National Academies Press: OpenBook

Nutrient Requirements of Mink and Foxes,: Second Revised Edition, 1982 (1982)


Suggested Citation:"TOXIC SUBSTANCES IN THE FEED SUPPLY." National Research Council. 1982. Nutrient Requirements of Mink and Foxes,: Second Revised Edition, 1982. Washington, DC: The National Academies Press. doi: 10.17226/1114.
Page 21
Suggested Citation:"TOXIC SUBSTANCES IN THE FEED SUPPLY." National Research Council. 1982. Nutrient Requirements of Mink and Foxes,: Second Revised Edition, 1982. Washington, DC: The National Academies Press. doi: 10.17226/1114.
Page 22
Suggested Citation:"TOXIC SUBSTANCES IN THE FEED SUPPLY." National Research Council. 1982. Nutrient Requirements of Mink and Foxes,: Second Revised Edition, 1982. Washington, DC: The National Academies Press. doi: 10.17226/1114.
Page 23

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Toxic Substances in the Feel] Supply The diverse nature of products and by-products used for feed- ing mink and foxes increases the possibility of incorporation of injurious substances into the diet. Excessive amounts of certain nutrients, as well as the presence of contaminants (both natu- ral and synthetic substances) in minute quantities in feed- stuffs, can cause severe problems in these forbearers. Tox- icities due to excessive dietary levels of certain nutrients are discussed along with the discussion of nutritional deficiencies in the section entitled "Recommended Dietary Allowances." Accounts of toxicity in mink and foxes due to some nonnutri- tive substances are presented below. SYNTHETIC ESTROGENS During the l9S0s, impaired reproduction and early kit losses in mink were attributed to the use of poultry and beef by- products that contained synthetic estrogen. Studies have shown that 10 ,ug of synthetic estrogens, such as diethylsti- bestrol (Travis et al., l9S6; Shackelford and Cochrane, 1962) or dienestrol diacetate (ruby and Travis, 1971), fed daily to female mink during the reproductive period, result in sterility, decreased litter size, and poor kit survival. One hundred fifty ,ug of diethylstilbestrol fed every third day after implantation also had adverse effects on mink reproduction and kit survival (Travis and Schaible, 1962~. Ahman (196S) reported mink fed 3 percent raw soybean oil that contained estrogenic compo- nents showed decreased litter size and increased kit mortality at birth. Clinical signs of estrogenic toxicity include loss of hair, anorexia, inactivity, excessive fatness, sterility, agalactia and abortion in breeders (Mills, 1961), and reduced body weight gain in young mink (Warner et al., 1958~. Single, oral 50-mg doses of diethylstilbestrol force-fed to female red foxes from 9 days before mating to 10 days after mating caused reproductive failure (Linhart and Enders, 1964~. Although mink and foxes are quite sensitive to synthetic estrogens, current regulations governing the use of these com- pounds have greatly reduced the chance for contamination of fur animal diets with these substances. THYROID GLANDS Mink fed products that contain thyroid-active compounds have been shown to exhibit reproductive complications. Diets that contained 15 percent "gullet trimmings', from calves (which included thyroid-parathyroid tissue) caused a marked decrease in the number of females that whelped, number of kits whelped, and kit birth weight and viability (Travis et al., 1966~. CHLORINATED HYDROCARBONS Chlorinated hydrocarbon pesticides, such as DDT and diel- drin, have had wide agricultural use and, because of their per- sistent nature, have become troublesome pollutants. Residues from these pesticides tend to concentrate in the fatty tissues of animals as they move up the food chain. Studies have shown that diets supplemented with 100 ppm DDT, 100 ppm DDE, or 100 ppm DDT plus 50 ppm DDD fed to mink from weaning through growth, furring, reproduc- tion, and lactation were not toxic, nor did they have an adverse effect on reproduction or kit growth and survival (Aulerich and Ringer, 1970). Duby (1970) reported similar results from feeding 100 ppm p,p'-DDT to mink for two suc- cessive generations, but noted a uterotropic response from in- traperitoneal injections of o,p'-DDT (ruby et al., 1971). Pro- longed feeding of diets that contained 2.5 ppm dieldrin were toxic to adult mink, especially if the animals were stressed, but the pesticide did not impair reproduction when fed at 5 ppm only during gestation (Aulerich and Ringer, 1970). The levels of pesticides employed in these studies were con- siderably higher than the residue levels one would expect to find in typical mink diets, which suggests that some margin of safety exists concerning these compounds. POLYCHLORINATED BIPHENYLS Polychlorinated biphenyls (PCBs) constitute a series of com- pounds of varying chlorine content that have had wide indus 21

22 Nutrient Requirements of Mink and Foxes trial use. Although PCBs are no longer manufactured in this country, some PCB use has continued in existing equipment. Consequently, they have become a major pollutant of many rivers and lakes and persist in the environment in a manner similar to the chlorinated hydrocarbon pesticides. Studies (Aulerich et al., 1973; Platonow and Karstad, 1973, Jensen, 1977) have shown that mink are extremely sensitive to these compounds. As little as 2 ppm PCB (Aroclor~ 1254*) fed to mink for 8 months caused reproductive failure. Diets that contained higher levels of PCl3s or PCB-contaminated fish or beef were lethal to adult mink. Clinical signs of PCB poisoning in mink consist of anorexia, bloody stools, fatty liver, kidney de- generation, hemorrhagic gastric ulcers, increased liver weights, and elevated hepatic cytochrome P450 levels (Aulerich and Ringer, 1977; Jensen, 1977~. It is thought that many of the reproductive problems in mink previously attributed to pesticide contamination may have been due to PCB residues. HISTAMINE Histamine, a potential toxicant in fur animal diets, is formed by the decarboxylation of histidine by certain bacteria (Clos- tridium, Proteus, Salmonella, and Escherichia coli) within a pH range of 5.0 to 8.0 (Wolfer, 1977~. Diets that contain high levels of acid-preserved feedstuffs are especially prone to histamine formation. According to Woller (19773, typical Scandinavian mink diets may contain from 0 to 30 ppm hista- mine at the time of mixing and up to 120 ppm after 24 hours storage. Mink kits fed diets containing from 15 to 847 ppm histamine showed diarrhea, decreased feed consumption, and reduced body weight gains in direct proportion to the level of hista- mine in the diet (Wolfer, 1977~. Other clinical signs of hista- mine poisoning included vomiting and dilated stomachs. HEAVY METALS Mercury and lead are two heavy metals that may have toxicity implications in mink and fox feeds. Mercenary contamination resulting from industrial pollution of lakes and rivers is widespread (Wobeser et al., 1975a), and, although mercury poisoning from consumption of contami- nated fish has been reported in humans, cats, and sea birds (Takeuchi, 1970), accounts of mercurialism in ranch mink are lacking except for a report of phenylmercuric acetate intoxica- tion by Borst and van Lieshout (1977~. Wobeser and Swift (1976) reported an incidence of mercury poisoning in wild mink, and it would appear that with diets high in fish, mer- cury poisoning could be a potential problem in ranch mink. Studies by Aulerich et al. (1974) have shown that mink are quite sensitive to methyl mercury but comparatively tolerant of mercury in an inorganic form. Mink fed diets that con- tained 5 ppm methyl mercury showed clinical signs of mer- cury poisoning within 25 days, with death occurring betweer~ *Trade name for a specific PCB containing 54 percer~t chlorine~ the 30th and 37th day. The degradation of methyl mercury by mink has been investigated by Jernelov et al. (1976~. Swedish investigators (Ahman and Kull, 1962) reported 0.24 and 2.4 mg mercury, as magnesium-bromalkylmercuric chloride, per kilogram of feed to be highly toxic to mink and noted a high correlation between the mercury content of the [eed and the mercury concentration in the organs. The clinical signs of mercury poisoning are incoordination, anorexia, weight loss, tremors, ataxia, paralysis, paroxysmal convulsions, and high-pitched vocalizations (Aulerich et al., 1974; Wobeser et al., 1975b). When suspended by the tail, mercury-treated mink show the typical limb-crossing phe- nomena indicative of mercury poisoning in several other species (Aulerich et al., 1974~. Lead poisoning (plumbism) in mink is usually associated with the use of red lead or paint containing lead on cages, [eed and water containers, or feed equipment. The clinical signs of acute plumbism in mink are anorexia, muscular incoordina- tion, stiffness, trembling, dehydration, convulsions, and a mu- copurulent discharge around the eyes (Gorham et al., 1972~. NITROSAMINES N-nitrosodimethylamine (dimethylnitrosamine) is a toxic sub- stance ~at forms in fish meals preserved with sodium nitrite, formaldehyde, or sodium benzoate (Koppang, 1974a>. Di- and trimethylamines present in the fish react with the preservative to form the toxin (Ender et al.' 1964; Stout and Adair, 1970b; Sen et al., 1972~. N-nitrosodimethylamine is extremely toxic to mink (Koppang, 1966; Koppang and ;Rimeslatten, 19763 as well as cattle (Koppang, 1974b), sheep (Koppang, lO74c), and pigs (Koppang, 1974a). Hepatotoxic disorders in mink from feeding fish meals that contained N-nitrosodimethylamine have been reported in Norway (Ender et al., 1964; Kop}?ang, 1966), England, and the United States (Stout and Adair' 1970b). The clinical signs associated with N-nitrosodime~ylamine poisoning in mink are ascites, pale necrotic livers with hae- mangiomatous tumors and obliterative degeneration of the hepatic veins, and adenomatous proliferation of the bile duct (Stout and Adair, 1970b; Koppang and Rimeslatten, 1976~. In mink, the LDso of N-nitrosodimethylamine adminis- tered by subcutaneous injection was reported to be 7 mg per kilogram of body weight, while daily ingestion of 0.2 mg per kilogram of body weight resulted ir~ toxic hepatosis (Koppang and Rimeslatten, 1976~. MYCOTOX.INS Mycotoxins are toxic substances produced by certain molds that grow on grain, forage, or other feedstuffs. They can cause serious economic loss and mortality when consumed by ani- mals. Although more than 100 mycotoxins have been identi- fied in feeds (Harms and Arafa, 1978), aflatoxins (produced by strains of Aspergillus flavus and A. parasiticus) appear to be the most important in terms of mink production. Mink are reported to be extremelY sensitive to aflatoxin poisoning (Kop

Nutrient Requirements of Mink and Foxes 23 pang and Helgebostad, 1972; Chou et al., 1976a,b), which has been reported to be responsible for the death of more than 3,000 animals in Russia (Astrakhantsev, 1967~. Within a species, the young are generally more susceptible to aflatoxin than mature animals (Patterson, 1973), although aflatoxin B1 and M1 are not passed to offspring via the milk (Chou and Marth, 1976~. In mink, the single LDso close of aflatox~n (40 percent Be and 60 percent G1) was estimated to be 500 to 600 ,ug per kg of body weight (Chou et al., 1976b). Daily ingestion of 5 fig of aflatoxin for 4 weeks produced fatty degeneration of the liver, catarrh in the stomach and intestine, and icterus (Koppang and Helgebostad, 1972~. Prolonged ex- posure to aflatoxin leads to anorexia, increased liver weight, hemorrhagic livers with pink-yellow spots, necrosis and fatty infiltration of the liver, hepatoma, bile duct proliferation, and increased alkaline phosphatase and plasma cholesterol levels (Chou et al., 1976a,b; Koppang and Helgebostad, 1972~. BOTULISM Botulism is a form of food poisoning causers by a potent toxin produced, in the absence of oxygen, by the organism Clostri dium botulinum, a bacterial contaminant frequently assort ated with spoiled meat or feed. There are several types of botul~num toxin. Mink are highly susceptible to type C, moderately susceptible to types A and B. and relatively resistant to type E (Quortrup and Gorham' 1949, Wagenaar et al., 1953; Skulberg and Valland, 1969~. Type A botulinum toxin has been reported to be toxic to silver foxes (Pyle and Brown, 1939; Shoop, 1939), although they are highly resistant to types G and E (Yndestad et al., 1977~. When an animal consumes feed that contains the toxm, the onset of the disease is rapid. The toxin affects the nerve centers, causing muscular incoordination and stiffness, fol- lowed by paralysis and death In from 12 to 96 hours in mink (Gorham et al., 1972~. Botulism outbreaks on mink farms ~n- volving considerable losses have been reported by Quortrup and Holt (1940), Gorham (1950), Dinter and Kull (1951), Kull and Moberg (1952), Anonymous (1957)j and Gustavsen et al. (1969~. Since the course of the disease is very rapid, treatment Is usually not effective.- The only successful control is annual vaccination of all kits with botulins toxoid (vaccine) shortly after weaning (Gorham et al., 1972~.

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