certain farmed populations of shellfish.

Geographic Range and Infected The diseaseaffects many speciesthroughout the world. Like many other shellfish diseases,it is probably more widely distributed than is now known. The following species and locations have been identified: Adula cali fornica, Pacific coast of ; Artica i slandica mahagany quahog!, Saund, Atlantic caast of Narth America; Ceras- todermaedule common cackle!, Cork Harbour, Ireland; Saccostrea commerciali,s Australian rockoyster!, Australia; Crassostreagigas Japaneseor Pacific !, Matsushima Bay, Japan; rhizophorae, Brazil; CrassostreaUirgi,mica Eastern or American oyster!, Atlantic coast of North America, discontinuously fram the Chesapeake Bay ta Long Island Soundand sites on the Gulf coast; Macoma calcarea, Baffin Island, Canada; Macoma nasuta andM. irus, Yaquina Bay, Oregon; arenaria soft shell !, Atlantic coast of North America,discontinuously from Chesapeake Bay to England; , BaRin Island, Canada;Mytilus edulis bay or blue !, Pacific caastof North America, discontinuously froni Yaquina Bay, Oregon, to sites in British Columbia, North Wales, Denmark, Finland, andsouthern coast of England; chilensis Chilean oyster!, Chiloe, Chile; Ostrea luri da Olympia oyster!, Yaquina Bay, Oregon; and European flat oyster!, Mali-Stonarea of Yugoslavia near Dubrovnic, Ria de Noya in Galicia, Spain, and the Brit- tany region of France.

29 80 / MOLLUSC DISEASES / Elston

Mortality Rate, Environmental Factors, and Seasonality Some cultured populations appear to be 100% infected if individual animals are monitored over severalmonths. Mortality rates due to the diseaseare reported to approach 100%over an annual period in soinespecies. In other cases,in cultured populations,annual mortality rates of 30%-50% are typical. Specific environmental factors that induce or enhance the disease are not known. Although much researchhas beenconducted to determine whether various types of pollu- tion contribute to the disease, no single factor which has these effects has been identified. Hemic neoplasia appears to be highly infectious, and dense populations of farmed shellfish maintain high disease levels because of ease of transnussion from one to another. In all speciesin which seasonalityhas beeninvestigated, the diseaseis reported to be most prevalent judging by percentageof infected individual shellfish! during fall and winter months, typically from Octoberthrough March. The prevalencedrops in the spring and summer, possibly because heavily infected individuals die in the winter and the disease does not start another cycle of infection until autumn.

Diagnosis Diagnosisis basedon microscopicexamination of blood or histological examination of tissuesby a qualifiedpathologist. Common signs of the diseasefor all affectedspecies are not established,but the followingare knownto applyin soinecases: failure to produce maturereproductive follicles; high levelsof mortality whichspread geographically; and tissues swollen from the massive proliferation of abnormal blood cells in individuals with advanced cases of the disease.

Prevention an8 Management Disease-free Areas Every effort should be made toavoid introducing infected shellfish into areas that do not have the disease, Hemic neoplasiais known to be contagiousfrom one animal to an- other within a given species. It is not known, however, if it can be transmitted from one speciesto another. It is possible,using techniquesof pathologicalexamination, to establish reasonableassurance of the presenceor absenceof the diseasein givenpopulations of shellfish.Field observationsindicate that somepopulations within a givenspecies may be more resistant than others. Areas Known to Have the Disease Eradication of the diseaseis not feasible sincethe diseasecan persist at low levels in natural populationsof shellfish. General managementmethods based on available knowl- edgeconsist of keepingcultured population densities as low as practicaland scheduling harvests so that market-sizedshellfish are harvested beforethe typical period of increased diseasein the fall and winter. Spat from wild spawn should not be allowed to collect on the shells of older infected bivalves. It alsoappears that the severityof infectionin individual shellfishand the percent- ageof individualsthat are infectedmay increaseas the animalsget older. Thus,it maybe desirableto harvest all individuals at as early an ageas possibleand to removeolder shellfish from the population. Other Diseases, Other Molluscs / 81

References Alderman,D. J., P. Van Banning,and P. Colomer.1977. Two European oyster Ostrea edulis! mortalities associatedwith an abnormal hernocyticcondition. Aquaculture 10:335- 340. Brousseau,D. J. 1987. Seasonalaspects of sarcomatousneoplasia in Mya arenaria soA;- shellclam! from Long Island Sound. Journal of InvertebratePathology 50:269-276. Cooper,K R,, R. S.Brown, and P. W. Chang.1982. Accuracy of bloodcytological screening techniquesfor thediagnosis of a possiblehematopoietic neoplasm in thebivalve mollusc, Myaarenaria. Journal of InvertebratePathology 39:281-289. Cooper,K. R.,R. S. Brown, and P. W. Chang.1982. The course and mortality of a hernato- poieticneoplasm in the soft-shellclam, Mya arenaria. Journal of InvertebratePathology 39;149-157. Cosson-Mannevy,M. A., C. S.Wong, and W, J, Cretney. 1984. Putativeneoplastic disor- dersin Mytilus edulis!from southernVancouver Island waters,British Columbia. Journal of Invertebrate Pathology 44:151-160. Elston,R. A., M. L. Kent, and A. S. Drum. 1988. Progression,lethality and remissionof hemicneoplasia in the bay mussel,Mytilus edulis. Diseasesof AquaticOrganisms 4.135- 142, Elston,R. A., M. L. Kent, and A. S. Drum. 1988. Transmissionof hemic neoplasiain the baymussel, Mytilus edulis,using whole cells and cell homogenate.Developmental and ComparativeImmunology 12:719-727. Farley,C, A, 1969.Sarcornatoid proliferative disease in a wild populationof bluemussels Mytilusedulis!. Journal of theNational CancerInstitute 43!:509-516. Farley,C. A. 1969. Probableneoplastic disease of the hematopoieticsystem in , Crassostreavirginica andCrassostrea gigas. National CancerInstitute Monographs31:541- ;5, Farley,C. A. 1976.Proliferative disorders in bivalvemollusks. Marine Fisheries Review 3Ht10!:30-33. Fsrley,C. A., andA. K. Sparks.1970. Proliferative diseases of hemocytes,endothelial cells, andconnective tissue cells in rnollusks. In ComparativeLeukemia Research 1969, ed. R, M. Dutcher,Bibl. Haemat.,No. 36 Karger,Basel/Munich/Paris/New York!, pp, 610-617. Farley,C. A., S.V. Otto, andC. L. Reinisch. 1986.New occurrence of epizooticsarcoma in .'hesapeakeBay soft shell ,Mya arenaria. FisheryBulletin U.S.!84!:851-857.

34 / MOLLUSC DISEASES / Elston

BrownC,, and G. Roland. 1984.Characterization of exotoxinproduced by a shellfish- pathogenic Vibrio sp. Journal of Fish Diseases 7:117-126. DiSalvo,L. H,, J. Blecka,and R. Zebal. 1978. Vibrio-anguillarum and larval mortality in a CaliforniaUSA coastalshellfish hatchery. Applied Environmental Microbiology 35!:219- 221,

Elston, R. A. 1984. Prevention and managementof infectious diseasesin intensive mollusc husbandry.Journal of the WorldMariculture Society 15:284-300,

Elston, R. A., and L. Leibovitz. 1980, Pathogenesisof experimental vibriosis in larval Americanoysters, Crassostrea virginica, CanadianJournal of Fisheriesand Aquatic Sciences 37:964-978.

Elston, R. A., L. Leibovitz, D. Relya, and J. Zatila. 1981.Diagnosis of vibriosis in a commer- cial oysterhatchery epizootic: diagnostic tools and management features. Aquaculture 24:53-62. Elston,R. A,, L, Elliot,and R. R. Colwell.1982. Conchiolin infection and surface coating Vibrio; shell fragility, growthdepression and mortalitiesin culturedoysters and clams Crassostreavirginica, Ostrea edulis and Mercenaria mercenaria. Journal of Fish Diseases 5:265-284, Guillard,R. R, L, 1959.Further evidence of thedestruction of bivalvelarvae by . Biological Bulletin 117:258-266. Jeffries,V. E. 1982.Three Vibrio strains pathogenic to larvaeof Crassostreagigas and Ostrea edulis. Aquaculture 29:201-226. Lodeiros,C., J. Bolinches,C. P. Dopazo,and A. E. Toranzo.1987. Bacillary necrosis in hatcheries of Ostreaedulis in Spain. Aquaculture 65:15-29. Tubiash,H. S,,P. E. Chanley,and E, Leifson. 1965. Bacillarynecrosis disease of larval and juvenilebivalve molluscs. I. Etiologyand epizootiology. Journal of Bacteriology90:1036- 1044.

Tubiash, H. S., R. R. Colwell, and R. Sakazaki. 1970. Marine vibrios associatedwith bacillarynecrosis, a disease oflarval and juvenile bivalve mollusks. Journal of Bacteriology 103:272-273 Walne,P, R. 1958.The importance of bacteria in laboratoryexperiments on rearing the larvaeof Ostreaedulis L.!. Journalof theMarine Biological Association of theUnited Kingdom 37:415-425. Other Diseases, Other Molluscs/ 85 Hinge Ligament Disease of Juvenile Bivalve Molluscs

In hinge ligament disease, the hinge or ligament that binds the two valves of a bivalvemollusc together is erodedor completelydestroyed by bacteria. Known as "gliding" bacteria because of their distinctive motion, this specialized group of microorganisms has notbeen well studied. The gliding bacteria are known to have the ability to decompose manyhighly organizedand complexbiological structures made of protein, such as the hinge ligamentof bivalve molluscs. Vast numbers of these bacteria are often found within the ligamentsof juvenile clams, oysters,or scallopsthat sicken and die in nursery areas. Once theligament is destroyed,the mollusc is unable to openits valves for feeding and respira- tion. Figure 9 shows in graphic form that these bacteria can cause the normally resilient ligamentto soften and even liquefy at temperaturesin the 5 C-10'C range and higher. It is alsopossible that the destruction of the ligament allows other bacteria to infect the tissues of the animals.

resilient

softened

gelatireus

liquefied

sa 15 20 INCUBATION TEMPERATURE 'C! II ~ I I II II Figure 9. Effect of gliding bacteria on the hinge ligaments of the oyster. Four different gliding haeteriaare compared with a fifth type of bacteria which is not capable of degrading the hinge liga- ment.The graph shows that gliding bacteria can causesoftened, gelatinous, or evenliquefied liga- mentsat temperaturesdown to about 10'C. The effectsare less pronouncedbelow 10'C. Graph courtesyof C. Dungan! 86 / MOLLUSC DISEASES / Elston

This diseaseis the most important known diseaseof juvenile bivalve molluscs. It can infect any species.It has beenreported from many locationswhere juvenile bivalves are intensivelycultured. It is not knownif the diseaseis importanton oysterbeds or among populations of wild oysters. The causativebacteria are probably commonin all marine environments,and thereforethe diseasemust be controlledby husbandrymanagement techniques.

Geographic Range and Species Infected Hinge ligament diseasehas beenfound in juvenile bivalves from both the east and the west coastof North America. It is likely that the diseaseoccurs wherever bivalve molluscsare cultivatedand potentiallyin any species.It hasbeen found in the following species: Crassostreagigas!, CrassostreaUirginica!, European flat oyster Ostreaedulis!, Mercenariamercenaria!, Manila clam Tapesphilippi- narum!, Siliqua patula!, and bay Argopectenirradians!. Mortality Rate, Environmental Factors, and Seasonality In manycases, aquaculturists have reported the completeloss of largegroups of clamsand oystersfrom this disease.Usually the bivalvesaffected by the diseaseare fram settleinentsize to 1 cmin shell height. The smalleranimals are probablymore susceptible, No typical seasonalcycle of the diseasehas been determined. It canoccur year- round,possibly because juvenile molluscsare usuallygrown in a controlledenvironment, oftenwith heatedwater. Researchon the diseasehas shown that the hingeligaments are degradedat an inc~easingrate as the water temperatureincreases over the rangefrom O'C to 20'C andthat the normallyhard ligament,when infected with the gliding bacteria,can becomejellylike at water temperatures as low as 10'C.

Diagnosis There is no known way to make a certain diagnosisof hinge ligament diseasewithout the microscopicexamination of the ligament.However, in any largemortality ofjuvenile molluscsthis diseaseshould be suspectand samplessubmitted for a pathologicalevalu- ation.

Prevention and Management Eradicationof hingeligament disease is not possiblebecause the causativeorganism is commonin marineenvironments. Thus, the disease must be prevented and limited by husbandrymanagement techniques see "Preventing and ManagingDisease in the Hatch- ery"!. The approachestried have beengeared toward the regular disinfection of the surface ofjuvenile molluscs.The mosteffective disinfectant has been sodium hypochlorite, other- wiseknown as commonhousehold bleach. Sucha treatmentcan be appliedonly whenthe juvenilesare in containersin a controlledenvironment, and the treatment is morepractical for single bivalves than for oysters attached to cultch. The concentration,frequency, and length of treatmentmay haveto be adjustedto OtherDiseases, Other Molluscs I 37 meetindividual circumstances. A suggested starting point for the treatment isa three- minutedipin 25 parts per million sodium hypochlorite dailyfor five days. This concentra- tionismade bydiluting household bleach,usually labeled 5.25% sodium hypochlorite, with seawaterbya factor of2,100. This should beperformed routinely if serious problems have beenexperienced fromthe disease. Thecontinuing needfor treatment willhave tobe determinedfor eachoperation. Threeantibiotics, penicillin, novobiocin, andtetracycline, areknown toinhibit growthofsome ofthe strains ofcausative bacteria. Penicillin iseffective atrestricting the growthofmost, if not all, strains ofthe ligament-degrading bacteria,while novobiocin restrictsgrowth ofthe least number ofstrains tested todate. Antibiotics arenot recom- mendedforroutine use and should beapplied only in a seriousdisease situation, withthe dosageestimated in consultation with a pathologist.

References Dungan,C.F. 1987. Pathological andmicrobiological studyofbacterial erosion ofthe hinge ligaiiientincultured juvenile Pacific oysters, Crassostrea gigas.Master's thesis,University of Washington, Seattle. Dui>gan,C.F., and R. A. Elston. 1988. Histopathological andultrastructural characteris- ticsofbacterial destruction ofhinge ligaments incultured juvenile Pacific oysters, Crassos- treagigas. Aquaculture 72:1-14. D>ingan,C.F., R. A. Elston, andM. Schiewe. 1989. Evidence forcolonization anddestruc- ii<>nofhinge ligaments ofcultured juvenile Pacific oysters, Crassostrea gigas, byCytophaga- likebacteria. Applied and Environmental Microbiology 55!:1128-1135, Elston, R.A. 1984. Prevention andmanagement ofinfectious diseases inintensive mollusc husbandry.Journal of the World Society 15:284-300. Flston,R.A., L. Elliot, and R. R. Colwell. 1982. Conchiolin infection andsurface coating Vibrio:shell fragility, growth depression andmortalities incultured oysters andclams '.rassostreavirginica,Ostrea edulis and Mercenaria mercenaria. Journal ofFish Diseases «:265-284.

AmebofiagellateDisease of Larval Clams Thisdisease ofthe larval geoduck clam Panope abrupta! iscaused bya parasitic piot<>zoanknownas an ameboflagellate andprobably belonging toa group known as iso>>ema,It wasrecently discovered inhatchery-reared larvalclams. 38 / MOL I VHC MS'RA,888 / E/ston

Geographic Range and Species Infected The diseasehas beendetected only in the one location where geoducklarvae are cultivatedin Washington.Only geoducklarvae are knownto be infectedby this flagellate ,kq; Mortality Rate, Environmental Factors, and Seasonality Kx Exact mortality rates of larvae due to the diseasehave not beendetermined, but hatchery persoiiiiel report losses to be "substantial." The mortalities have occurred throughoutthe time in which the larvaeare cultured,from Februarythrough May.

Diagnosis A preliminarydiagnosis can be mademicroscopically by examiningwet mountsof sick larvaefor the characteristicprotozoan see Figure 10!. The diagnosisshould be con- firmed by havinga shellfishpathologist microscopically examine tissues for the presenceof +/N the parasitesin the mantle and body cavity of the larvae.

1~~4!

v>

Figure 10. C~eoducklarva infected with the parasiteIsonema, The parasites are located between the:-,, valves arrows!and can be identified with a low-powermicroscope. Other Diseases, Other Molluscs l 89

Frevention and Management No specificmethods are known for the managementof the disease. It is nat known to infectjuvenile or adult geoduckclams and doesnot infectoyster larvae grown in the same vicinity as the larval .

Reference Kent,M. L., R. A. Elston, T. A. Nerad, and T. K. Sawyer. 1987. An Isonema-likeflagellate Protozoa:Mastigophora! infection in larval geoduckclams, Panope abrupta. Journal of Invertebrate Pathology 50:221-229.

Diseases of

The abalonegroup of molluscs,long cultured in Japan, are being increasingly farmed in North America. Several diseases have been reported, but relatively little is known about the diseasesor health management of the abalone. Vibriasis has beenreported in the red abalone, rufescens,as it has beenin manyintensively cultured molluscs. This diseaseis consideredto be cosmopolitan,that is, causedby a cornrnanmarine bacterium, and the eA'ectsof the diseasecan be controlledby goodhusbandry practices. One of the most common bacteria in the marine environment, Vibrio alginolyticus, invadesdamaged epithelium or skin af the cultured abalone,then grows through the circu- latorysystem of the animals, causing a fatal disease. Abalone stressedby high tempera- turesand supersaturatedoxygen conditions are particularly subjectto the disease. Nothing specificis reported for the managementof this disease,but controlling temperature and oxygenlevels as well as minimizing the number of vibrias in the system should reduce losses. In Australia, a parasite known as olseni, similar to the one causing derma ipcrkinsiosis!in oysters,is reported in the black-lipped abalone,Hali otis ruber. The disease i.' found in wild harvested abalone. It causes saA, cream-colored or yellow-to-brown pus- tulcs in the adductor muscle, in mantle tissue, and an body surfaces. Animals with these lesionsare considered unacceptable for processing. Infection appears to depend, at least in part,upon temperature; abaloneat 15'C had the lesions filled with dead parasites,while abaloneat 20'C had active lesions containing live parasites. Another parasite, Labyrinthuloides haliotidis, is reparted to cause mortalities in hnuhery-rearedred and pinto abalone and H. kamtschatkana!in British Columbia.The parasite is consideredto be a protozoan single-celledanimal!, It was lethal to alialoneunder six months of age in an intensive culture facility. Parasites are found in thehead and foot tissues of infected abalone. The parasites are reported to grow best at a temperatureof 10'C but not above 28'C! and a salinity af 30 parts per thousand in experi- mental studies. 40 / MOLLUSC DISEASES / Elston

Mortalities of cultured seed abalone of the three important species in Japan, Nordotis discus, N. gigantea, and N. sieboldii, have been attributed to bacterial pathogens. Mortal- ites were reported to be reduced by treatment with dihydro-streptoniycin sulphate at 100 parts per million in the 32 days following development of the veliger larvae.

References Bower, S. M. 1986, The life cycle and ultrastructure of a new species of thraustochytrid Protozoa: Labyrinthomorpha! pathogenic to small abalone. Second International Collo- quium on Pathology and Marine Aquaculture, September 7-11, 1986, Porto, Portugal, pp. 35-36.

Bower, S. M, 1987, Labyrinthuloides haliotidis n. sp. Protozoa: Labyrinthomorpha!, a pathogenic parasite of small juvenile abalone in a British Columbia mariculture facility. Canadian Journal of Zoology 65:1996-2007.

Bower, S. M. 1987. Pathogenicity and host specificity of Labyrinthuloides haliotidis Proto- zoa: Labyrinthomorpha!, a parasite of juvenile abalone. Canadian Journal of Zoology 65:2008-2012.

Bower, S. M. 1987. Artificial culture of Labyrinthuloides hali otidis Protozoa: Labyrintho- morpha!, a pathogenic parasite of abalone. Canadian Journal of Zoology 65:2013-2020.

Elston, R. A., and G. S. Lockwood. 1983. Pathogenesis of vibriosis in cultured juvenile red abalone, Haliotis rufescens Swainson. Journal of Fish Diseases 6:111-128.

Lester, R. J. G., and G, H, D, Davis. 1981, A new Perkinsus species Apicomplexa, Perkin- sea! from the abalone Haliotis ruber, Journal of Invertebrate Pathology 37:181-187.

Tanaka, Y. 1969. Studies on reducing mortality of larvae and juveniles in the course of the mass-production of seed abalone-I. Satisfactory result with streptomycin to reduce inten- sive mortality. Bulletin of the Tokai Regional Fisheries Research Laboratory 58:155-158.