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OCR for page 21
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
OCR for page 22
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
OCR for page 23
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~.
Representative terms from entire chapter:
mercury poisoning
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