- Email: [email protected]
Diseases in wild and cultured salmon: possible interaction
fyrrrlt*u/:rvi.. 98 ( ! 99 I ) 27’7-258 Else\ :er Science Pubhshets B.V.. Amsterdam
277
Diseasesin wild and cultured salmon: possible interacth
;iislan.
./
T. ;il~u uIdsiti~.
1.. i 49 I. Diseases in wild and ruhured
s;llmon: possible Intcractlon.
.+ra-
c~rtilltrc~. 98: 277-x3.
An overview of some of the POSI impurtant infcctiousdiseases in wild and farmed salmon IS g!vc~ and possible disease inwrxtions are discussed. ilumdn activities like fish farming. r,stc. k!n&“f fish in river system;. pollution of water5 rhrough lnduslrral and agnculttiral activities may howcypr he the grcatcst factor causing porenIlat inlcraclions bctwecn ~113 and farmrd populations.
Aquacultllre has increased considerably in importrlnce throughout the world during the last dc;ades compared with the exploitation of wild fish for food 2nd sportfishing ptirposes. In I\Jors,ay the economic importance of fish farm ing is now far ahe;ld cf that af wiild salmoniti fish. However, it is somewhat difftcult to foresee and evaluate the importtince and economic value of sportfishing from a recreational point of vkw, bJ.I t it should not be undercstirnaterl. of infcc:ious disease in farmed fish is due to The occurrence and the qx~d the high densities at which the fish are held. Such disease in farmed fish is now 2 very serious problem and when compared to disease r.1 wild fish, the latter is seen as a phenomenon rather than a problem . This comparison has led to an assumption in some quarters thdi the fish farm ing industry was the origin of infectious diseases iq wild stocks. Such an assumption cannot be correct because the available etiidence indicates that these infectious diseases existed previously in wild stocks, e.g. as early as 15ri3, Gessner’s book describes carp pox ( Tlofer, 1904). It must be emph;!sized that the environment in which the fish lives usuallv barbours a varied iilicrof’lora that may inch& many bacteria, viruses, fungi and parasites that are capable of creating serious diseases in f?,h in farms as well as in wild populations, Nevertheless the mere presence of a disease-prop0044-8486!9
I /‘sUS.50
0 I99 I Elsevier
Science Pubhshers
B.V.
All rights reserved.
178
T HAsTErN
AND
r. LINESTAD
agating organism does not necessarily mean that a disease condition will arise. as the devJopment of disease will be a complex interaction between the host, the environment and the disease agent involved (Warren, 1983). The interaction between wild and farmed stocks will most probably take place through water. fish and other sources that may be contaminated with infectious material, e.g. contaminzted fishinggear. Disease transmission through water will either take place by the shedding of infectious agents into the water from diseased farmed or wild fish and it rn::. take place over long distances. It has been proven that IPN-virus has been detected in wild fish in Scotland scme 7 km away from an aditicent fish farm (Munrr, and Dunca:i, 1377). Similar figures have been reported from Norway in ,-;rlnection with disease outbreaks. Disease transmission and interaction of fish is most likely to occur by contact between f;rmcd fish and wild fish on each side c?fthe cage cr by Gcape of residing farmed fish migrating up imo nearby river systems. The USC of csc;lprd farmed fish irs hro.)rl tish for restocking purposes may also lead 10 tran;rnission af &ease into hatcheries especially those diseases that may be transferred by verrical transmission. Horizontal transmission may Jso trrke place if current hygienic procedures I:uch as egg disinfection is not followed In this paper some of the currently more important fish diseases and their etiulogical agents arc described.
1 ‘irui ;rcwtc~rrth,q.k~z,ptic*rrnicl (VHS. Egtved diseaszj, is an acute rhabdo-
virus infection dtiscribed in rainbow trout from Denmark in 1949, and in Germany possibly as early as 1938 (Schaperklaus, I938, 1954). The virus is now believed to be disseminated in farmed as wel! as wild populations of saimonids Ltnd non-salmonid fishes in Europe. The chscase is characterized by dark pigr,ientation. exophthalmus. accites and hemorrhages in internal organs. This disrase ~3s originally believed to be a disease condition in farmed rainbcbv trout (Ultl.r,rlr)~~z~l~ll.s nrj*kiscf), and that the disetise could only be transmitted through experimental infections to other salmonid such as Atlantic salmon (Salrno sahr). However, Enzmann and Konrad ( 1985 ) reported that I O-4 1% of’wild brown trout (Sufmo rrlttta ) cafrght upstream and downstream from a formerly infected rainbow trout hatchery showed VHSVspecific &;ntibodies in their sera. Such fish could thus be regarded as a possible source for the distiibution of the virus which largely takes p!ace through virus laden water i.c. lateral spread. Escaped fish are another p lssible source of virus. VHS was originally only thought to be sndemic in Elropean waters, but in 1988 VHSV was detected in two hatcheries in Washington &te, USA in spawni.ri; coho (0. k~\rctc%) and chinook salmon (0. tshmytdr~). The
source of infection is still unknown, and the disease has re-appeared in migratory Pacific salmon in I989 (Tebb, 1989). There is reason to believe that the virus might have existed in these fish specie; without causing disease problems. These findings may however result in a tkreat to the US rainbow trout farming industry as well as wild stocks of rainbow trout, It should also be mentioned that the virus has been detected in cod (Gadus rnorht~a) in Danish waters (Vestergard Jorgensen and Olesen. I?87 ). In 1990 VHSV was also isolated from Pacific cod (G. macrwc~phah) off the coast of Alaska. I~~ficliolrs nrvtlulrywiivic sc.i.I’ii.iij (IHN) is another rhnbdoviral infection with similar clinical and pathological signs as those described for V ES. The principal species of salmonids susceptible to IHN1’ are rainbow trout, sockeye salmon (O~cc~l?~‘rfr’lrfi.sX&Z) as well as iiokanee and chir.cok salmon (ii. rsha~.~tscha). Naiti.3 occurring epizootics have also beer, observed in Pacific salmon (B.H. Hill, pers. commun , 1989). Susceptible species of salrnonids are considered to be the only knowr? reservoir of the IHN virus and the release of virus usually occurs at the time of spawring. This may provide ample concentrations of virus released with sexual products for vertical transmission to occur. IHNV can retain infecti ity in wa!er al 10°C for up to 7 weeks (Wedemeyer et al., 1978 ), thtis allowing sufficient time to infect fish of the same year class or newly hatched salmon and trout fry. but ma) also result in initiation of infection among other fish (Muicahy et al.. 1983a. b). High carrier rates of the virus among feral fish populations and epizootics in such populations (Williams and Amend. 1976; Muicahy et al., I983s: Ttaxier, 1986) clearly demonstrate the perpetuation of IHNV in wild stocks of salmonids which, when used for brood fish in commercial hatcF&cs. could rcprcsent a threat to ;he fish iarming indust,.y. There is reason tct hcii~vc that IHN has been t:ansferrci to Europe by ilnportation of infcctcd ceqs I’rom enzootic areas of the USA.
H~?rpc~s~linrssaimc)nis is a virus isolated from normal-appearing adult stocks of caplive as well as anadromous steeihcad trout with as much as 50% mortality post spawning. Since the virus i; prcserlt in adult tish, this may indicate possible vzticar ’ ‘.ransmission. So far this virus has been diagnosed only in fish from Northern America (Wolf, 198S). The h’~J7?4 virus 1sanother herpes virus infection first recognized in Japan in lS72 (Sano. 1976) on Honshu Island where it was found in moribund landlocked sockeye salmon. This virus was responsible for annual cpizootic., in progeny of himemasu or kokanee. The NeVTA virus was named from the specie: an3 iof:ation (Nerka virus, Towzdo Lake, Akits Prefecture). It caused considerable mortality among progeny of himemasu ( kokanee), a landlocked form of 0. wrka In 1978 ;dnothcr herpesvirus was diagnosed on Hokkaido Island among yamame (landlocked) masou saLnon (0. rrtcrsr~lc)from ovar-
180
1. HASTEIN AND T. LINDST4D
fit-id of normai brood fish with poor progeny. That virus was named Oncorlrytr~~hus rnuwl/ rinr.~ (OMV ) (Kimura et al., 198 1 ). OMV has been shown to be pathogenic to several salmomds and in survivors given epithelial tumors ma\* occur subsequently. Another herpesvirus was isolated in I98 1 from natur;i occurring tumors in yamame (Sano et at. 1983 j and named Yamame rlrttror rYrrrs (YTV). Yet an;:her herpesvirus was Lctated from ocean pen cultured adult cohu jalmor ~0)ncorh~~hus kisurch) and named c&o salmon /wwr virus (CSTV ) ( Sano. I 388 ) . Many inue~+igatc:~ ‘ixlicvc ihat OMV, I’TV and CSW to be &nilar viruses from which NeVTA virus can be differentiated. These viruses are so far found only in Japan. but mJy represfnt a future risk for transmission to other countries Ir!,5~imv putrct~~a~i~~r~c~~.si.v(IPN ) is a hirnavirus infection which is now rccc!g:.ised it, ix ividc:y spccad throughout the world and within a variety of populations of aquatic organisms since its first discovery in 1946. Among salmonids the principal source of IPNV is infected brood stock which transfer the :pirus to the offspring. ‘jurvivots of clinical disease may become carriers and sllrd the virus. SuLh 5sh shouid cf course not be used for breeding pur;)c)ses.As with other infectious agents lPNV has most probably been derived from wild s;ocks and secondarily been transferred into aquaculture which in turn hrs spread the disease :lnd virus through shipment ofcontaminated eggs or live fish. IPNV has been isolated from fish from the McKenzie delta, Canadr: \B,hzreno fish. according to information received, have been stocked (T.G. Carey. pcrs. cornmun.. 1084). ian
.~i~ton ~NWIII~*.W irrrs has so far or;ly been isolated from apparcntly Norman .4;nook slirrul, luring health monitoring programmes and its r0ie i:~ ;L pu~,silil; ii;,,.,,***In t:lrtr-r Illt.. .. ic .” nnt ..-. determined. _.. ~‘CLIW v +:;il~ I~~OI*~WS was tirst isolated from healthy appearing 0. keta returning to Hokkaido Island. but has later been reported to cause some mortality in 0. WUSOU.The only pathological change reported has been focal necrosis in liver of chum and chinook salmon fry in early stzges of Infection (Wolf. 1988). C‘i~irtrwk
.dllunlic.
.~ctltwtt switdh
I&r
surtwrr~a virrrs infection was reported from
Scottish cage culture and whcl L’massive swimbladder tumors were associated with some mortality in I-year-old smelts and 2-year-old Atlantic salmon ( McKnight. I978 j. SO far this discasc has only been reported from cage culturc in Scotland ;ind this prohlem has not been recorded in wiid stocks.
Several a~mic conditions ha\ * been described from wild ~n3 farmed WImonids. Most common among these cxGtions are I-,‘rr~lrrcq*r 4, irtctrtsion hd4* f EIBS j. In/kWms .saltr7
Papillomatnsis ot’ Atlantic salrn~~~nhas been kilown for many years in wild stocks and was first reported from Sweden in i 97 i ( Wircu. I97 I ). The papillomas are usually detected in parr and smolt In fresh water, but irri* sometimes also found in migratory salmon x-turning irom the sea. The prev&llce is reported to be 5-55 o/u, hut in most outhrcaks the pr~valcncc is I~w. The disease has also been reported under farming condition>, but neither in rage culture nor in wild stocks does the discase yccrn to cause mortality of ;Iny significance. :‘!~‘L’ruli~‘L’ij(Jr777uI ~7ccr~~.vi.s (UDN ) is rl rlicrase with an unrcs4vcd ctic?ogy, but possibly of viral origin. Though the affected fish in terminal stages WI!
die from secondary fungal infection of the Saprolegnia parasiricc /diclina complex, UDN is still only observed in wild stocks of Atlantic S~~~IKMI and sea trout. The disease is initially characterized by small grcy erosions on thi: head and adipose fin. Only adult fish are affected upon ‘their entry into fresh water. The history of this disease goes as far back as 1873-I 5 1 I when it was reported from several rivers in Britain where it spread frcr.1 watershed to watershed. In I964 a recrudescence of the disease took place, starting in salmo,l ri\*ers in the south of Ireland and then spreading to &itain and later to rivers in France. In Sweden the disease was detected in 1976 and later spread to rivers in the ana LJungberg, 1977: Popp, castern p,7rt5 uf ?lorwriy by :%7 ~~~J~ldllwm 1989).
~l,irllcllioc:r:~riv IS a chlamydial infection that may result in hypertrophied
cprthclial crlls of the gills of several marinc species includ& s&Tonids. Under normal circumstances the condition is ofbenigrl character, but may cause respiratory problems in hdl.
~‘lcrrrrt(,rrlovi.v.also named ‘The Great Red Plaque’, ‘B;tctcrial i!emorrhagic Scpticcmia’. ‘Fururiculosis Salmonidarum’. and ‘Boil Disease’, was first described in connection with a disease out.>reak in Bavaria in 1894. Where the disease initially originated will possibly rover be revealed although there i)re descriptions indicating the cxistencc of the disease since I868 (Forel, 1868). Tilcre is some discussion whether it was spread to Europe from USA or vice versa. Some indication of the former may be that rainbow trout introduced front USA to Europe IS more rk i&ant to .!K disease than the brown trout and Atlantic salmon. In the beginni IS of tht 20th century, the disease spread rapidly in Europe in wild stocks as 1: !I as +I farmed fish and Plehn i 1909, 19! 1) showed that the disease C. %ted ir wlrC : . ?ut populations in 25 river systems. Irk Great Britain considerablr: mortality was .?bserved in several salmon rivers in I9 I I ( Wyc. Exe. Teige, Dart) (Arkwright. 19 12) and the disctise is still reported to be endemic in rivers in BtiIain. In Finland, furunculosis was first detected in Atlantic salm,>n brood fish caught in Bothnian Bay, but later also in rainbow trout, char and brook trout in hatcheries. In Norway the disease was first rcportcd in 1964 after importation of rainbow trout from Denmark, and the dibease was probably transferred to the river Numedalsl&n due to
DISEA!iSES IN WILD 4N11 CL’LTl!RFD
WLMIJS:
POSSIBLE lNTtR4C‘TION
283
stocking of latent carrier iish in a tributary. The mortality rat\: in this river system, however, seemed not to be of any significance compared to the mortality rirtes reported under farming condition where it may vary considerably, and can range from ! O-20% up to 50% (Hastein and Holt, 1970). From 1985. furunculosis has been epidemic in Norwegian fish farms in some regions after initial reintroduction of the disease due to importa?ion of latent infected Atlantic salmon smelts from Scot!and. Due to escaped fish, the disease has now been introduced in some 20 Norwegian salmon rivers. The significance ofthis is still not known and and the investigations into the epizootiology of .4. .vulmonicidu ;hus far have not provided unequivocal answers to several crucial questions concerning the dissemination of the pathogen. Controversy still exists whether tne pathogen is able to exist in a free-living stage in the natural environment or if it is a true parasitic pathogen which does not have any existence outside the fish host. Several experiments concerning the survival of the bacterium in water h:ive been carried out. giving different results. The existence of latent carriers is however the most likely way that the infection persists in a watershed system from one season to another. Ir$vtions by atypical Aeromonaq salmonicidu. Pigmented as well as nonpigmented striains are most likc!y to be Gdely distributed in nature and in different species of fish. ln Ntirway we have expericrlccd disease outbreaks in wild populations of salmomds and non-salmonid fish as well as in farmed I,-**nn n+ salmoni& . Or . .;ntrnA . . . ,y,~,,l,.. “.’ whitefish from the Norwegian lake Mjosa into an aquarium facility, disease appeared in the whitefish (C’c)r~~~rn~rs ult~rlu) and in pollan (inrt~~onrts Iu~~rctt~s). The same observation was experienced upon transfer of Arctic char (Sal~v~lin:~.vufprtrrts) from the lake TakL,atn to a hatchery. Z’ihricrsis. While coldwatcr vibriosis caused h>, l’r3~~0 ~~/;)totrl( ij,, 1s nt)t recovered in disease outbreaks of wild fish, classicrrl VI~I iosls cus?d by 1 ‘Ihrio anguillarum has been registeved in both wild and fnrmcd populGtlons of salmonids. While Smith ( I96 I ) rcportcd the disease lo or-cur in finnock from the river Dee, the disease was encountered in several Norwegian salmon river systems as far away from the river mouth as 10 km and cvcn in regions where no fish farmmg took place. There is reason tJ believe that I ‘. crngtrikmrtn constitutes part of the normal microflol 1 of the aquatic environment and in maximum and minimum numbers in summer and winter rcspectivcly (Larsen, 1982). The onl) kimwhat I~V spp. infection in wild migratory broodstock of Atlantic salmon reported by Roald and HAstein ( 1980 ), is now bclicved to have been caused by 1‘ihrio spp. Buwrial kidmy diwuw ( HKL), Ucc discasi ) caused by Kenihu!?eriwn .;~imoninuntm was initially described in 1930 in connection with disease In the river Dee, and the river Spcy in Scotl;z,ld (Mackie zt al.. 1933). In 1935, the disease was reported from hatchery-reared rainbow (n;tit. bro\\n trout and
break trout in USA ( Balding and Merill, 1935 ). Since that time, the disease is reported in at ‘c-rs: 13 different sahnonid species from many ccuntries throughout the world. Today this disease represents a great threat to fish farming. especraily to rhe farming tif Pacific salmon. It is only occasionally found in wild fish populations (Mitchurn and Sherma;l, i 98 I ). There is no doubt that wild tish may represent a greater risk to the farmed popuiarioas than vice verse. This is due to the chronic appearance of the disease and the difficulties in the eradication ofthe bacterium in wild stocks. However, a heavy infestation oi BKD in farmed fish will also pose considerable infectious taressure on wild fish populations. ~i~~inio.v~s (entrrir red mouth, ERM) was initially diagnosed as ti systemic infection among farmed rainbow trout in Hagerman Valley. ID. USA. Thr: disease is still mostly restricted to salmonid species. but has been reported from scvcral countries outside USA in the 1950’s and seems to be more widespread than Ii rs’ rhtiught. Its significance in wild populations of salmonids is not known. but is prc?;umably of little significance since the disease usually only results ir disease problems in f’armed fish when stressed. 4% WC‘ ozcasion we have recovcrzd Yor.sirriti rlr&ri in one wild sea trout brocld fish from a river on the vvcst coast of Norway.
.~(ll!rr’l(:~rriu-inf~~tions vauscd by the S. rmrusilic.a/~ic.linu car lplcx is the most common fungirl i1iseJsc in fish and is likely ?o occur in wild fish as weil a< farmed fish. Gcncrall;. it resu!ts in infections of the skin. but the pathogencsis is complex. Although th r: fungus has hair structures on the surface of the s~conclar~ c\ ~!r which may~n.~ble !hc penetration into the skin, ieveral other trrct~s are of great signific;rncc in the dcvclopment of Su~nl/~~rriu-infection. Such factors arc rnicroscupic as well as macroscopic lesions in conrrection with iraumstic injuries in the skin due to handling, spawning and parasitic infestations. The disease may be serious to sexually mature fish in connection with spawning. but may also be ot’ importance in fish not sext.alIy mature if the primary Icsions arc‘ scvcrc enough. ,ul)rokDx~riu-iniection; have a more dcletcrious cffcct on wild fish than t’armed fish. as no treatment is possible in ;1 constant manner. t‘.l~tll~.ol~ltf)~~r~.s h&v-i infection is a systemic fungal infectiolfwidesprcad in nature and reported io ‘cause significant mortality in herring, but was alsc reported to caJse infection in salmonids 2’; uar;y as 1893 (Hofer. 1893 ). It normaiiy dt;t’s not cause any disease problems ccither in wild fish, no: in farmed tish, but should ncvcrtSclcss bc considcrec! as a potential problem. I::\-c’C’lriLc!~-i?icctic,n is unoth~r fungal infection in freshwater fish first described to cause so-called ccrc:;r’al mycctoma in cutthroat trout (Carmichael, lqt(j) anj iids >i;*ILL ..LI? b. I\ 8*..b** b.1I.” .I* ;t L,‘;?*Asc LI*L.l bp8l%.* ,k.u crf systemic and spo~a&~ fuug;il
DISE*SES
IN WILD
4NDCC:LTIIREl~S~LLION:
POSS;BLt
Ih’Tf!?.~(‘l!OK
285
infections in farmed salmonids. Its economic significance is however lim ited as are the fungal infections caused ty Paccilliom~vw spp., Phumu spp. and kricillitrm spp. ( Neish anti Hughes. I 980 ) . PAR.4SITIC DISEASES
Many different parasites, protczoans as well as metazoan parasites have been described causing disease in salmonids. Most of these parasites do not cause significant problerx in wild stocks, but may cause large mortality within a fish farm, especially in hatcheries. O f the protozoan parasites. Jc~l;rh~dwd~c! rw~wr, \“/iilld~ncll(~ spp. and Trichdtna spp. may cause severe infestations under farming ci?nditions if river/surface water with a freeliving fish population is used as a \xtet supply. /L.;II/1)~~}ililiir;IrS rntr!l~fi/,% (~ch ) as well as My~oboftrs cerebrah may even cause disease problems in wild fish. but then only in singIe specimens compared to a f8rm situation. J~ertnqpya spp. maybe a problem for wild whitefish populations. W ith the m irnogenean GymductJ~l~tssalaris however, the situatton is the opposite. This parasite constitutes a large disease problem In Norwegian salmon rivers where it has caused considerahre problems and over years has resulted in an almost total eradication of young salmonids. This subject is dealt with elsewhere in this issue (Johnsen and Jensen, I99 1 ), but it is stressed that the reason why this parcsite is a problem in the wild popukltions and nor in farmed populations is that the latter are amendable to treatment. while the wild fish are not. Digenic flukes .nay cause problems in single fish both in wild salmonids as well as in farmed fish, but in fish cultured iu earthen ponds, considembtc effects caused by the eye fluke. Dipk~omtrm .~palhucwtm have been ohserved. The trematode P~~~llodistontttm wnbiac~is quite common in wild popu:ations of char and brown trout in densely populated waters. Under unfdvorable conditions this parasite may cause some under natural condit;ons. The parasite is so far not known to cause prohlcms in farmed stccks. O ther important metazoan diseases tha! have been reported in both’wild and farmed populations of salmonids are the salmon louse ( Lqwop~~~~.~.7%’ salmonis), plerocerco& of different cestodes such as D~~~it~~llubo~itrrtrrlr dendriricum as well as adult specimens of Llrho hrizim ;ww*,: & ‘!+,;1-.. The salmon lo~rn&v~s~tgrne nrrrV3x 1.. ~~+-;I:44;~igTatCiyZmon in sea hater, burrepresent no proolem in the freshwater chase unless large skin $sions have been created resulting in secondary fungdl infecticns. On the co$trary. the parasite may cause considerable problems among Tarmcd salmon finless treated. Etrborhritrm cruxwm, being a ‘normal” finding in the gut of wild s ilmon I and trout populations, causes some problems iu rnarirx rearing of A:lauric salmon by ixreased mortality u!tCer certain circumstances and a red3ction in growth due to reduced feed uptahe. In farmed fish, one may red&e the
problem sufficiently by medical treatment. Significant numbers of other ~,(IIasites have also been rectirded in wiid and farmed salmonids. but their importance is low. In xti;lin arcas E;lochiJie-lar*/ar: oi the frcshwa.ter pearl mussel Afugmiti,WYJtrruq~i~$~ may cause some disease problems under hatchery conditic nc unless the water is Cltcrcd through fine ~i~~s;iitlj fiibs. This probicm IS not transmissable to -.vild tush populations, but nature may use farmed fish as a WV of introclr;c;nr! the iieshwhtcr pear: mussel to other u-atorsheds by stocking ~f!j:h
llke fjsh farming, restocking of fish ii; :Iver systems, poi!ution of waters through industrlaf and agricultural ncticrties. man is Johaps the greatest t’actcr of causing potential interactions between wild and farmed populations axi \?~henxting “uncons~*iously” may create the largest damage to the rviturc. Sii:~ hUii\tili diiiviid
‘JlStr4fF.S
iX H ILI?.\?:I~(‘I’LT~~HEI~S\LS~O~’
I’OS!dHLi
IS~EK~W‘T1~JS
787
the wrus ofr~tl;loc>tic lncltwon hod!, s>ndrom:. CBt’. drtccrcxi in Atlantic salmon ( .\~I/~u~I .ru!;;,i in Norw~. Pull. Eur. Xssoc. Fish Fathol.. IO ( 1 ): Z!-23. H’.D. dnd hllvwt*s. A?wkic. T.J.. Ark&right. J..-\.. Pycc-Tanatt. ‘.‘.E.. Xlollram. .I (‘ l!*hnwn ~~\‘.J.Xl., 1933. The Second Interim Kcport ol’ t:~c Fururrcz!- nsir Commlttw. HXlSO. lidlnburgh. 8 I pp. McKnight I.J.. 1978. Sarcoma of the swim bladder of -\tlan!r: Amon (.r;(J:‘f~lJ ~r,/uv). Aq 1;~ cuhutc. ! 3: 45-w. .-:c\-r Mitchurn. D.L. and Sherman. L.E.. 1981, Transmission of bact:riat k-4 . . A.ic~:~w t’ram briu I 1 stocked hat&e? trout. Tan. ! Fish. :\~sa~. Sci.. 3X: 547-55 I. Alulcahy. D.. Paw”? v.! ?n
kobcrts. K.J.. 1989. Fish Patholog!,. Bzillicrtb T~ndall, 467 I?;‘ Qno. T.. 1976 v,:al diseases of cultured lishrr in Jawn. Fish 1’31hol.. IO: 22 I -Z?tp. .hi!I:i‘ I . . 1y8k. Characicrifation. plctlwgwlcit> nvd onc:ycniL.lth ot’hcrpc+vlru\ In tish In. Inr. Fish Hcah I Cont.. Vancouver. B(‘. C‘onCcrcnrc H?ndhotbk. Fish !linlth %,C.IIIP:I ~.xrr t.‘ln Flshcrics Scvxly. p 157. Saw. T.. I-uk .:da. H.. Okamoto, N. and Kzwku. F.. ! Vk;. k’3m:irhic I:Lmor \ lrus: Lcth3111> ;*nd oncogcnic I>. Bull. Jpn. Sot. Sci. Fish.. 49 (8): 1 159-l IG?. Sih~pcrklaus W.. I YJ8. Die Schadlgul.$;n dcr dcutschcn I ischcr*:l d,rr i ~;II:;~c ~rrwdd~nlhruC, og 54, I61 - I(yh forslag til b *iirmpcl:< her&f. Fcrskl Andsti\kcr!h!. Smith. 1.w.. 1941, ,A discasc in linnoch due 10 i’r/rrrc~ c~rr~tt!!/nr,rr,rl. J. (;ci:. klicrol6.?l.. J-1: z-1?252 icbh. T.. 1989. aquaculturc llpdatc. W: I-2. Thorud. K.. Lundcr. t.. ‘h’llk. 5. ,nrl Engcland. E.. I YYO. tlcc~ ron microscopic obwr\ ation of EIBSV-liks >drtlcla:s and IUO lntracqrl;wc!,tic virus-like pw~~clcs diffcrcnt from El&A’ in . L) itlanlic salmon. W~JJ~~~JI. L.. in Norway. BII,.It Eur. .Aw~c. Fish Pathol,. I (J: 2 l-23. Ti-tid~~. G.S. 1~1(6. An eptrootic of i!:fcctious h~~rnal~pr~i:~‘w t~t~~~rw~ In 2-!,ear-old hokancc
288
T HbTFlY
\SDT
LINDST!.
(Of.c,orb!,trl,hrr\ rwrh) (Walbaum ) ar Lake Cowichan. British Columbia. J. Fish DIS.. 9: 545-549. Vestergard Jorgensen, P.E. and Olcscz~. N.J.. 1987. Cod uicus syndrome rhabdovirus is indistingulshablc lorm the Egtved (Vt is) virus. Bull. Eur. Assoc. Fish Pathol., 7 (3 ): 73-74. Warren. J.W.. IY83. The nature of fish diseases. In: F.P. Meyer. J.W. Warren and T.G Care) (Editors). -\ guide to inlegralcd Fish Health Manag ; r Ilcn: in rhc Great Lakes Basin. Grcdl Lakes Flshrries Commission. Sp x. Publ.. 83-J. pp. 7-l 3. U’cdcmcyer. G.r\., Nelson, N.c_‘. and Smith. C..A.. 1978. Survival of the salmonid viruses infect~ous hcmatopoietic necrosis ( IHh” t and infectious pancreatic necrosis (IPNV ) III ozonatcd. chlorinated and untrcaxd tiatcrs. J. k:sh. Res. Board Can.. 35: 1564-l 567. ‘~w’:‘lIdl~i,. 1.V. aqd Arnc’l,d. D,F.. 1976. .A natural cpixotic of infcctlous hcmatopoirtic necrosis (Orrlorll~.r/,‘hlr.\ rwrC,J) at I hllko Lake, British Columbia. J. Fish. rn f’~ ol’sockc)c Amon Kc5. Board Can.. 33: I 564-i 31~7. %‘lrcn. H.. I Y71. Wart discasc in .A,lantlc salmon (.S~lr)r,: .SL(/LITL. ): Hislologlcal studies ofcpidcrmal I:apllloma in rcurcd salmon ( I’artsJuka hos lx ; Suftm .x~frr L. ) histologiska studwr 0% cr cpidcrmala paplllnm has odlad lax ). Swed. Sstmr )n Rcs. Inst. Rep.. LFI Mcddclandc. 7: I-IO. bolt, h.. I Y&d. l,i,h Vlrusti\ a11J Vlrdl IIiwascs. (‘orncll Ilnlxcrsltb Pwss. Ithaca. NY. 476 rp.
277
Diseasesin wild and cultured salmon: possible interacth
;iislan.
./
T. ;il~u uIdsiti~.
1.. i 49 I. Diseases in wild and ruhured
s;llmon: possible Intcractlon.
.+ra-
c~rtilltrc~. 98: 277-x3.
An overview of some of the POSI impurtant infcctiousdiseases in wild and farmed salmon IS g!vc~ and possible disease inwrxtions are discussed. ilumdn activities like fish farming. r,stc. k!n&“f fish in river system;. pollution of water5 rhrough lnduslrral and agnculttiral activities may howcypr he the grcatcst factor causing porenIlat inlcraclions bctwecn ~113 and farmrd populations.
Aquacultllre has increased considerably in importrlnce throughout the world during the last dc;ades compared with the exploitation of wild fish for food 2nd sportfishing ptirposes. In I\Jors,ay the economic importance of fish farm ing is now far ahe;ld cf that af wiild salmoniti fish. However, it is somewhat difftcult to foresee and evaluate the importtince and economic value of sportfishing from a recreational point of vkw, bJ.I t it should not be undercstirnaterl. of infcc:ious disease in farmed fish is due to The occurrence and the qx~d the high densities at which the fish are held. Such disease in farmed fish is now 2 very serious problem and when compared to disease r.1 wild fish, the latter is seen as a phenomenon rather than a problem . This comparison has led to an assumption in some quarters thdi the fish farm ing industry was the origin of infectious diseases iq wild stocks. Such an assumption cannot be correct because the available etiidence indicates that these infectious diseases existed previously in wild stocks, e.g. as early as 15ri3, Gessner’s book describes carp pox ( Tlofer, 1904). It must be emph;!sized that the environment in which the fish lives usuallv barbours a varied iilicrof’lora that may inch& many bacteria, viruses, fungi and parasites that are capable of creating serious diseases in f?,h in farms as well as in wild populations, Nevertheless the mere presence of a disease-prop0044-8486!9
I /‘sUS.50
0 I99 I Elsevier
Science Pubhshers
B.V.
All rights reserved.
178
T HAsTErN
AND
r. LINESTAD
agating organism does not necessarily mean that a disease condition will arise. as the devJopment of disease will be a complex interaction between the host, the environment and the disease agent involved (Warren, 1983). The interaction between wild and farmed stocks will most probably take place through water. fish and other sources that may be contaminated with infectious material, e.g. contaminzted fishinggear. Disease transmission through water will either take place by the shedding of infectious agents into the water from diseased farmed or wild fish and it rn::. take place over long distances. It has been proven that IPN-virus has been detected in wild fish in Scotland scme 7 km away from an aditicent fish farm (Munrr, and Dunca:i, 1377). Similar figures have been reported from Norway in ,-;rlnection with disease outbreaks. Disease transmission and interaction of fish is most likely to occur by contact between f;rmcd fish and wild fish on each side c?fthe cage cr by Gcape of residing farmed fish migrating up imo nearby river systems. The USC of csc;lprd farmed fish irs hro.)rl tish for restocking purposes may also lead 10 tran;rnission af &ease into hatcheries especially those diseases that may be transferred by verrical transmission. Horizontal transmission may Jso trrke place if current hygienic procedures I:uch as egg disinfection is not followed In this paper some of the currently more important fish diseases and their etiulogical agents arc described.
1 ‘irui ;rcwtc~rrth,q.k~z,ptic*rrnicl (VHS. Egtved diseaszj, is an acute rhabdo-
virus infection dtiscribed in rainbow trout from Denmark in 1949, and in Germany possibly as early as 1938 (Schaperklaus, I938, 1954). The virus is now believed to be disseminated in farmed as wel! as wild populations of saimonids Ltnd non-salmonid fishes in Europe. The chscase is characterized by dark pigr,ientation. exophthalmus. accites and hemorrhages in internal organs. This disrase ~3s originally believed to be a disease condition in farmed rainbcbv trout (Ultl.r,rlr)~~z~l~ll.s nrj*kiscf), and that the disetise could only be transmitted through experimental infections to other salmonid such as Atlantic salmon (Salrno sahr). However, Enzmann and Konrad ( 1985 ) reported that I O-4 1% of’wild brown trout (Sufmo rrlttta ) cafrght upstream and downstream from a formerly infected rainbow trout hatchery showed VHSVspecific &;ntibodies in their sera. Such fish could thus be regarded as a possible source for the distiibution of the virus which largely takes p!ace through virus laden water i.c. lateral spread. Escaped fish are another p lssible source of virus. VHS was originally only thought to be sndemic in Elropean waters, but in 1988 VHSV was detected in two hatcheries in Washington &te, USA in spawni.ri; coho (0. k~\rctc%) and chinook salmon (0. tshmytdr~). The
source of infection is still unknown, and the disease has re-appeared in migratory Pacific salmon in I989 (Tebb, 1989). There is reason to believe that the virus might have existed in these fish specie; without causing disease problems. These findings may however result in a tkreat to the US rainbow trout farming industry as well as wild stocks of rainbow trout, It should also be mentioned that the virus has been detected in cod (Gadus rnorht~a) in Danish waters (Vestergard Jorgensen and Olesen. I?87 ). In 1990 VHSV was also isolated from Pacific cod (G. macrwc~phah) off the coast of Alaska. I~~ficliolrs nrvtlulrywiivic sc.i.I’ii.iij (IHN) is another rhnbdoviral infection with similar clinical and pathological signs as those described for V ES. The principal species of salmonids susceptible to IHN1’ are rainbow trout, sockeye salmon (O~cc~l?~‘rfr’lrfi.sX&Z) as well as iiokanee and chir.cok salmon (ii. rsha~.~tscha). Naiti.3 occurring epizootics have also beer, observed in Pacific salmon (B.H. Hill, pers. commun , 1989). Susceptible species of salrnonids are considered to be the only knowr? reservoir of the IHN virus and the release of virus usually occurs at the time of spawring. This may provide ample concentrations of virus released with sexual products for vertical transmission to occur. IHNV can retain infecti ity in wa!er al 10°C for up to 7 weeks (Wedemeyer et al., 1978 ), thtis allowing sufficient time to infect fish of the same year class or newly hatched salmon and trout fry. but ma) also result in initiation of infection among other fish (Muicahy et al.. 1983a. b). High carrier rates of the virus among feral fish populations and epizootics in such populations (Williams and Amend. 1976; Muicahy et al., I983s: Ttaxier, 1986) clearly demonstrate the perpetuation of IHNV in wild stocks of salmonids which, when used for brood fish in commercial hatcF&cs. could rcprcsent a threat to ;he fish iarming indust,.y. There is reason tct hcii~vc that IHN has been t:ansferrci to Europe by ilnportation of infcctcd ceqs I’rom enzootic areas of the USA.
H~?rpc~s~linrssaimc)nis is a virus isolated from normal-appearing adult stocks of caplive as well as anadromous steeihcad trout with as much as 50% mortality post spawning. Since the virus i; prcserlt in adult tish, this may indicate possible vzticar ’ ‘.ransmission. So far this virus has been diagnosed only in fish from Northern America (Wolf, 198S). The h’~J7?4 virus 1sanother herpes virus infection first recognized in Japan in lS72 (Sano. 1976) on Honshu Island where it was found in moribund landlocked sockeye salmon. This virus was responsible for annual cpizootic., in progeny of himemasu or kokanee. The NeVTA virus was named from the specie: an3 iof:ation (Nerka virus, Towzdo Lake, Akits Prefecture). It caused considerable mortality among progeny of himemasu ( kokanee), a landlocked form of 0. wrka In 1978 ;dnothcr herpesvirus was diagnosed on Hokkaido Island among yamame (landlocked) masou saLnon (0. rrtcrsr~lc)from ovar-
180
1. HASTEIN AND T. LINDST4D
fit-id of normai brood fish with poor progeny. That virus was named Oncorlrytr~~hus rnuwl/ rinr.~ (OMV ) (Kimura et al., 198 1 ). OMV has been shown to be pathogenic to several salmomds and in survivors given epithelial tumors ma\* occur subsequently. Another herpesvirus was isolated in I98 1 from natur;i occurring tumors in yamame (Sano et at. 1983 j and named Yamame rlrttror rYrrrs (YTV). Yet an;:her herpesvirus was Lctated from ocean pen cultured adult cohu jalmor ~0)ncorh~~hus kisurch) and named c&o salmon /wwr virus (CSTV ) ( Sano. I 388 ) . Many inue~+igatc:~ ‘ixlicvc ihat OMV, I’TV and CSW to be &nilar viruses from which NeVTA virus can be differentiated. These viruses are so far found only in Japan. but mJy represfnt a future risk for transmission to other countries Ir!,5~imv putrct~~a~i~~r~c~~.si.v(IPN ) is a hirnavirus infection which is now rccc!g:.ised it, ix ividc:y spccad throughout the world and within a variety of populations of aquatic organisms since its first discovery in 1946. Among salmonids the principal source of IPNV is infected brood stock which transfer the :pirus to the offspring. ‘jurvivots of clinical disease may become carriers and sllrd the virus. SuLh 5sh shouid cf course not be used for breeding pur;)c)ses.As with other infectious agents lPNV has most probably been derived from wild s;ocks and secondarily been transferred into aquaculture which in turn hrs spread the disease :lnd virus through shipment ofcontaminated eggs or live fish. IPNV has been isolated from fish from the McKenzie delta, Canadr: \B,hzreno fish. according to information received, have been stocked (T.G. Carey. pcrs. cornmun.. 1084). ian
.~i~ton ~NWIII~*.W irrrs has so far or;ly been isolated from apparcntly Norman .4;nook slirrul, luring health monitoring programmes and its r0ie i:~ ;L pu~,silil; ii;,,.,,***In t:lrtr-r Illt.. .. ic .” nnt ..-. determined. _.. ~‘CLIW v +:;il~ I~~OI*~WS was tirst isolated from healthy appearing 0. keta returning to Hokkaido Island. but has later been reported to cause some mortality in 0. WUSOU.The only pathological change reported has been focal necrosis in liver of chum and chinook salmon fry in early stzges of Infection (Wolf. 1988). C‘i~irtrwk
.dllunlic.
.~ctltwtt switdh
I&r
surtwrr~a virrrs infection was reported from
Scottish cage culture and whcl L’massive swimbladder tumors were associated with some mortality in I-year-old smelts and 2-year-old Atlantic salmon ( McKnight. I978 j. SO far this discasc has only been reported from cage culturc in Scotland ;ind this prohlem has not been recorded in wiid stocks.
Several a~mic conditions ha\ * been described from wild ~n3 farmed WImonids. Most common among these cxGtions are I-,‘rr~lrrcq*r 4, irtctrtsion hd4* f EIBS j. In/kWms .saltr7
Papillomatnsis ot’ Atlantic salrn~~~nhas been kilown for many years in wild stocks and was first reported from Sweden in i 97 i ( Wircu. I97 I ). The papillomas are usually detected in parr and smolt In fresh water, but irri* sometimes also found in migratory salmon x-turning irom the sea. The prev&llce is reported to be 5-55 o/u, hut in most outhrcaks the pr~valcncc is I~w. The disease has also been reported under farming condition>, but neither in rage culture nor in wild stocks does the discase yccrn to cause mortality of ;Iny significance. :‘!~‘L’ruli~‘L’ij(Jr777uI ~7ccr~~.vi.s (UDN ) is rl rlicrase with an unrcs4vcd ctic?ogy, but possibly of viral origin. Though the affected fish in terminal stages WI!
die from secondary fungal infection of the Saprolegnia parasiricc /diclina complex, UDN is still only observed in wild stocks of Atlantic S~~~IKMI and sea trout. The disease is initially characterized by small grcy erosions on thi: head and adipose fin. Only adult fish are affected upon ‘their entry into fresh water. The history of this disease goes as far back as 1873-I 5 1 I when it was reported from several rivers in Britain where it spread frcr.1 watershed to watershed. In I964 a recrudescence of the disease took place, starting in salmo,l ri\*ers in the south of Ireland and then spreading to &itain and later to rivers in France. In Sweden the disease was detected in 1976 and later spread to rivers in the ana LJungberg, 1977: Popp, castern p,7rt5 uf ?lorwriy by :%7 ~~~J~ldllwm 1989).
~l,irllcllioc:r:~riv IS a chlamydial infection that may result in hypertrophied
cprthclial crlls of the gills of several marinc species includ& s&Tonids. Under normal circumstances the condition is ofbenigrl character, but may cause respiratory problems in hdl.
~‘lcrrrrt(,rrlovi.v.also named ‘The Great Red Plaque’, ‘B;tctcrial i!emorrhagic Scpticcmia’. ‘Fururiculosis Salmonidarum’. and ‘Boil Disease’, was first described in connection with a disease out.>reak in Bavaria in 1894. Where the disease initially originated will possibly rover be revealed although there i)re descriptions indicating the cxistencc of the disease since I868 (Forel, 1868). Tilcre is some discussion whether it was spread to Europe from USA or vice versa. Some indication of the former may be that rainbow trout introduced front USA to Europe IS more rk i&ant to .!K disease than the brown trout and Atlantic salmon. In the beginni IS of tht 20th century, the disease spread rapidly in Europe in wild stocks as 1: !I as +I farmed fish and Plehn i 1909, 19! 1) showed that the disease C. %ted ir wlrC : . ?ut populations in 25 river systems. Irk Great Britain considerablr: mortality was .?bserved in several salmon rivers in I9 I I ( Wyc. Exe. Teige, Dart) (Arkwright. 19 12) and the disctise is still reported to be endemic in rivers in BtiIain. In Finland, furunculosis was first detected in Atlantic salm,>n brood fish caught in Bothnian Bay, but later also in rainbow trout, char and brook trout in hatcheries. In Norway the disease was first rcportcd in 1964 after importation of rainbow trout from Denmark, and the dibease was probably transferred to the river Numedalsl&n due to
DISEA!iSES IN WILD 4N11 CL’LTl!RFD
WLMIJS:
POSSIBLE lNTtR4C‘TION
283
stocking of latent carrier iish in a tributary. The mortality rat\: in this river system, however, seemed not to be of any significance compared to the mortality rirtes reported under farming condition where it may vary considerably, and can range from ! O-20% up to 50% (Hastein and Holt, 1970). From 1985. furunculosis has been epidemic in Norwegian fish farms in some regions after initial reintroduction of the disease due to importa?ion of latent infected Atlantic salmon smelts from Scot!and. Due to escaped fish, the disease has now been introduced in some 20 Norwegian salmon rivers. The significance ofthis is still not known and and the investigations into the epizootiology of .4. .vulmonicidu ;hus far have not provided unequivocal answers to several crucial questions concerning the dissemination of the pathogen. Controversy still exists whether tne pathogen is able to exist in a free-living stage in the natural environment or if it is a true parasitic pathogen which does not have any existence outside the fish host. Several experiments concerning the survival of the bacterium in water h:ive been carried out. giving different results. The existence of latent carriers is however the most likely way that the infection persists in a watershed system from one season to another. Ir$vtions by atypical Aeromonaq salmonicidu. Pigmented as well as nonpigmented striains are most likc!y to be Gdely distributed in nature and in different species of fish. ln Ntirway we have expericrlccd disease outbreaks in wild populations of salmomds and non-salmonid fish as well as in farmed I,-**nn n+ salmoni& . Or . .;ntrnA . . . ,y,~,,l,.. “.’ whitefish from the Norwegian lake Mjosa into an aquarium facility, disease appeared in the whitefish (C’c)r~~~rn~rs ult~rlu) and in pollan (inrt~~onrts Iu~~rctt~s). The same observation was experienced upon transfer of Arctic char (Sal~v~lin:~.vufprtrrts) from the lake TakL,atn to a hatchery. Z’ihricrsis. While coldwatcr vibriosis caused h>, l’r3~~0 ~~/;)totrl( ij,, 1s nt)t recovered in disease outbreaks of wild fish, classicrrl VI~I iosls cus?d by 1 ‘Ihrio anguillarum has been registeved in both wild and fnrmcd populGtlons of salmonids. While Smith ( I96 I ) rcportcd the disease lo or-cur in finnock from the river Dee, the disease was encountered in several Norwegian salmon river systems as far away from the river mouth as 10 km and cvcn in regions where no fish farmmg took place. There is reason tJ believe that I ‘. crngtrikmrtn constitutes part of the normal microflol 1 of the aquatic environment and in maximum and minimum numbers in summer and winter rcspectivcly (Larsen, 1982). The onl) kimwhat I~V spp. infection in wild migratory broodstock of Atlantic salmon reported by Roald and HAstein ( 1980 ), is now bclicved to have been caused by 1‘ihrio spp. Buwrial kidmy diwuw ( HKL), Ucc discasi ) caused by Kenihu!?eriwn .;~imoninuntm was initially described in 1930 in connection with disease In the river Dee, and the river Spcy in Scotl;z,ld (Mackie zt al.. 1933). In 1935, the disease was reported from hatchery-reared rainbow (n;tit. bro\\n trout and
break trout in USA ( Balding and Merill, 1935 ). Since that time, the disease is reported in at ‘c-rs: 13 different sahnonid species from many ccuntries throughout the world. Today this disease represents a great threat to fish farming. especraily to rhe farming tif Pacific salmon. It is only occasionally found in wild fish populations (Mitchurn and Sherma;l, i 98 I ). There is no doubt that wild tish may represent a greater risk to the farmed popuiarioas than vice verse. This is due to the chronic appearance of the disease and the difficulties in the eradication ofthe bacterium in wild stocks. However, a heavy infestation oi BKD in farmed fish will also pose considerable infectious taressure on wild fish populations. ~i~~inio.v~s (entrrir red mouth, ERM) was initially diagnosed as ti systemic infection among farmed rainbow trout in Hagerman Valley. ID. USA. Thr: disease is still mostly restricted to salmonid species. but has been reported from scvcral countries outside USA in the 1950’s and seems to be more widespread than Ii rs’ rhtiught. Its significance in wild populations of salmonids is not known. but is prc?;umably of little significance since the disease usually only results ir disease problems in f’armed fish when stressed. 4% WC‘ ozcasion we have recovcrzd Yor.sirriti rlr&ri in one wild sea trout brocld fish from a river on the vvcst coast of Norway.
.~(ll!rr’l(:~rriu-inf~~tions vauscd by the S. rmrusilic.a/~ic.linu car lplcx is the most common fungirl i1iseJsc in fish and is likely ?o occur in wild fish as weil a< farmed fish. Gcncrall;. it resu!ts in infections of the skin. but the pathogencsis is complex. Although th r: fungus has hair structures on the surface of the s~conclar~ c\ ~!r which may~n.~ble !hc penetration into the skin, ieveral other trrct~s are of great signific;rncc in the dcvclopment of Su~nl/~~rriu-infection. Such factors arc rnicroscupic as well as macroscopic lesions in conrrection with iraumstic injuries in the skin due to handling, spawning and parasitic infestations. The disease may be serious to sexually mature fish in connection with spawning. but may also be ot’ importance in fish not sext.alIy mature if the primary Icsions arc‘ scvcrc enough. ,ul)rokDx~riu-iniection; have a more dcletcrious cffcct on wild fish than t’armed fish. as no treatment is possible in ;1 constant manner. t‘.l~tll~.ol~ltf)~~r~.s h&v-i infection is a systemic fungal infectiolfwidesprcad in nature and reported io ‘cause significant mortality in herring, but was alsc reported to caJse infection in salmonids 2’; uar;y as 1893 (Hofer. 1893 ). It normaiiy dt;t’s not cause any disease problems ccither in wild fish, no: in farmed tish, but should ncvcrtSclcss bc considcrec! as a potential problem. I::\-c’C’lriLc!~-i?icctic,n is unoth~r fungal infection in freshwater fish first described to cause so-called ccrc:;r’al mycctoma in cutthroat trout (Carmichael, lqt(j) anj iids >i;*ILL ..LI? b. I\ 8*..b** b.1I.” .I* ;t L,‘;?*Asc LI*L.l bp8l%.* ,k.u crf systemic and spo~a&~ fuug;il
DISE*SES
IN WILD
4NDCC:LTIIREl~S~LLION:
POSS;BLt
Ih’Tf!?.~(‘l!OK
285
infections in farmed salmonids. Its economic significance is however lim ited as are the fungal infections caused ty Paccilliom~vw spp., Phumu spp. and kricillitrm spp. ( Neish anti Hughes. I 980 ) . PAR.4SITIC DISEASES
Many different parasites, protczoans as well as metazoan parasites have been described causing disease in salmonids. Most of these parasites do not cause significant problerx in wild stocks, but may cause large mortality within a fish farm, especially in hatcheries. O f the protozoan parasites. Jc~l;rh~dwd~c! rw~wr, \“/iilld~ncll(~ spp. and Trichdtna spp. may cause severe infestations under farming ci?nditions if river/surface water with a freeliving fish population is used as a \xtet supply. /L.;II/1)~~}ililiir;IrS rntr!l~fi/,% (~ch ) as well as My~oboftrs cerebrah may even cause disease problems in wild fish. but then only in singIe specimens compared to a f8rm situation. J~ertnqpya spp. maybe a problem for wild whitefish populations. W ith the m irnogenean GymductJ~l~tssalaris however, the situatton is the opposite. This parasite constitutes a large disease problem In Norwegian salmon rivers where it has caused considerahre problems and over years has resulted in an almost total eradication of young salmonids. This subject is dealt with elsewhere in this issue (Johnsen and Jensen, I99 1 ), but it is stressed that the reason why this parcsite is a problem in the wild popukltions and nor in farmed populations is that the latter are amendable to treatment. while the wild fish are not. Digenic flukes .nay cause problems in single fish both in wild salmonids as well as in farmed fish, but in fish cultured iu earthen ponds, considembtc effects caused by the eye fluke. Dipk~omtrm .~palhucwtm have been ohserved. The trematode P~~~llodistontttm wnbiac~is quite common in wild popu:ations of char and brown trout in densely populated waters. Under unfdvorable conditions this parasite may cause some under natural condit;ons. The parasite is so far not known to cause prohlcms in farmed stccks. O ther important metazoan diseases tha! have been reported in both’wild and farmed populations of salmonids are the salmon louse ( Lqwop~~~~.~.7%’ salmonis), plerocerco& of different cestodes such as D~~~it~~llubo~itrrtrrlr dendriricum as well as adult specimens of Llrho hrizim ;ww*,: & ‘!+,;1-.. The salmon lo~rn&v~s~tgrne nrrrV3x 1.. ~~+-;I:44;~igTatCiyZmon in sea hater, burrepresent no proolem in the freshwater chase unless large skin $sions have been created resulting in secondary fungdl infecticns. On the co$trary. the parasite may cause considerable problems among Tarmcd salmon finless treated. Etrborhritrm cruxwm, being a ‘normal” finding in the gut of wild s ilmon I and trout populations, causes some problems iu rnarirx rearing of A:lauric salmon by ixreased mortality u!tCer certain circumstances and a red3ction in growth due to reduced feed uptahe. In farmed fish, one may red&e the
problem sufficiently by medical treatment. Significant numbers of other ~,(IIasites have also been rectirded in wiid and farmed salmonids. but their importance is low. In xti;lin arcas E;lochiJie-lar*/ar: oi the frcshwa.ter pearl mussel Afugmiti,WYJtrruq~i~$~ may cause some disease problems under hatchery conditic nc unless the water is Cltcrcd through fine ~i~~s;iitlj fiibs. This probicm IS not transmissable to -.vild tush populations, but nature may use farmed fish as a WV of introclr;c;nr! the iieshwhtcr pear: mussel to other u-atorsheds by stocking ~f!j:h
llke fjsh farming, restocking of fish ii; :Iver systems, poi!ution of waters through industrlaf and agricultural ncticrties. man is Johaps the greatest t’actcr of causing potential interactions between wild and farmed populations axi \?~henxting “uncons~*iously” may create the largest damage to the rviturc. Sii:~ hUii\tili diiiviid
‘JlStr4fF.S
iX H ILI?.\?:I~(‘I’LT~~HEI~S\LS~O~’
I’OS!dHLi
IS~EK~W‘T1~JS
787
the wrus ofr~tl;loc>tic lncltwon hod!, s>ndrom:. CBt’. drtccrcxi in Atlantic salmon ( .\~I/~u~I .ru!;;,i in Norw~. Pull. Eur. Xssoc. Fish Fathol.. IO ( 1 ): Z!-23. H’.D. dnd hllvwt*s. A?wkic. T.J.. Ark&right. J..-\.. Pycc-Tanatt. ‘.‘.E.. Xlollram. .I (‘ l!*hnwn ~~\‘.J.Xl., 1933. The Second Interim Kcport ol’ t:~c Fururrcz!- nsir Commlttw. HXlSO. lidlnburgh. 8 I pp. McKnight I.J.. 1978. Sarcoma of the swim bladder of -\tlan!r: Amon (.r;(J:‘f~lJ ~r,/uv). Aq 1;~ cuhutc. ! 3: 45-w. .-:c\-r Mitchurn. D.L. and Sherman. L.E.. 1981, Transmission of bact:riat k-4 . . A.ic~:~w t’ram briu I 1 stocked hat&e? trout. Tan. ! Fish. :\~sa~. Sci.. 3X: 547-55 I. Alulcahy. D.. Paw”? v.! ?n
kobcrts. K.J.. 1989. Fish Patholog!,. Bzillicrtb T~ndall, 467 I?;‘ Qno. T.. 1976 v,:al diseases of cultured lishrr in Jawn. Fish 1’31hol.. IO: 22 I -Z?tp. .hi!I:i‘ I . . 1y8k. Characicrifation. plctlwgwlcit> nvd onc:ycniL.lth ot’hcrpc+vlru\ In tish In. Inr. Fish Hcah I Cont.. Vancouver. B(‘. C‘onCcrcnrc H?ndhotbk. Fish !linlth %,C.IIIP:I ~.xrr t.‘ln Flshcrics Scvxly. p 157. Saw. T.. I-uk .:da. H.. Okamoto, N. and Kzwku. F.. ! Vk;. k’3m:irhic I:Lmor \ lrus: Lcth3111> ;*nd oncogcnic I>. Bull. Jpn. Sot. Sci. Fish.. 49 (8): 1 159-l IG?. Sih~pcrklaus W.. I YJ8. Die Schadlgul.$;n dcr dcutschcn I ischcr*:l d,r
288
T HbTFlY
\SDT
LINDST!.
(Of.c,orb!,trl,hrr\ rwrh) (Walbaum ) ar Lake Cowichan. British Columbia. J. Fish DIS.. 9: 545-549. Vestergard Jorgensen, P.E. and Olcscz~. N.J.. 1987. Cod uicus syndrome rhabdovirus is indistingulshablc lorm the Egtved (Vt is) virus. Bull. Eur. Assoc. Fish Pathol., 7 (3 ): 73-74. Warren. J.W.. IY83. The nature of fish diseases. In: F.P. Meyer. J.W. Warren and T.G Care) (Editors). -\ guide to inlegralcd Fish Health Manag ; r Ilcn: in rhc Great Lakes Basin. Grcdl Lakes Flshrries Commission. Sp x. Publ.. 83-J. pp. 7-l 3. U’cdcmcyer. G.r\., Nelson, N.c_‘. and Smith. C..A.. 1978. Survival of the salmonid viruses infect~ous hcmatopoietic necrosis ( IHh” t and infectious pancreatic necrosis (IPNV ) III ozonatcd. chlorinated and untrcaxd tiatcrs. J. k:sh. Res. Board Can.. 35: 1564-l 567. ‘~w’:‘lIdl~i,. 1.V. aqd Arnc’l,d. D,F.. 1976. .A natural cpixotic of infcctlous hcmatopoirtic necrosis (Orrlorll~.r/,‘hlr.\ rwrC,J) at I hllko Lake, British Columbia. J. Fish. rn f’~ ol’sockc)c Amon Kc5. Board Can.. 33: I 564-i 31~7. %‘lrcn. H.. I Y71. Wart discasc in .A,lantlc salmon (.S~lr)r,: .SL(/LITL. ): Hislologlcal studies ofcpidcrmal I:apllloma in rcurcd salmon ( I’artsJuka hos lx ; Suftm .x~frr L. ) histologiska studwr 0% cr cpidcrmala paplllnm has odlad lax ). Swed. Sstmr )n Rcs. Inst. Rep.. LFI Mcddclandc. 7: I-IO. bolt, h.. I Y&d. l,i,h Vlrusti\ a11J Vlrdl IIiwascs. (‘orncll Ilnlxcrsltb Pwss. Ithaca. NY. 476 rp.