Erp. Eye Rrs. (1990)
50, 439442
LETTER
Possible
Causes
of Cataract
TO THE EDITORS
in Atlantic
We read with interest the letter by Fraser, Duncan and Tomlinson (1989). We feel that this letter contained several inaccuracies which deserve correction and would like to comment on the hypothesis and conclusions drawn. We were somewhat disturbed by the use of a registered trade mark (Nuvan) throughout a scientific publication without a mention of its manufacturer (Ciba-Geigy Limited, Basel). Much more disturbing was the identification of several misquoted references. Ross and Horsman (19 8 8) did not implicate Nuvan ’ in a number of cases involving loss of marine life ’ as stated in Fraser et al. (1989). In fact they detail losses of marine life associated with the routine use of trichlorfon [Neguvon Vet (Bayer)]. Ross and Horsman (1988) quote various papers establishing the toxicity of dichlorvos to marine organisms, but the routine use of dichlorvos has not been implicated in any actual cases involving the loss of marine life. Salte et al. (1987) again describe losses of marine life associated with the use of trichlorfon. Although trichlorfon is a precursor of dichlorvos and gradually breaks down to release dichlorvos, its breakdown is temperature and pH dependent. Because of the high dosesemployed for lice control on salmonids, reports of losses of marine life, and because of its extremely unpredictable rate of breakdown, trichlorfon use has been largely superseded by that of dichlorvos. Iwata et al. (1987) did not state that osmotically caused cataracts are unlikely to occur in wild fish on a regular basis. Their paper in fact describes an investigation of osmotically caused cataract in salmon and includes a detailed discussion of several causes of cataract in wild salmon, including dietary effects. Wooten, Smith and Needham (1982) did not state that ‘dichlorvos is known to cause cataracts when ingested at relatively high concentration in food’. In fact, this particular reference referred to original work by Brandal and Egidius (19 77) which reports on the administration of trichlorfon, not dichlorvos, in food and in fact records blindness, not cataract formation. Some of our own work with salmon in solutions of dichlorvos at lethal overdoses have also demonstrated apparent blindness before death, but without any cataracts being observed. Dichlorvos has in fact been widely tested and used as an in-feed substance in many species. including man (it is widely used worldwide as an anthelmintic). In all the toxicity work involving up to a lifetime feeding of dichlorvos to several species, dichlorvos has not been recorded as causing cataracts (World Health Organisation, 1989). We are somewhat concerned that the paper gives 00144835/90/040439+04
$03.00/O
Salmon
(Saho
salar)
no information as to how, and by whom, the estimates of the incidence of cataracts were made, nor the number of fish examined in each individual year. Other authors have commented on the diiculty of judging whether a fish had or did not have cataracts (Allison, 1962b). Cornea1 opacity also occurs (Brandt and Jones, 1986), and time elapsed since death is very important, as transient opacity may occur postmortem. Although a number of possible causes of cataract other than dichlorvos are described in the letter and dismissed, the review of the relevant literature is somewhat incomplete. Many other cataractogens in fish have been described including several which may cause unilateral cataracts. Steucke et al. (1968) describe unilateral cataracts in trout related to nutritional status, but suggests that this condition is purely an early stage in the development of bilateral cataracts. Fraser et al. (1989). however, suggest that the high incidence of unilateral cataract is most probably due to a macroscopic agent. Although zinc and methionine deficiences are indeed usually associated with accompanying symptoms of retarded growth and mortality, many dietary deficiences causing cataract are not associated with any effect on growth rate or mortality. Akiyama, Mori and Murai (1986) studied the effects of tryptophan deficiency in chum salmon fry. They found that cataract is apt to occur when metabolism is high due to high water temperatures, or when fish are fed a diet low in tryptophan rather than a complete deficiency. With such a diet, there is no effect on growth rate or mortality. Poston and Rumsey (1983) showed that cataract did not develop as rapidly in slow growing fish fed a diet extremely low in tryptophan. They conclude that a shortage, rather than a lack, of substrate for protein synthesis in continually growing epithelial structures such as eye lenses induces cataract formation. Hughes, Rumsey and Nickum (198 1) reported that a riboflavin-deficient diet caused cataracts in rainbow trout with no effect on body growth. Cataract has also been induced in juvenile chinook salmon Oncorhynchus tsh~wytscha by feeding riboflavin-deficient diets (Halver, 19 5 3 ), and similar results have been found for brook trout Salvelinus fontinalis and brown trout Salmo trutta (Phillips et al., 19 56. 19 5 7). A cataractogenic diet for juvenile chinook salmon 0. tshawytscha has been described by Richardson, Higgs and Beames (1986), which contained high levels of calcium, phosphorus and phytate. Light, specifically UV, is also implicated in cataract formation, and susceptibility to light is related to 0 1990 Academic Press Limited
440
nutritional status (Steuke et al., 1968). For example, Allison (1962a) studied a group of 18 3 1 lake trout Salvelinus namaycush where no cataracts were observed in October. However, by May, cataract had developed in 5 50 of 8 7 3 fish exposed to direct sunlight, but in only one of 858 held in shaded raceways. Susceptibility to UV light is ameliorated in diets rich in niacin (Allison, 1960, 1962a). Niacin can only be utilized by fish if tryptophan is also present (c.f. Akiyama et al., 1986). In a further study (Allison, 1962b) of lake trout reared for 4-6 yr as broodstock, cataract was noted in a high proportion of the fish, commonly in the range of 40-60x, with both unilateral and bilateral cataracts occurring. Experiments with different diets, light intensities, handling and injections of riboflavin did not provide control of cataract. AIlison (1962b) identified inflammation in the choroid layer of the eye which caused an oedema that displaced the retina. Most of the salmon examined in the Fraser et al. (1989) paper were caught in coastal bag nets. These fish were presumably stressed by capture and to be susceptible to mechanical injury. Ubels and Edelhauser (1987) showed that abrasions of the cornea of fish caused cataracts within 24 hr and usually within a few hours, which clear as the cornea1 epithelium heals. The structural integrity of the cornea1 epithelium is essential as a barrier to fluxes of water and ions between the environment and the cornea1 stroma and aqueous humor of the fish (Edelhauser, Geroski and Stern, 1980). Changes in aqueous humor composition reflect the osmolality and salinity of the external medium and may lead to cataract formation as a result of osmotic effects on lens water content (Smelser, 1962). Abrasion is likely to occur in salmon caught in nets and this could be unilateral. Stress has been shown to induce cornea1 opacity in largemouth bass Micropterus salmoides within 6 hr during simulated transportation (Brandt and Jones, 1986). In this species, as with all teleosts so far studied, stress causes rapid increases in cortiscosteroid hormones, and secondary effects include elevated plasma glucose concentrations and plasma electrolyte changes (Eddy, 1981; Carmichael et al., 1984; Specker and Schreck, 1980). Plasma ions increase in stressed sea water-adapted fish and decrease in stressed fresh water-adapted fish. Steroids (in man, Kopp and Tow, 1989) and glucose, water and electrolyte disturbance as a consequence of cornea1 injury, or stress as described above, or due to changes in external medium salinity (Iwata et al., 1987), may separately or in combination, be factors related to cataracts in captured salmon. Salmon smolts and adults both experience osmotic stress while making the transition between fresh and sea water. The formation of cataracts referred to by lwata et al. (19 8 7) describes a general phenomenon in fish which are experiencing osmotic and ionic disturbance per se. These may be through external
D. P. DOBSON
AND
H. J. SCHUURMAN
factors, (i.e. altering salinity), or internal factors such as secondary stress responses. Iwata et al. ( 1987) incubated isolated lenses of fresh water-adapted Masu salmon 0. masou in media of various osmolalities. The transparency of lenses was maintained in media of 308 and 388 mOsmo1 kg-’ (plasma was 310 mOsmo1 kg-‘) but became opaque within 1 hr in other solutions of both higher and lower concentrations. Migrating adult salmon could show cataracts as an effect of exposure to fresh water in the same way as might smolts moving into sea water. A number of other agents are known to cause cornea1 necrosis and cataract in fish, e.g. sublethal concentrations of copper (Bodammer, 1985) pH (Daye and Garside, 1976). and thioacetamide (Von Sallman et al., 1966). Parasites and bacterial and viral pathogens have been mentioned as possible causes of cataracts in salmon. Secondary cataract following anterior uveitis caused by bacterial or viral infections is also recognised in other species (Blood, Henderson and Radostits, 19 79 ; West and Barrie, 1986). In the absence of proper investigation, none of these potential causes can be ruled out. For example. discounting parasitic infection based on the fact that they were not observed on microscopic examination does not preclude this being the cause some time prior to capture. The same argument applies to bacterial and viral pathogens where the infection could have cleared but any cataract persists. Dichlorvos is used as a treatment for salmon lice on farmed Atlantic salmon (Salmo s&r). Treatments are performed by enclosing cages in tarpaulin and adding Nuvan SOOEC at 2 ppm (1 ppm dichlorvos) to the enclosed water. Salmon are exposed to this concentration for up to 1. hr, after which the tarpaulin is lifted and the treatment solution allowed out to the open sea. Recent trials to Good Laboratory Pratice (GLP) status (Dobson and Tack, in press) have been unable to identify dichlorvos outside a 2 5-m perimeter of a treated pen at any depths [Level of Detection (LOD) of 2 ppb]. Bearing these points in mind, we are surprised that Fraser et al., (1989) selected a concentration of 1.34 x 10e4 M dichlorvos to test their hypothesis. This concentration is equivalent to 30 ppm dichlorvos (60 ppm Nuvan 500EC). Such a concentration in sea water would kill Atlantic salmon in less than 15 min. In addition, subjecting a lens to a 24-hr period of such a concentration of dichlorvos does not take into account the replenishment rate of aqueous humor. Maren et al. ( 19 75) reported work on dogfish (Sgualus acanthias) demonstrating 40% of the aqueous humor being replenished every hour. There is no reason to suppose that the rate of replenishment in salmonids is dramatically different. All these latter facts combine to produce the major flaw in the hypothesis of Fraser et al. (1989), i.e. the fact that farmed fish regularly treated with Nuvan SOOEC are not affected by cataracts. Researchers at the Institute of Aquaculture, University of Stirling,
SALMO
SALAR
CATARACT
441
CAUSES
having monitored the health of both farmed and wild salmon in Scotland for the past 21 yr, have concluded (pers. commun.): ‘There is no evidence, despite, with a team of veterinary pathologists examining many thousands of farmed fish at all stages of their growth, to suggest any connection between the use of Nuvan SOOEC and cataracts or other ophthalmic pathology’. Cataracts in farmed salmon have only been observed in specific instances after excessive handling or following identifiable dietary imbalances. These latter facts have been communicated to Dr Fraser on numerous occasions prior to the publication of his letter, and indeed, the Scottish Salmon Growers Association have also invited Dr Fraser to examine the incidence of cataracts in farmed salmon for himself.
We note that this point has not been addressed in Fraser et al. (1989), however. The suggestion that a product with a short half life in sea water (approximately 6 days) could somehow affect wild salmon some miles away from its point of release, but not affect the salmon actually treated by the substance is not credible, particularly when dichlorvos is indisputably non-bioaccumulative and undergoes no biomagnification in soil, water, plants, vertebrates or invertebrates (World Health Organisation, 1989). There appears to be no logic behind the hypothesis in Fraser et al. (1989) and there exists many other less far fetched explanations to account for cataract formation in the Atlantic salmon (Salmo s&r).
Ciba - Geigy Agrochemicals, Whittlesford, Cambridge, CB2 4Q T, U.K. Ciba - Geigy Limited, CH-4002, Basel, Switzerland (Received
D. PHILIP
HESSEL
6 November
1989 and accepted
References Akiyama. T., Mori, K. and Murai, T. (1986). Effects of temperature on the incidence of scoliosis and cataract in chum salmon fry caused by tryptophan deficiency. Bull. Jpn. Sot. Sci. Fish 52, 2039. Allison, L. N. (1960). Sunburning fingerling lake trout with ultra-violet light and the effect of a niacin-fortified diet. Prog. Fish-Cult. 22. 114-6. Allison, L. N. (1962a). Cataract among hatchery-reared lake trout. Prog. Fish-Cult. 24, 155. Allison, L. N. (1962b). Cataract in hatchery lake trout. Trans.Am. Fish. Sot. 92, 34-8. Blood, D. C., Henderson,J. A. and Radostits,0. M. (19 79). VeterinaryMedicine.(5th edn)BailliereTindall: London. Bodammer.J. E.(1985). Cornea1damagein larvae of striped bassMoronesaxatilisexposedto copper.Trans. Am. Fish. sot. 113, 577-83. Brandal, P. 0. and Egidius,E. (1977). Preliminary report on oral treatment against salmon lice, Lepeophtheirus salmonis,with Neguvon. Aquaculture10, 177-8. Brandt, T. M. andJones,R. M. (1986). Cornea1cloudinessin transported largemouth bass Prog. Fish-Cult. 48, 199-201. Carmichael,G. J.. Tomasso,J. R., Simco, B. A. and Davis,
K. B. (1984). Characterization and alleviation of stress associatedwith hauling largemouth bass.Trans.Am. Fish. Sot. 113, 778-85.
Daye. P. G. and Garside, E.T. (1976). Histopathologic changesin superficialtissuesof brook trout. Salvelinus fontinalis(Mitchell), exposedto acuteand chronic levels of PH. Can. 1. ZooZ. 54. 2140-55. Eddy, F. B. (1981). Effects of stresson osmotic and ionic regulation in fish in Stressin Fish (Ed.Pickering,A. D.). Pp. 77-102. AcademicPress:London. Edelhauser,H. F., Geroski,D. H. and Stern, M. E. (1980). Glucose metabolism in the cornea and lens in
in revised form 18 December
DOBSON
J. SCHUURMAN
1989)
elasmobranchs,teleostsand mammals: responseto thioloxidation. Fed. Proc. 39. 32 13-2 1. Fraser,P. J., Duncan, G. and Tomlinson,J. (1989). Faectsof a cholinesteraseinhibitor on salmonidlens: A possible causefor the increasedincidenceof cataract in salmon (Salmosalar).Exp. Eye Res.49, 293-8. Halver, J. E. (1953). Nutrition of salmonidfishes.III. Watersoluble vitamin requirementsof Chinook salmon. I. Nutr. 62, 22543. Hughes, S. G., Rumsey, G. L. and Nickum, J. G. (1981). Riboflavin requirement of fingerling rainbow trout. Prog. Fish-Cult.43, 167-72. Iwata, M., Komatsu, S., Collie, N. L., Nishioka, R. S. and Bern, H. A. (1987). Ocular cataract and sea water adaptationin salmonids.Aquaculture66, 315-28. Kopp. S.J. and Tow, J. P. (1989). Species-dependant differencesin ATP half-life of glucosedeprived crystalline lens.Camp.Biochem.Physiol.93B. 5 7 5-8 1. Maren, T. H., Wistrand. P., Swendon. E. R. and Talalay, A. B. C. (1985). Theratesof ion movementfrom plasma to aqueoushumor in the dog fish (Squalusacauthias). Invest. OpthaJmoJ. 14, 662-73. Philips,A. M., Podoliak,H. A., Brockway, D. R. and Balzer, G. C. (1956). CortlundHatchery Report No. 25. New York ConservationDepartment: Albany, New York. Philips,A. M., Podoliak,H. A., Brockway, D. R. and Vaughn, R. R. (1957). CortlandHatchery Report No. 26. New York ConservationDepartment:Albany, New York. Poston, H. A. and Rumsey,G. L. (1983). Factors affecting dietary requirementand deficiencysignsof L-trytophan in rainbow trout. J. Nutr. 113, 2568-77. Richardson,N. L., Higgs,D. A. and Beames,R. M. (1986). The susceptibility of juvenile Chinook Salmon (Oncorhynchustschawytscha)to cataract formation in relation to dietary changesin early life. Aquaculture52. 23743.
Ross,A. and Horsman, P. V. (1988). The Useof Nuvan
442
D. P. DOBSON
500EC in the Salmon Farming Industry. Marine Conservation Society : Ross-on-Wye. Salte, R., Syvertsen, C. Kjoennoey, M. and Frode F. (1987). Fatal acetylcholinesterase inhibition in salmonids subject to a routine organophosphate treatment. Aquaculture 61, 17 3-9. Smelser, G. K. (1962). Cornea1 hydration: Comparative physiology of fish and mammals. Invest. Opthalmol. 1. 11-32. Speker. J. L. and Schreck, C. B. (1980). Stress responses to transportation and fitness for marine survival in Coho Salmon (Oncorhynchus kisutch). Can. 1. Fish. Aquat. Sci. 37, 765-9. Steuke, E. W.. Allison, L. H.. Piper, R. G. and Robertson, K. (1968). Effects of light and diet on the incidence of cataract in hatchery-reared lake trout. Prog. Fish-Cult.
30.220-6. Ubels, J. L. and Fdelhauser, H. F. (1987). abrasion on cornea1 transparency,
EfTects of cornea1 aqueous humor
AND
H J. SCHUURMAN
composition, and lens of fish. Prog. Fish-Cult. 49, 219-224. Von Sallman, L., Halver. J. E.. Collins, E. and Grimes. f’. (1966). Thioacetamide-induced cataract with invasive proliferation of the lens epithelium, in rainbow trout. Cancer Res. 26, 1819-925. West, C. S. and Barrie, K. P. (1986). Disorders of the Anterior Uvea Current Veterinary Therapy IX: 64%656. W. B. Saunders : Philadelphia. Wooten, R.. Smith, J. W. and Needham, K. A. (1982). Aspects of the biology of the parasitic copepods Lepeophtheirus salmonis and Caligus elongaqus on farmed salmonids, and their treatment. hoc. R. Sor. Edin. 81 B. 185-97. World Health Organisation (1989). International programme on chemical safety. Environmental Health Criteria 79. Dichlorvos. United Nations Environment Programme. the International Labour Organisation. and the World Health Organization : Geneva.
50, 439442
LETTER
Possible
Causes
of Cataract
TO THE EDITORS
in Atlantic
We read with interest the letter by Fraser, Duncan and Tomlinson (1989). We feel that this letter contained several inaccuracies which deserve correction and would like to comment on the hypothesis and conclusions drawn. We were somewhat disturbed by the use of a registered trade mark (Nuvan) throughout a scientific publication without a mention of its manufacturer (Ciba-Geigy Limited, Basel). Much more disturbing was the identification of several misquoted references. Ross and Horsman (19 8 8) did not implicate Nuvan ’ in a number of cases involving loss of marine life ’ as stated in Fraser et al. (1989). In fact they detail losses of marine life associated with the routine use of trichlorfon [Neguvon Vet (Bayer)]. Ross and Horsman (1988) quote various papers establishing the toxicity of dichlorvos to marine organisms, but the routine use of dichlorvos has not been implicated in any actual cases involving the loss of marine life. Salte et al. (1987) again describe losses of marine life associated with the use of trichlorfon. Although trichlorfon is a precursor of dichlorvos and gradually breaks down to release dichlorvos, its breakdown is temperature and pH dependent. Because of the high dosesemployed for lice control on salmonids, reports of losses of marine life, and because of its extremely unpredictable rate of breakdown, trichlorfon use has been largely superseded by that of dichlorvos. Iwata et al. (1987) did not state that osmotically caused cataracts are unlikely to occur in wild fish on a regular basis. Their paper in fact describes an investigation of osmotically caused cataract in salmon and includes a detailed discussion of several causes of cataract in wild salmon, including dietary effects. Wooten, Smith and Needham (1982) did not state that ‘dichlorvos is known to cause cataracts when ingested at relatively high concentration in food’. In fact, this particular reference referred to original work by Brandal and Egidius (19 77) which reports on the administration of trichlorfon, not dichlorvos, in food and in fact records blindness, not cataract formation. Some of our own work with salmon in solutions of dichlorvos at lethal overdoses have also demonstrated apparent blindness before death, but without any cataracts being observed. Dichlorvos has in fact been widely tested and used as an in-feed substance in many species. including man (it is widely used worldwide as an anthelmintic). In all the toxicity work involving up to a lifetime feeding of dichlorvos to several species, dichlorvos has not been recorded as causing cataracts (World Health Organisation, 1989). We are somewhat concerned that the paper gives 00144835/90/040439+04
$03.00/O
Salmon
(Saho
salar)
no information as to how, and by whom, the estimates of the incidence of cataracts were made, nor the number of fish examined in each individual year. Other authors have commented on the diiculty of judging whether a fish had or did not have cataracts (Allison, 1962b). Cornea1 opacity also occurs (Brandt and Jones, 1986), and time elapsed since death is very important, as transient opacity may occur postmortem. Although a number of possible causes of cataract other than dichlorvos are described in the letter and dismissed, the review of the relevant literature is somewhat incomplete. Many other cataractogens in fish have been described including several which may cause unilateral cataracts. Steucke et al. (1968) describe unilateral cataracts in trout related to nutritional status, but suggests that this condition is purely an early stage in the development of bilateral cataracts. Fraser et al. (1989). however, suggest that the high incidence of unilateral cataract is most probably due to a macroscopic agent. Although zinc and methionine deficiences are indeed usually associated with accompanying symptoms of retarded growth and mortality, many dietary deficiences causing cataract are not associated with any effect on growth rate or mortality. Akiyama, Mori and Murai (1986) studied the effects of tryptophan deficiency in chum salmon fry. They found that cataract is apt to occur when metabolism is high due to high water temperatures, or when fish are fed a diet low in tryptophan rather than a complete deficiency. With such a diet, there is no effect on growth rate or mortality. Poston and Rumsey (1983) showed that cataract did not develop as rapidly in slow growing fish fed a diet extremely low in tryptophan. They conclude that a shortage, rather than a lack, of substrate for protein synthesis in continually growing epithelial structures such as eye lenses induces cataract formation. Hughes, Rumsey and Nickum (198 1) reported that a riboflavin-deficient diet caused cataracts in rainbow trout with no effect on body growth. Cataract has also been induced in juvenile chinook salmon Oncorhynchus tsh~wytscha by feeding riboflavin-deficient diets (Halver, 19 5 3 ), and similar results have been found for brook trout Salvelinus fontinalis and brown trout Salmo trutta (Phillips et al., 19 56. 19 5 7). A cataractogenic diet for juvenile chinook salmon 0. tshawytscha has been described by Richardson, Higgs and Beames (1986), which contained high levels of calcium, phosphorus and phytate. Light, specifically UV, is also implicated in cataract formation, and susceptibility to light is related to 0 1990 Academic Press Limited
440
nutritional status (Steuke et al., 1968). For example, Allison (1962a) studied a group of 18 3 1 lake trout Salvelinus namaycush where no cataracts were observed in October. However, by May, cataract had developed in 5 50 of 8 7 3 fish exposed to direct sunlight, but in only one of 858 held in shaded raceways. Susceptibility to UV light is ameliorated in diets rich in niacin (Allison, 1960, 1962a). Niacin can only be utilized by fish if tryptophan is also present (c.f. Akiyama et al., 1986). In a further study (Allison, 1962b) of lake trout reared for 4-6 yr as broodstock, cataract was noted in a high proportion of the fish, commonly in the range of 40-60x, with both unilateral and bilateral cataracts occurring. Experiments with different diets, light intensities, handling and injections of riboflavin did not provide control of cataract. AIlison (1962b) identified inflammation in the choroid layer of the eye which caused an oedema that displaced the retina. Most of the salmon examined in the Fraser et al. (1989) paper were caught in coastal bag nets. These fish were presumably stressed by capture and to be susceptible to mechanical injury. Ubels and Edelhauser (1987) showed that abrasions of the cornea of fish caused cataracts within 24 hr and usually within a few hours, which clear as the cornea1 epithelium heals. The structural integrity of the cornea1 epithelium is essential as a barrier to fluxes of water and ions between the environment and the cornea1 stroma and aqueous humor of the fish (Edelhauser, Geroski and Stern, 1980). Changes in aqueous humor composition reflect the osmolality and salinity of the external medium and may lead to cataract formation as a result of osmotic effects on lens water content (Smelser, 1962). Abrasion is likely to occur in salmon caught in nets and this could be unilateral. Stress has been shown to induce cornea1 opacity in largemouth bass Micropterus salmoides within 6 hr during simulated transportation (Brandt and Jones, 1986). In this species, as with all teleosts so far studied, stress causes rapid increases in cortiscosteroid hormones, and secondary effects include elevated plasma glucose concentrations and plasma electrolyte changes (Eddy, 1981; Carmichael et al., 1984; Specker and Schreck, 1980). Plasma ions increase in stressed sea water-adapted fish and decrease in stressed fresh water-adapted fish. Steroids (in man, Kopp and Tow, 1989) and glucose, water and electrolyte disturbance as a consequence of cornea1 injury, or stress as described above, or due to changes in external medium salinity (Iwata et al., 1987), may separately or in combination, be factors related to cataracts in captured salmon. Salmon smolts and adults both experience osmotic stress while making the transition between fresh and sea water. The formation of cataracts referred to by lwata et al. (19 8 7) describes a general phenomenon in fish which are experiencing osmotic and ionic disturbance per se. These may be through external
D. P. DOBSON
AND
H. J. SCHUURMAN
factors, (i.e. altering salinity), or internal factors such as secondary stress responses. Iwata et al. ( 1987) incubated isolated lenses of fresh water-adapted Masu salmon 0. masou in media of various osmolalities. The transparency of lenses was maintained in media of 308 and 388 mOsmo1 kg-’ (plasma was 310 mOsmo1 kg-‘) but became opaque within 1 hr in other solutions of both higher and lower concentrations. Migrating adult salmon could show cataracts as an effect of exposure to fresh water in the same way as might smolts moving into sea water. A number of other agents are known to cause cornea1 necrosis and cataract in fish, e.g. sublethal concentrations of copper (Bodammer, 1985) pH (Daye and Garside, 1976). and thioacetamide (Von Sallman et al., 1966). Parasites and bacterial and viral pathogens have been mentioned as possible causes of cataracts in salmon. Secondary cataract following anterior uveitis caused by bacterial or viral infections is also recognised in other species (Blood, Henderson and Radostits, 19 79 ; West and Barrie, 1986). In the absence of proper investigation, none of these potential causes can be ruled out. For example. discounting parasitic infection based on the fact that they were not observed on microscopic examination does not preclude this being the cause some time prior to capture. The same argument applies to bacterial and viral pathogens where the infection could have cleared but any cataract persists. Dichlorvos is used as a treatment for salmon lice on farmed Atlantic salmon (Salmo s&r). Treatments are performed by enclosing cages in tarpaulin and adding Nuvan SOOEC at 2 ppm (1 ppm dichlorvos) to the enclosed water. Salmon are exposed to this concentration for up to 1. hr, after which the tarpaulin is lifted and the treatment solution allowed out to the open sea. Recent trials to Good Laboratory Pratice (GLP) status (Dobson and Tack, in press) have been unable to identify dichlorvos outside a 2 5-m perimeter of a treated pen at any depths [Level of Detection (LOD) of 2 ppb]. Bearing these points in mind, we are surprised that Fraser et al., (1989) selected a concentration of 1.34 x 10e4 M dichlorvos to test their hypothesis. This concentration is equivalent to 30 ppm dichlorvos (60 ppm Nuvan 500EC). Such a concentration in sea water would kill Atlantic salmon in less than 15 min. In addition, subjecting a lens to a 24-hr period of such a concentration of dichlorvos does not take into account the replenishment rate of aqueous humor. Maren et al. ( 19 75) reported work on dogfish (Sgualus acanthias) demonstrating 40% of the aqueous humor being replenished every hour. There is no reason to suppose that the rate of replenishment in salmonids is dramatically different. All these latter facts combine to produce the major flaw in the hypothesis of Fraser et al. (1989), i.e. the fact that farmed fish regularly treated with Nuvan SOOEC are not affected by cataracts. Researchers at the Institute of Aquaculture, University of Stirling,
SALMO
SALAR
CATARACT
441
CAUSES
having monitored the health of both farmed and wild salmon in Scotland for the past 21 yr, have concluded (pers. commun.): ‘There is no evidence, despite, with a team of veterinary pathologists examining many thousands of farmed fish at all stages of their growth, to suggest any connection between the use of Nuvan SOOEC and cataracts or other ophthalmic pathology’. Cataracts in farmed salmon have only been observed in specific instances after excessive handling or following identifiable dietary imbalances. These latter facts have been communicated to Dr Fraser on numerous occasions prior to the publication of his letter, and indeed, the Scottish Salmon Growers Association have also invited Dr Fraser to examine the incidence of cataracts in farmed salmon for himself.
We note that this point has not been addressed in Fraser et al. (1989), however. The suggestion that a product with a short half life in sea water (approximately 6 days) could somehow affect wild salmon some miles away from its point of release, but not affect the salmon actually treated by the substance is not credible, particularly when dichlorvos is indisputably non-bioaccumulative and undergoes no biomagnification in soil, water, plants, vertebrates or invertebrates (World Health Organisation, 1989). There appears to be no logic behind the hypothesis in Fraser et al. (1989) and there exists many other less far fetched explanations to account for cataract formation in the Atlantic salmon (Salmo s&r).
Ciba - Geigy Agrochemicals, Whittlesford, Cambridge, CB2 4Q T, U.K. Ciba - Geigy Limited, CH-4002, Basel, Switzerland (Received
D. PHILIP
HESSEL
6 November
1989 and accepted
References Akiyama. T., Mori, K. and Murai, T. (1986). Effects of temperature on the incidence of scoliosis and cataract in chum salmon fry caused by tryptophan deficiency. Bull. Jpn. Sot. Sci. Fish 52, 2039. Allison, L. N. (1960). Sunburning fingerling lake trout with ultra-violet light and the effect of a niacin-fortified diet. Prog. Fish-Cult. 22. 114-6. Allison, L. N. (1962a). Cataract among hatchery-reared lake trout. Prog. Fish-Cult. 24, 155. Allison, L. N. (1962b). Cataract in hatchery lake trout. Trans.Am. Fish. Sot. 92, 34-8. Blood, D. C., Henderson,J. A. and Radostits,0. M. (19 79). VeterinaryMedicine.(5th edn)BailliereTindall: London. Bodammer.J. E.(1985). Cornea1damagein larvae of striped bassMoronesaxatilisexposedto copper.Trans. Am. Fish. sot. 113, 577-83. Brandal, P. 0. and Egidius,E. (1977). Preliminary report on oral treatment against salmon lice, Lepeophtheirus salmonis,with Neguvon. Aquaculture10, 177-8. Brandt, T. M. andJones,R. M. (1986). Cornea1cloudinessin transported largemouth bass Prog. Fish-Cult. 48, 199-201. Carmichael,G. J.. Tomasso,J. R., Simco, B. A. and Davis,
K. B. (1984). Characterization and alleviation of stress associatedwith hauling largemouth bass.Trans.Am. Fish. Sot. 113, 778-85.
Daye. P. G. and Garside, E.T. (1976). Histopathologic changesin superficialtissuesof brook trout. Salvelinus fontinalis(Mitchell), exposedto acuteand chronic levels of PH. Can. 1. ZooZ. 54. 2140-55. Eddy, F. B. (1981). Effects of stresson osmotic and ionic regulation in fish in Stressin Fish (Ed.Pickering,A. D.). Pp. 77-102. AcademicPress:London. Edelhauser,H. F., Geroski,D. H. and Stern, M. E. (1980). Glucose metabolism in the cornea and lens in
in revised form 18 December
DOBSON
J. SCHUURMAN
1989)
elasmobranchs,teleostsand mammals: responseto thioloxidation. Fed. Proc. 39. 32 13-2 1. Fraser,P. J., Duncan, G. and Tomlinson,J. (1989). Faectsof a cholinesteraseinhibitor on salmonidlens: A possible causefor the increasedincidenceof cataract in salmon (Salmosalar).Exp. Eye Res.49, 293-8. Halver, J. E. (1953). Nutrition of salmonidfishes.III. Watersoluble vitamin requirementsof Chinook salmon. I. Nutr. 62, 22543. Hughes, S. G., Rumsey, G. L. and Nickum, J. G. (1981). Riboflavin requirement of fingerling rainbow trout. Prog. Fish-Cult.43, 167-72. Iwata, M., Komatsu, S., Collie, N. L., Nishioka, R. S. and Bern, H. A. (1987). Ocular cataract and sea water adaptationin salmonids.Aquaculture66, 315-28. Kopp. S.J. and Tow, J. P. (1989). Species-dependant differencesin ATP half-life of glucosedeprived crystalline lens.Camp.Biochem.Physiol.93B. 5 7 5-8 1. Maren, T. H., Wistrand. P., Swendon. E. R. and Talalay, A. B. C. (1985). Theratesof ion movementfrom plasma to aqueoushumor in the dog fish (Squalusacauthias). Invest. OpthaJmoJ. 14, 662-73. Philips,A. M., Podoliak,H. A., Brockway, D. R. and Balzer, G. C. (1956). CortlundHatchery Report No. 25. New York ConservationDepartment: Albany, New York. Philips,A. M., Podoliak,H. A., Brockway, D. R. and Vaughn, R. R. (1957). CortlandHatchery Report No. 26. New York ConservationDepartment:Albany, New York. Poston, H. A. and Rumsey,G. L. (1983). Factors affecting dietary requirementand deficiencysignsof L-trytophan in rainbow trout. J. Nutr. 113, 2568-77. Richardson,N. L., Higgs,D. A. and Beames,R. M. (1986). The susceptibility of juvenile Chinook Salmon (Oncorhynchustschawytscha)to cataract formation in relation to dietary changesin early life. Aquaculture52. 23743.
Ross,A. and Horsman, P. V. (1988). The Useof Nuvan
442
D. P. DOBSON
500EC in the Salmon Farming Industry. Marine Conservation Society : Ross-on-Wye. Salte, R., Syvertsen, C. Kjoennoey, M. and Frode F. (1987). Fatal acetylcholinesterase inhibition in salmonids subject to a routine organophosphate treatment. Aquaculture 61, 17 3-9. Smelser, G. K. (1962). Cornea1 hydration: Comparative physiology of fish and mammals. Invest. Opthalmol. 1. 11-32. Speker. J. L. and Schreck, C. B. (1980). Stress responses to transportation and fitness for marine survival in Coho Salmon (Oncorhynchus kisutch). Can. 1. Fish. Aquat. Sci. 37, 765-9. Steuke, E. W.. Allison, L. H.. Piper, R. G. and Robertson, K. (1968). Effects of light and diet on the incidence of cataract in hatchery-reared lake trout. Prog. Fish-Cult.
30.220-6. Ubels, J. L. and Fdelhauser, H. F. (1987). abrasion on cornea1 transparency,
EfTects of cornea1 aqueous humor
AND
H J. SCHUURMAN
composition, and lens of fish. Prog. Fish-Cult. 49, 219-224. Von Sallman, L., Halver. J. E.. Collins, E. and Grimes. f’. (1966). Thioacetamide-induced cataract with invasive proliferation of the lens epithelium, in rainbow trout. Cancer Res. 26, 1819-925. West, C. S. and Barrie, K. P. (1986). Disorders of the Anterior Uvea Current Veterinary Therapy IX: 64%656. W. B. Saunders : Philadelphia. Wooten, R.. Smith, J. W. and Needham, K. A. (1982). Aspects of the biology of the parasitic copepods Lepeophtheirus salmonis and Caligus elongaqus on farmed salmonids, and their treatment. hoc. R. Sor. Edin. 81 B. 185-97. World Health Organisation (1989). International programme on chemical safety. Environmental Health Criteria 79. Dichlorvos. United Nations Environment Programme. the International Labour Organisation. and the World Health Organization : Geneva.
