10.2 Naturally Occurring Toxins in Formulated
10.2.2. Toxins of Animal Origin 1. Introduction
The previous section lists the limited number of plant foodstuffs used routinely in pelleted fish rations. When we consider the number of animal- derived foodstuffs used in fish diets the number is even smaller: fish meal (herring, anchovy, menhaden and whitefish), whey, blood meal, poultry by- products meal, feather meal, meat meal, wet fish (hake, herring, bottom fish fillet scrap), shrimp or crab meal, krill, and fish oil. In general, there are no toxins, of a significant nature, associated with any of animals from which these products are derived. Two toxins found naturally in the liver, ovaries, and roe of certain fish could potentially enter fish diets if these fish species were inadvertently included with fish being prepared for fish meal or wet fish. These are tetrodotoxin and dinogunellin.
10.2.2.2. Tetrodotoxin
About 80 species of the order Tetraodontiformes (the puffer fish or globefish) produce and store tetrodotoxin, a complex cyclic compound (Fig. 10.10) which is highly toxic to all vertebrate animals tested except those species that produce it (Fuhrman 1974). I am not aware of tests that specifically determine its toxicity to other fish species. In humans and labora- tory mammals it causes numbness of the lips, tongue, and fingers, muscular paralysis, and eventual respiratory paralysis and death. Most of the fish con- taining this toxin are from the western Pacific and Indian oceans, but some species of puffers also inhabit the coastal waters of the eastern United States (Fuhrman 1985). It is conceivable that these fish could enter the fishery and end up in fish meal or wet fish but the risk in fish diets is very low. The effects of the toxin on the various species of commercially fed fish are not known.
FIG. 10.10 Tetrodotoxin.
10.2.2.3. Dinogunellin
Dinogunellin is a toxic lipoprotein that is produced in the roe of two fish, the northern blenny (Stichaeus grigorgjewi), from northern Japan, and the cabezon or marbled sculpin (Scorpaenichthys marmoratus), a fish com- mon to the Pacific coast of North America. This toxin is not as potent as tetrodotoxin, but it causes diarrhea, nausea, vomiting, epigastric distress, and liver and spleen necrosis (Fuhrman 1974, 1985). I am not aware of any exposures of fish such as trout to dinogunellin. Since the cabezon is a com- mon inhabitant of the Pacific coastline, it is conceivable that some of these fish could end up in the fillet scrap of groundfish used as wet fish in Oregon Moist Pellets. In practice, however, these fish rarely enter the troll fishery since they prefer rocky bottoms near the coastline. Thus the potential for fish toxicity due to dinogunellin in pelleted fish diets is very low.
10.2.2.4. Dinoflagellate Toxins
Under undefined climatic and hydrographic conditions, certain blue–
green algae known as dinoflagellates reproduce very rapidly to produce
“blooms” which can actually turn the water of the estuary red or whatever color predominates in the organism. Several of these bloom-forming organ- isms are toxic and create dangerous conditions for fish as well as humans and terrestrial animals. Mollusks filter these organisms from the water, di- gest them, and accumulate the toxin in various tissues. Mollusks are not affected by the toxin but humans or other mammals that eat toxic shell- fish are very sensitive and significant mortalities of humans, livestock, wild animals, and pets have resulted from eating these toxic animals. Fish also seem to be sensitive to algal blooms, since massive fish kills have occurred in bloom areas. Blooms ofGymnodinium brevishave resulted in large fish kills off the Florida coast, and the toxin appears to be released into the water because fish die soon after swimming into a bloom area. The dinoflagellate
FIG. 10.11 Histamine.
Prymnesium parvum also releases toxins into the water that are extremely toxic to brackish-water fish.
The potential for these dinoflagellate toxins to appear in formulated fish diets is rare, though not impossible. Because mollusks are rarely used in fish diet formulations, and fish that would contain dangerous levels of these toxins would probably already be dead, the chances of these toxins entering fish diets is remote. Some crustacean products, such as shrimp and crab meal or oil, may be used in fish diets to impart carotenoid pigmentation to fish flesh, so these products could carry certain amounts of dinoflagellate toxins. Overall, however, it is not a significant problem.
10.2.2.5. Histamine
Under conditions of improper storage (warm temperatures and extended periods of time), scombroid fishes may develop high levels of histamine (Fig. 10.11). This is due to the action of the bacteriumProteus morganiion the high histidine content of these fish. Little is known about the effects of histamine on fish, but since the chances of scombroid fish (tuna, swordfish, and mackerel) being incorporated into fish diets is low, it is, again, only a potential problem that has little possibility of actually affecting cultured fish.
10.2.2.6. Oxidized Fats
Marine fish oils, high in polyunsaturated fatty acids, are very susceptible to autoxidation when exposed to atmospheric oxygen (Watanabe 1982).
The use of oxidized or rancid fish oils in diet preparation, along with the additional oxidation that can occur during diet preparation and storage, results in the presence of undesirable lipid-derived toxins in the diet. These toxic components of the diets may affect fish by direct toxicity or indirectly through vitamin deficiencies caused by greater demands for vitamins, es- pecially vitamin E (Hardyet al.1983). The effects of oxidized lipids in fish diets have been investigated in at least three groups of cultured fish, the salmonids, catfish, and carp. Smith (1979) reported growth depression, increased mortality, microcytic anemia, and liver lipoid degeneration in
rainbow trout fed rancid diets deficient in both vitamin C and vitamin E.
Supplementing the diets with adequate levels of vitamins C and E prevented the described symptoms. The symptoms are those of vitamin E deficiency (Woodallet al.1964; Postonet al.1976) in rainbow trout rather than vitamin C deficiency, indicating that adequate vitamin E was the most important factor in preventing the symptoms. Sinnhuberet al.(1968b) and Hunget al.
(1980) also reported that adequate levels of vitamin E prevented adverse effects of feeding oxidized fish oils to rainbow trout. Murai and Andrews (1974) tested the effects ofα-tocopherol and ethoxyquin on oxidized men- haden oil in channel catfish. Oxidized menhaden oil in diets, without sup- plementalα-tocopherol or ethoxyquin, resulted in poor growth, food con- version, and survival rates; high incidences of exudative diathesis, muscular dystrophy, and depigmentation; and fatty livers, anemia, and pronounced histological changes in muscle fibers, kidney, and pancreas. Adequate levels of α-tocopherol in the rancid diets reversed all the above symptoms, but ethoxyquin was only partially effective, not reversing the anemic and mus- cular dystrophic conditions. Hashimotoet al.(1966) described a muscular dystrophy condition in carp resulting from oxidized fat in the diet and re- ported that vitamin E would prevent the condition. Watanabeet al.(1966, 1967) reported that vitamin E was effective in preventing carp muscular dys- trophy but that synthetic antioxidants such as ethoxyquin, BHA, methylene blue, ethyl gallate, and DPPD were not.
These results clearly indicate the deleterious effects of oxidized lipids on fish health. They also clearly demonstrate the essential requirement for adequate vitamin E in fish diets since at least some degree of lipid oxidation is almost inevitable, particularly in dry diets. The use of high-quality, unox- idized oils in diet preparation is recommended, but supplementation with adequate levels of vitamin E, which will vary depending on the fish species and the quality of the lipid, is absolutely essential.