Mercury and Mink. II. Experimental methyl mercury intoxication.

Adult female mink were fed rations containing 1.1, 1.8, 4.8, 8.3 and 15.0 ppm mercury as methyl mercury chloride over a 93 day period. Histopathological evidence of injury was present in all groups. Mink fed rations containing 1.8 to 15.0 ppm mercury developed clinical intoxication within the experimental period. The rapidity of onset of clinical intoxication was directly related to the mercury content of the ration. Mercury concentration in tissue of mink which died were similar, despite differences in mercury content of the diets and time of death. The average mercury concentration in the brain of mink which died was 11.9 ppm. The lesions of methyl mercury poisoning are described and criteria for diagnosis are discussed.     

Pathologic features of polybrominated biphenyl toxicosis in the rat and guinea pig.

Young male rats were fed a diet containing 0, 1, 10, 100, or 500 ppm of a commercial mixture of polybrominated biphenyls (PBB) that had been accidentally incorporated into a mineral mixture and fed to Michigan livestock and poultry. After 30 days, 9 of the 12 rats in each group were killed and tissues were examined. Liver weight to body weight ratios were significantly increased at all feeding levels; at 500 ppm, liver weight had more than doubled. Kidney weight was not affected. Microscopic lesions were mostly confined to the liver and consisted of extensive swelling and vacuolation of hepatocytes in rats fed diets containing 100 and 500 ppm of PBB. Slight swelling and vacuolation were seen in rats fed the diet containing 10 ppm, and lesions were not found at 0 or 1 ppm. There was a significant increase in hepatic mitochondrial size at 1 ppm, and smooth endoplasmic reticulum was markedly increased at 100 and 500 ppm. Myelin bodies were present at 100 and 500 ppm, and vacuoles were numerous. Rats killed at 60 days had similar lesions. The activity of hepatic microsomal enzymes increased at all levels of feeding of PBB. Rat pups nursing dams fed a diet containing 10 ppm of PBB had microscopic and ultrastructural hepatic lesions. When guinea pigs were fed PBB at the same amounts as were rats, the results were strikingly different. Guinea pigs fed a diet containing 500 ppm of PBB died within 15 days; at 100 ppm, only 2 of 6 survived for 30 days. Effects on liver weight were inconsistent, but 2 of 6 fed a diet containing 10 ppm had enlarged livers.     

Chronic copper toxicity in a dairy cow

A three year old Holstein dairy cow fed a ration containing a copper supplement died of chronic copper poisoning. The concentration of copper in the liver was 331 ppm (wet weight). The typical lesions of chronic copper toxicity including icterus, hepatic fibrosis and hemoglobinemic nephrosis were found at necropsy. The chronic copper toxicity was not considered to be a herd problem since the liver copper concentration in a slaughtered cull animal and blood samples taken from five animals in the same herd were within normal limits.     

The Distribution and Some Effects of Polychlorinated Biphenyls (Aroclor 1254) in Cockerels During Prolonged Feeding Trial

A ration containing 500 ppm of polychlorinated biphenyls (PCB) was fed to one month old cockerels for periods up to 12 weeks. The distribution of PCB was determined in the brain, liver, kidneys and blood as well as in the muscular and adipose tissues. Tissue concentrations of PCB increased linearly with time. Small changes were detected on the chromatograms of the liver, fat and blood extracts.

A significant decrease in the size of the combs and testicles in PCB-treated birds was noted. This decrease appeared as early as one week after the start of PCB administration.

     

Chronic toxicity of dietary fluorine to mink

Seventy-two 3-mo-old pastel mink were fed diets that contained 0, 33, 60, 108, 194 or 350 ppm supplemental fluorine (F), as NaF, for 382 d to assess its effects on growth, fur quality, reproduction and survivability. The basal diet contained 35 ppm F as fed. No significant differences were observed in body weight gains or fur quality between the controls and any of the F-treated groups (P greater than .05). Some males fed 350 ppm supplemental F for a 4-mo period prior to pelting had weakened frontal, parietal and femoral bones that fractured during the pelting process. The F treatments had no measurable adverse effects on breeding, gestation, whelping or lactation, although only 14% of the kits whelped by females fed 350 ppm F survived to 3 wk of age. The survivability of the adult mink was adversely affected only at 350 ppm supplemental F. At the termination of the study, no differences were observed in hematologic parameters or serum calcium concentrations between the controls and treated mink (P greater than .05), but serum alkaline phosphatase activities were increased (P less than .05) by the two highest dietary F levels. Serum F levels were elevated (P less than .01) only in mink fed 194 and 350 ppm F, and urinary and femoral F concentrations in the treated animals were generally greater (P less than .05; P less than .01) than control values and were closely related with dietary F levels. Femoral ash contents of the 194 and 350 ppm F-treated mink were less than the control values (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Mercury and mink. I. The use of mercury contaminated fish as a food for ranch mink.

Adult female and juvenile ranch mink were fed rations containing 50 and 75% of fish containing 0.44 ppm total mercury over a 145 day period. There was no clinical or pathological evidence of intoxication in these animals and mercury concentrations in tissue appeared to be at a level below that associated with toxicity.     

Proliferation of maxillary and mandibular periodontal squamous cells in mink fed 3,3',4,4',5-pentachlorobiphenyl (PCB 126).

This report characterizes squamous cell proliferation in young farm mink (Mustela vison) fed a diet supplemented with 0.024 ppm 3,3',4,4',5-pentachlorobiphenyl (polychlorinated biphenyl [PCB] congener 126). One to 2 months of dietary exposure to PCB 126 resulted in gross lesions of the upper and lower jaws consisting of mandibular and maxillary nodular proliferation of the gingiva and loose teeth. The maxilla and mandible of the PCB-treated mink were markedly porous because of loss of alveolar bone. Histologically, this osteoporosis was caused by proliferation of squamous cells that formed infiltrating cords. This report clearly documents the fact that the environmental contaminant PCB 126 can cause osteoinvasive squamous proliferation in young mink, although the dose used in the present study was 7 and 36 times higher than what is typically encountered in contaminated bird eggs and fish, respectively.     

Tissue Distribution of Polychlorinated Biphenyls (Aroclor 1254) in Cockerels: Relation to the Duration of Exposure and Observations on Pathology

Day old cockerels were given a ration containing 500 ppm of polychlorinated biphenyls (PCB) as Aroclor 1254. Mortality was recorded and various tissues analyzed for PCB levels. Tissue concentrations of PCB increased in direct relation with the time of the experiment and with the survival period of birds. The PCB ratios between liver, kidney and muscle to that in the brain were constant through the duration of the study. Pathological examination revealed extensive hydropericardium and edema in the lung, muscle and subcutis; hemorrhages in muscles, digestive tract, lung and kidney; myocarditis; kidney and liver necrosis and hepatitis.     

The Effects of Polychlorinated Biphenyls (Aroclor 1254) on Chicken Egg Production, Fertility and Hatchability

Laying hens and roosters were given rations containing 0, 5 or 50 ppm of polychlorinated biphenyls (PCB) as Aroclor 1254 for up to 39 weeks. Due to drastic decline in production and hatchability of fertile eggs, the 50 ppm treatment was replaced with control ration at 14 weeks and the residual effects were investigated. Following the withdrawal of PCB from the ration, the affected parameters slowly returned to the control range. The 5ppm level of PCB reduced egg production but not hatchability of fertile eggs. Fertility for the 5ppm PCB group in the first 14 weeks was similar to the other groups but showed a significantly greater decline in the last 14 weeks.

Concentration of PCB in eggs of both treatment groups increased until maximum concentrations were reached. These maxima persisted until the end of the experiment or until the withdrawal of PCB from the ration. Following withdrawal of higher level of PCB, the PCB declined in concentration but persisted in eggs over a five month period.

     

Effects of Different Fat Supplements on Growth and Hepatic Lipids and Fatty Acids in Male Mink

Male mink kits (n=10 for each group) were fed diets supplemented with different fats for 12 weeks (September-November). The levels of digestible fat (8%) and energy content (7 MJ kg-1) of the diets were equal. The supplements used were beef pork fat, mink fat, broiler offal, rainbow trout offal, capelin oil, soybean oil and linseed oil. The growth and hepatic lipids (analysed by a thin-layer chromatography- flame ionization detection analyser) and fatty acid composition (analysed by gas-liquid chromatography) were studied. The pattern of weight gain of the mink fed the beef pork diet differed from that of the other mink. These kits reached high but delayed weight maxima compared with the other mink but then during November they lost weight rapidly. In liver, both the capelin oil- and linseed oil-fed mink had large concentrations of total lipids and triacylglycerols. The mink fed capelin oil were significantly heavier. The fatty acid analyses of hepatic total lipids and phospholipids revealed that the f -linolenic acid (18:3 n-3) of linseed oil was not efficiently metabolized to longer chain and more unsaturated fatty acids important for cellular membranes. It is discussed that 18:3 n-3 may not be as valuable for growing mink kits as the polyunsaturated fatty acids of the fish oils.     

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. I. Chukar partridge

Chukar partridges were fed diets containing 1.25, 2.5, or 5 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Toxin-induced mortality was seen during the third week with 4 ppm OA (12.5%) and 16 ppm T-2 toxin (15%), compared with the mortality in control chukars fed no toxin (2.5%). Body weights were significantly decreased by the highest level of aflatoxin at 3 weeks of age, by the highest level of OA by 2 weeks of age, and by 8 and 16 ppm T-2 toxin by 1 week of age. Aflatoxin did not affect liver weight and OA did not increase kidney weight in 3-week-old chukars. There was a slight decrease in kidney weight in chukars fed 4 ppm OA; however, the decrease was related to the decrease in body weight produced by the toxin. Mouth lesions were seen at all levels of T-2 toxin fed.     

Reversibility of furazolidone-induced cardiotoxicosis in ducklings

Furazolidone cardiotoxicosis was induced in 2 groups (FZ and FZ-CR groups) of newly hatched male Pekin ducklings (100/group) by feeding a ration containing 650 mg of furazolidone/kg of feed (ppm) for 28 days. A third group (control ration, CR group; n = 100) was fed the same ration without furazolidone. On day 28, the control ration was initiated for the FZ-CR group initially given the furazolidone-containing ration, to allow recovery from the effects of the drug, whereas ducklings of the FZ group continued to consume the furazolidone-containing ration. Biweekly, beginning with week 4, ducklings were euthanatized to assess severity of gross lesions and to obtain sections of myocardium for histologic and ultrastructural examination. Clinical evidence (increased weight gain, increased feed consumption, decreased mortality, reduced prevalence of palpable ascites) of regression of cardiotoxicosis of ducklings of the FZ-CR group was nearly complete by day 56 (28 days after cessation of furazolidone intake). Likewise, regression of gross lesions, as measured by overall prevalence of gross lesions, left ventricular volume, and ascites prevalence and severity, were also essentially complete by day 56. Myofibrillar lysis was not seen in sections from the heart (examined ultrastructurally) obtained from ducklings of the CR group that were euthanatized on day 28, 56, or 98. Myofibrillar lysis was detected in all ducklings (4/4) fed furazolidone (FZ and FZ-CR groups) and euthanatized on day 28. Myofibrillar lysis was not seen in the heart of ducklings of the FZ-CR group that were euthanatized on day 56 or 98. Myofibrillar lysis was detected in the heart from all ducklings of the FZ group that were euthanatized on day 56.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mortality in mink kits from birth to weaning

In 1988, a necropsy survey of the pattern and major causes of mortality in mink kits from birth to weaning was undertaken. The overall preweaning mortality rate was 20%. Mortalities occurring within the first three days after birth accounted for 91% of submissions, and 78% of the kits in this age group had no lesions or bacterial isolates. The average weight of kits which died within one day of birth (7.9 g) was significantly lower than the average birthweight of healthy kits (10.7 g). In kits under four days of age and with lesions, the most common diagnoses were dystocia (12%), systemic infection (4%), anasarca (2%), and congenital defects (1%). In unweaned kits four days of age or older, the most common diagnoses were systemic infection (19%), external trauma (6%), dystocia (5%), and cervical adenitis (2%).     

Pathological Changes in Virus Enteritis of Mink

The lesions which characterize viral enteritis of mink (VEM) were studied in twenty-six, ten-week-old mink which had been infected by force feeding a tissue suspension containing a Wisconsin strain of mink enteritis virus. The pathogenesis of the lesions was reconstructed from gross and histopathological changes observed in animals which were selected randomly from the group each day for necropsy during the course of the disease.

Alterations were observed in the tissues of all mink examined from post-inoculation day (PID) 4 through 13. The principal macroscopic lesions which consisted of fibrinous enteritis, enlargement and hemorrhage of the spleen and edema of mesenteric and hepatic lymph nodes were most conspicuous on PID 7 and 8. Histopathological changes including necrosis and desquamation of intestinal epithelium, depletion of mature lymphocytes in lymph nodes, thymus and spleen and loss of partly differentiated myeloid and erythroid cells from spleen and bone marrow also reached full development on PID 7 and 8. However, nuclear inclusion bodies which were presumed to be a product of the causative agent and, therefore, of diagnostic significance were most prevalent on PID 3, 4 and 5. The inclusions were observed in mucosal epithelial cells of the intestine, parenchymal cells of the liver and in lymphocyte precursor cells of the spleen, intestinal lymph nodules and masenteric and hepatic lymph nodes.

     

The formaldehyde content in fish in relation to anemia in mink (author's transl)]

The fish-induced anemia in mink is an alimentary disease produced by feeding high amounts of some raw marine fishes. The anemiogenic properties of the fish has been related mainly to its content of the iron binding agent-trimethylaminoxide. The aim of the present investigation was to examine how far formaldehyde could also play a part as an anemiogenic factor. The content of formaldehyde has been analysed in all species of raw, cold stored fish known to be used in mink food and in a few samples of ready made food (Table II). The content of formaldehyde varied within wide limits from 12 to 105 ppm, but none of the measured contents reached the high values obtained by Costly (1970). The mean values of formaldehyde in gutted coalfish, fillet waste of coal fish, cod and haddock prepared for the feeding experiments, were all close to 50 ppm. 175 female mink and 632 mits were tested during the whole of the breeding period from 15.2-30.6, 80 per cent of the diet (page 1) was fish products with and without supplements of formaldehyde. Amounts from 200 to 50 ppm were tried (Table I). The supplement of 200 ppm formaldehyde had an appetite-decreasing and anemiogenic effect, but the supplement of 50 ppm, i.e. a formaldehyde content up to the highest value observed in fillet waste, had no effect on appetite or hemoglobin synthesis neither in females nor in kits. This content of formaldehyde did not counteract the anti-anemiogenic effect of iron glutamate. The fish-induced anemia occurred in mink thus appears unaffected by the quantities of formaldehyde found in fish diets to fur bearing animals. Triox must be regarded as the dominant anemiogenic factor in raw fish diets.     

Toleration of high concentrations of dietary zinc by mink

Adult and kit male and female natural dark ranch mink (Mustela vison) were fed a conventional diet supplemented with 0, 500, 1,000, or 1,500 ppm zinc, as ZnSO4.7H2O, for 144 days. No marked adverse effects were observed in feed consumption, body weight gains, hematologic parameters, fur quality, or survival. Zinc concentrations in liver, kidney, and pancreas of the mink increased in direct proportion to the zinc content of the diet. Histopathologic examination of the livers, kidneys, and pancreata revealed no lesions indicative of zinc toxicosis. The results indicate that mink can tolerate at least 1,500 ppm dietary zinc, as ZnSO4.7H2O, for several months without apparent adverse effects.     

Efficacy of selected coccidiostats in sandhill cranes (Grus canadensis) following challenge.

The anticoccidial efficacy of amprolium, clazuril, and monensin were studied in sandhill cranes (Grus canadensis) infected with a mixture of Eimeria spp. oocysts. Five groups of four 1-day-old sandhill crane chicks were maintained on a crumbled ration containing no coccidiostat, amprolium at 2.2 ppm, clazuril at 1.1 ppm, clazuril at 5.5 ppm, or monensin at 99 ppm. After 2 wk on their respective feeding regimens, birds in each of the five groups were administered 25 x 10(3) pooled sporulated Eimeria spp. oocysts per os and observed for another 3 wk. A sixth group of four chicks served as nonmedicated, nonchallenged control during the study. Clinical signs and lesions consistent with disseminated visceral coccidiosis were observed in all challenged controls and birds fed amprolium and clazuril. Birds in these groups died 9-10 days after challenge. In contrast, only one monensin-medicated bird had clinical signs of disseminated visceral coccidiosis, and it died 13 days after challenge (DAC). This and an asymptomatic bird that were necropsied at study termination had less-severe gross and microscopic lesions of disseminated visceral coccidiosis. Two of three monensin-treated birds that survived challenge passed from 50 to 500 coccidial oocysts 11 to 18 DAC but were negative at study termination. Of the coccidiostats tested, monensin, at the dietary level of 99 ppm, was the only anticoccidial drug that provided protection against experimentally induced disseminated visceral coccidiosis in sandhill cranes.     

Tissue residues from feeding pentachloronitrobenzene (quintozene) to White Leghorn chickens

One-day-old White Leghorn chicks were fed graded levels (0, 10, 50, 100 and 1,000 ppm) of pentachloronitrobenzene (PCNB; quintozene) up to 8 weeks. Each treatment group consisted of 90 randomly selected birds (2 replications of 45 birds each). Body weight gains were significantly lower at the 1,000-ppm treatment level. Histopathologic examination of brain, liver, pancreas, small intestine, gizzard, spleen, kidney, lung, and heart failed to reveal lesions in either control or treated groups. Bioaccumulation of PCNB or its metabolites (pentachloroaniline and pentachlorophenylmethylsulfide) in tissues only occurred in trace or very low concentrations. However, trace contaminating of PCNB, eg, hexachlorobenzene (HCB) and pentachlorobenzene (PCB) accumulated in tissues to a significant degree. Tetrachloronitrobenzene, another contaminant of PCNB, was found in only the adipose and cardiac tissues following the feeding of 1,000 ppm PCNB. Storage of PCNB, HCB, and PCB in adipose and other tissues was linearly related to the amount of PCNB in the ration.     

Selenium toxicity and porcine focal symmetrical poliomyelomalacia: description of a field outbreak and experimental reproduction.

An acute afebrile paretic condition was diagnosed in 18 of 225 feeder pigs between eight to ten weeks of age. Nine pigs died acutely, seven pigs were euthanatized and two appeared to recover. Macroscopic lesions in the ventral horns of the cervical and lumbar/sacral spinal cord enlargements consisted of focal, bilateral, depressed areas. Histopathologically, the lesion consisted of endothelial proliferation, glial cell reaction and microcavitation. Similar lesions were observed in some brain stem motor nuclei. High selenium levels were detected in the pig feed and in pig tissues and blood. Two of five experimental pigs fed a commercial grower ration and supplemented with 52 ppm selenium as sodium selenite developed paresis and paralysis after a 29 day feeding trial. Histopathological lesions of focal symmetrical poliomyelomalacia confined to the cervical and lumbar/sacral spinal cord enlargements, and identical to those in the field cases, were produced. Select brain stem motor nuclei were also affected.     

Effects of long-term feeding of a diet supplemented with clinoptilolite to dairy cows on the incidence of ketosis, milk yield and liver function

Fifty-two clinically healthy Holstein cows were randomly assigned to one of three groups according to their age and parity. The first group (A) consisted of 17 cows that were fed a concentrate ration supplemented with 1.25 per cent clinoptilolite, the second group (B) consisted of 17 cows fed a ration supplemented with 2.5 per cent clinoptilolite, and the third group (C) consisted of 18 cows, which were fed the basal ration containing no clinoptilolite. The rations were fed from four weeks before the cows' expected parturition dates until the beginning of the next dry period. Blood samples were collected from each animal at the start of the experiment, on the day of calving and then monthly, and analysed for serum glucose, ketone bodies, liver enzymes, blood urea nitrogen (BUN) and total proteins. The milk yield of each cow was recorded monthly. The cows in group B had significantly fewer cases of clinical ketosis during the first month after calving and a higher total milk yield. Feeding the cows with clinoptilolite for a long period had no apparent adverse effects on their liver function, and did not significantly affect the concentrations of glucose, ketone bodies, BUN and total proteins in their serum.