Abstract. Histologic, histochemical and atomic absorption studies on liver tissue from 7 1 West H... more Abstract. Histologic, histochemical and atomic absorption studies on liver tissue from 7 1 West Highland white terriers are reported. Twenty-seven dogs had histologically normal liver and copper concentration com-parable to mongrel control dogs. Forty-four dogs had hepatic copper concentrations up to 22 times the mean copper concentration found in clinically normal mongrel dogs. Hepatitis, hepatic necrosis and cirrhosis were associated with the increased copper concentration in some dogs. Matings between dogs with high liver copper concentration produced pups with high liver concentration. The copper storage defect is inherited. Abnormally high copper concentrations have been found in the cirrhotic liver from dogs of different breeds.8J6J8 The cause or effect relationship between cirrhosis and increased hepatic copper is unclear except among Bedlington terriers. Some Bedlington terriers are affected with an inherited inborn error of metab-olism that results in excessive copper accum...
There is a need for efficient storage and retrieval of information about poisonous plants. The pu... more There is a need for efficient storage and retrieval of information about poisonous plants. The purpose of this article is to describe the Poisonous Plant Information System (PPIS) and to discuss basic issues in building and maintaining databases within the larger context of combined veterinary databases. This paper defines the database of PPIS and discusses its contents. Access methods are explained and sample search techniques are given.
Journal of the American Veterinary Medical Association, 1990
Accidental monensin toxicosis developed in 5 Stone sheep (Ovis dalli stonei), 5 blesbok (Damalisc... more Accidental monensin toxicosis developed in 5 Stone sheep (Ovis dalli stonei), 5 blesbok (Damaliscus dorcas phillipsi), and a Bactrian camel (Camelus bactrianus) at the St Louis Zoological Park. Eight animals died acutely and 1 was euthanatized because of chronic hind limb paresis. All affected animals had clinicopathologic evidence of severe muscle necrosis, serum electrolyte disturbances, and hemoconcentration.
Five captive-raised pronghorn antelope (Antilocapra americana) were fed an alfalfa- grass hay die... more Five captive-raised pronghorn antelope (Antilocapra americana) were fed an alfalfa- grass hay diet containing 15 ppm total dietary selenium (Se) for 164 days. Four additional captive- raised pronghorns fed a similar diet containing approximately 0.3 ppm total dietary Se served as controls. None of the pronghorns had clinical signs attributable to the high Se hay. Plasma Se increased more rapidly than blood Se concentrations, from baseline concentrations (<0.15 g/ml) to >0.40 g/ml within the first 50 days on the high selenium diet, but thereafter declined to approximately 0.30 pg/ml. Mean primary antibody response to hen egg albumin was less in pronghorn on Se hay. No significant gross or histological lesions attributable to selenosis were found, nor was there any evidence of dystrophic hoof growth. The greatest Se tissue concentra- tions were found in liver and kidney (5.67 to 10.4 pg/g and 2.36 to 3.14 pg/g, respectively) from experimental animals; liver and kidney from the c...
Gram negative endotoxins play a contributory role in the syndrome which results from over consump... more Gram negative endotoxins play a contributory role in the syndrome which results from over consumption of carbohydrates by horses and ponies. Since the antibiotic polymyxin B exerts a direct anti-endotoxin effect by chemically modifying the active lipid A moiety of endotoxin, it might be expected to protect horses after carbohydrate overload and provide a new therapeutic and experimental tool for this condition. The present study was undertaken to evaluate the effect of polymyxin B on hemostatic, hemodynamic, acid-base, and clinical aspects of the syndrome resulting from carbohydrate overload. Experimentally-induced carbohydrate overload resulted in lactic acidosis, hypercoagulability, hypovolemic shock and lameness. Although there was a slight delay in the onset of clinical signs resulting from experimental carbohydrate overload in treated animals, polymyxin B administered iv at 2.5 mg/kg every 6 hr failed to significantly ameliorate the coagulopathy, acidosis, lameness and shock in...
Poisoning by plants, mycotoxins and related toxins, 2011
During a 7 week period in the winter of 2004 approximately 400-500 elk (Cervus canadensis) in sou... more During a 7 week period in the winter of 2004 approximately 400-500 elk (Cervus canadensis) in south-central Wyoming were poisoned by a lichen (Xanthoparmelia chlorochroa) which was previously described as good winter feed for wildlife (Thomas and ...
Disruption of redox homeostasis is a prominent feature in the pathogenesis of Huntington&amp;... more Disruption of redox homeostasis is a prominent feature in the pathogenesis of Huntington&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s disease (HD). Selenium an essential element nutrient that modulates redox pathways and has been reported to provide protection against both acute neurotoxicity (e.g. methamphetamine) and chronic neurodegeneration (e.g. tauopathy) in mice. The objective of our study was to investigate the effect of sodium selenite, an inorganic form of selenium, on behavioral, brain degeneration and biochemical outcomes in the N171-82Q Huntington&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s disease mouse model. HD mice, which were supplemented with sodium selenite from 6 to 14 weeks of age, demonstrated increased motor endurance, decreased loss of brain weight, decreased mutant huntingtin aggregate burden and decreased brain oxidized glutathione levels. Biochemical studies revealed that selenite treatment reverted HD-associated changes in liver selenium and plasma glutathione in N171-82Q mice and had effects on brain selenoprotein transcript expression. Further, we found decreased brain selenium content in human autopsy brain. Taken together, we demonstrate a decreased selenium phenotype in human and mouse HD and additionally show some protective effects of selenite in N171-82Q HD mice. Modification of selenium metabolism results in beneficial effects in mouse HD and thus may represent a therapeutic strategy.
Selenosis is thought to be a significant problem among waterfowl populations in selenium-contamin... more Selenosis is thought to be a significant problem among waterfowl populations in selenium-contaminated wetlands in the western United States. Chemical analysis of avian tissues is currently the principal basis for diagnosis. The purpose of these two 150-day studies was to establish whether morphological criteria for selenosis could be developed to supplement chemical analysis. Forty-eight flightling male mallard ducks were fed either a proprietary waterfowl ration (&lt; 1 ppm selenium) or the same ration amended to contain 10, 25, and 60 ppm selenium supplied as seleno-L-methionine (n = 12/group). In a separate study, 12 birds fed twice daily were offered either a proprietary ration or a selenium-supplemented ration (120 microg/g) for one of two daily feedings. Selenium in whole blood increased from baseline concentrations (&lt; 0.4 microg/ml) to means of 4.5, 8.9, and 16.0 microg/ml in the 10-, 25-, and 60-ppm groups, respectively. All birds in the 60-ppm-dose group rapidly lost weight and were killed (11/12) or died (1/12) between 22 and 50 days of dietary exposure. In addition to emaciation, six of 12 birds (50%) fed the 60-microg/g diet developed mild to moderate generalized hepatopathy with single-cell necrosis, karyomegaly of hepatocytes, hyperplastic bile duct epithelium, and/or iron accumulation in Kupffer cells. The principal lesions in birds exposed to other dietary concentrations of selenium involved integumentary structures containing hard keratin. Gross lesions developed after 76 days of dietary exposure and consisted of bilaterally symmetrical alopecia of the scalp and dorsal cervical midline, broken or lost digital nails, and necrosis of the tip of the beak (maxillary nail). One or more of these three lesions were present in 0/12 birds (0%) fed 10 ppm selenium, 5/12 birds (42%) fed 25 ppm selenium, and 4/9 (44%) birds fed a split-feed diet containing 120 ppm selenium. Controls were unaffected. Histologic lesions in digital and maxillary nails consisted of single-cell to full-thickness necrosis of keratinocytes and multifocal parakeratosis in stratum corneum. Histologic lesions in alopecic skin (necrosis of the epidermal collar, inflammation of the feather pulp, and follicular keratosis) were mild. Some birds with alopecia had no detectable lesions in feather follicles from affected areas of skin. The highest tissue concentrations of selenium were in liver, kidney, and feathers, respectively. Mean hepatic tissue concentrations were 14.5 microg/g (10 ppm group), 29.6 microg/g (25 ppm group), 60.6 microg/g (60 ppm group), 13.0 microg/g (120 ppm split-feed group), and 2.0 microg/g (controls). Integumentary and hepatic lesions may be of value in corroborating a diagnosis of selenosis based on chemical analysis of tissues from naturally intoxicated waterfowl. Some birds with fatal selenosis may have no morphologic lesions other than emaciation.
Toxicity following ingestion of the vagrant, foliose lichen Xanthoparmelia chlorochroa was identi... more Toxicity following ingestion of the vagrant, foliose lichen Xanthoparmelia chlorochroa was identified as the putative etiology in the death of an estimated 400-500 elk on the Red Rim-Daley Wildlife Habitat Management Area in Wyoming during the winter of 2004. A single, unsubstantiated report in 1939 attributed toxicity of X. chlorochroa in cattle and sheep to usnic acid, a common lichen secondary metabolite. To test the hypothesis that usnic acid is the proximate cause of death in animals poisoned by lichen, domestic sheep were dosed PO with (+)-usnic acid. Clinical signs in symptomatic ewes included lethargy, anorexia, and signs indicative of abdominal discomfort. Serum creatine kinase, aspartate aminotransferase, and lactate dehydrogenase activities were considerably elevated in symptomatic sheep. Similarly, only symptomatic ewes exhibited appreciable postmortem lesions consisting of severe degenerative appendicular skeletal myopathy. The median toxic dose (ED(50)) of (+)-usnic acid in domestic sheep was estimated to be between 485 and 647 mg/kg/day for 7 days.
Histologic, histochemical and atomic absorption studies on liver tissue from 71 West Highland whi... more Histologic, histochemical and atomic absorption studies on liver tissue from 71 West Highland white terriers are reported. Twenty-seven dogs had histologically normal liver and copper concentration comparable to mongrel control dogs. Forty-four dogs had hepatic copper concentrations up to 22 times the mean copper concentration found in clinically normal mongrel dogs. Hepatitis, hepatic necrosis and cirrhosis were associated with the increased copper concentration in some dogs. Matings between dogs with high liver copper concentration produced pups with high liver concentration. The copper storage defect is inherited.
Journal of Veterinary Diagnostic Investigation, 1995
Prolonged oral exposure of cattle to elevated dietary selenium (Se) in forage and seleniferous pl... more Prolonged oral exposure of cattle to elevated dietary selenium (Se) in forage and seleniferous plants in seleniferous areas of the western United States is associated historically with 2 clinical syndromes: alkali disease and &quot;blind staggers.&quot; The potential for Se-induced disease in cattle and other species is considerable in areas with seleniferous shales, Se-accumulating plants, arid climates, and alkaline soils. These 2 Se-associated conditions were defined in the 1930s and 1940s, and the nosology of blind staggers is questionable. Seventeen yearling steers fed 0.15, 0.28, and 0.8 mg Se/kg body weight as selenomethionine or selenite for 120 days were euthanized and examined postmortem. Significant lesions were confined to 4 steers in the medium- and high-dose selenomethionine group and to 1 steer in the high-dose selenite group. Grossly, dystrophic hoof lesions developed in 2 steers, 1 of which had extensive separation of horn from lamellar and coronary epidermis and also lost hair from the tail switch. Histologically, tubules in the stratum medium of hooves from these 5 steers were replaced by islands of parakeratotic cellular debris, separated by more normal hoof matrix. Two of the 5 steers also had hyperplasia, acanthosis, parakeratosis, and disorganized germinal epithelium of varying severity in hoof epithelium, particularly at the tips of epidermal lamellae. These changes may distinguish the hoof lesions of chronic selenosis from those of chronic laminitis in cattle, in which dermal (chorial) changes predominate. In skin from the distal part of the tail of the animal that lost its switch, most follicles were atrophic and devoid of hairshafts and displayed dyskeratosis and mild superficial follicular keratosis. No significant lesions developed in tissues other than integument. Autometallographic staining for catalytic Se bonds in various tissues, including skin, liver, and kidney, revealed no positive staining of hair shafts; the correlation between stain intensity and dose group was poor. These findings indicate that dietary exposure for 4 months to 0.28 and 0.8 mg Se/kg in the form of selenomethionine and to 0.8 mg Se/kg in the form of sodium selenite reproduces in some cattle mild (subclinical) to severe (clinical) forms of alkali disease. No significant neurological, renal, or hepatic lesions developed, supporting the contention that blind staggers is caused by factors other than excessive dietary selenium.
Abstract. Histologic, histochemical and atomic absorption studies on liver tissue from 7 1 West H... more Abstract. Histologic, histochemical and atomic absorption studies on liver tissue from 7 1 West Highland white terriers are reported. Twenty-seven dogs had histologically normal liver and copper concentration com-parable to mongrel control dogs. Forty-four dogs had hepatic copper concentrations up to 22 times the mean copper concentration found in clinically normal mongrel dogs. Hepatitis, hepatic necrosis and cirrhosis were associated with the increased copper concentration in some dogs. Matings between dogs with high liver copper concentration produced pups with high liver concentration. The copper storage defect is inherited. Abnormally high copper concentrations have been found in the cirrhotic liver from dogs of different breeds.8J6J8 The cause or effect relationship between cirrhosis and increased hepatic copper is unclear except among Bedlington terriers. Some Bedlington terriers are affected with an inherited inborn error of metab-olism that results in excessive copper accum...
There is a need for efficient storage and retrieval of information about poisonous plants. The pu... more There is a need for efficient storage and retrieval of information about poisonous plants. The purpose of this article is to describe the Poisonous Plant Information System (PPIS) and to discuss basic issues in building and maintaining databases within the larger context of combined veterinary databases. This paper defines the database of PPIS and discusses its contents. Access methods are explained and sample search techniques are given.
Journal of the American Veterinary Medical Association, 1990
Accidental monensin toxicosis developed in 5 Stone sheep (Ovis dalli stonei), 5 blesbok (Damalisc... more Accidental monensin toxicosis developed in 5 Stone sheep (Ovis dalli stonei), 5 blesbok (Damaliscus dorcas phillipsi), and a Bactrian camel (Camelus bactrianus) at the St Louis Zoological Park. Eight animals died acutely and 1 was euthanatized because of chronic hind limb paresis. All affected animals had clinicopathologic evidence of severe muscle necrosis, serum electrolyte disturbances, and hemoconcentration.
Five captive-raised pronghorn antelope (Antilocapra americana) were fed an alfalfa- grass hay die... more Five captive-raised pronghorn antelope (Antilocapra americana) were fed an alfalfa- grass hay diet containing 15 ppm total dietary selenium (Se) for 164 days. Four additional captive- raised pronghorns fed a similar diet containing approximately 0.3 ppm total dietary Se served as controls. None of the pronghorns had clinical signs attributable to the high Se hay. Plasma Se increased more rapidly than blood Se concentrations, from baseline concentrations (<0.15 g/ml) to >0.40 g/ml within the first 50 days on the high selenium diet, but thereafter declined to approximately 0.30 pg/ml. Mean primary antibody response to hen egg albumin was less in pronghorn on Se hay. No significant gross or histological lesions attributable to selenosis were found, nor was there any evidence of dystrophic hoof growth. The greatest Se tissue concentra- tions were found in liver and kidney (5.67 to 10.4 pg/g and 2.36 to 3.14 pg/g, respectively) from experimental animals; liver and kidney from the c...
Gram negative endotoxins play a contributory role in the syndrome which results from over consump... more Gram negative endotoxins play a contributory role in the syndrome which results from over consumption of carbohydrates by horses and ponies. Since the antibiotic polymyxin B exerts a direct anti-endotoxin effect by chemically modifying the active lipid A moiety of endotoxin, it might be expected to protect horses after carbohydrate overload and provide a new therapeutic and experimental tool for this condition. The present study was undertaken to evaluate the effect of polymyxin B on hemostatic, hemodynamic, acid-base, and clinical aspects of the syndrome resulting from carbohydrate overload. Experimentally-induced carbohydrate overload resulted in lactic acidosis, hypercoagulability, hypovolemic shock and lameness. Although there was a slight delay in the onset of clinical signs resulting from experimental carbohydrate overload in treated animals, polymyxin B administered iv at 2.5 mg/kg every 6 hr failed to significantly ameliorate the coagulopathy, acidosis, lameness and shock in...
Poisoning by plants, mycotoxins and related toxins, 2011
During a 7 week period in the winter of 2004 approximately 400-500 elk (Cervus canadensis) in sou... more During a 7 week period in the winter of 2004 approximately 400-500 elk (Cervus canadensis) in south-central Wyoming were poisoned by a lichen (Xanthoparmelia chlorochroa) which was previously described as good winter feed for wildlife (Thomas and ...
Disruption of redox homeostasis is a prominent feature in the pathogenesis of Huntington&amp;... more Disruption of redox homeostasis is a prominent feature in the pathogenesis of Huntington&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s disease (HD). Selenium an essential element nutrient that modulates redox pathways and has been reported to provide protection against both acute neurotoxicity (e.g. methamphetamine) and chronic neurodegeneration (e.g. tauopathy) in mice. The objective of our study was to investigate the effect of sodium selenite, an inorganic form of selenium, on behavioral, brain degeneration and biochemical outcomes in the N171-82Q Huntington&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s disease mouse model. HD mice, which were supplemented with sodium selenite from 6 to 14 weeks of age, demonstrated increased motor endurance, decreased loss of brain weight, decreased mutant huntingtin aggregate burden and decreased brain oxidized glutathione levels. Biochemical studies revealed that selenite treatment reverted HD-associated changes in liver selenium and plasma glutathione in N171-82Q mice and had effects on brain selenoprotein transcript expression. Further, we found decreased brain selenium content in human autopsy brain. Taken together, we demonstrate a decreased selenium phenotype in human and mouse HD and additionally show some protective effects of selenite in N171-82Q HD mice. Modification of selenium metabolism results in beneficial effects in mouse HD and thus may represent a therapeutic strategy.
Selenosis is thought to be a significant problem among waterfowl populations in selenium-contamin... more Selenosis is thought to be a significant problem among waterfowl populations in selenium-contaminated wetlands in the western United States. Chemical analysis of avian tissues is currently the principal basis for diagnosis. The purpose of these two 150-day studies was to establish whether morphological criteria for selenosis could be developed to supplement chemical analysis. Forty-eight flightling male mallard ducks were fed either a proprietary waterfowl ration (&lt; 1 ppm selenium) or the same ration amended to contain 10, 25, and 60 ppm selenium supplied as seleno-L-methionine (n = 12/group). In a separate study, 12 birds fed twice daily were offered either a proprietary ration or a selenium-supplemented ration (120 microg/g) for one of two daily feedings. Selenium in whole blood increased from baseline concentrations (&lt; 0.4 microg/ml) to means of 4.5, 8.9, and 16.0 microg/ml in the 10-, 25-, and 60-ppm groups, respectively. All birds in the 60-ppm-dose group rapidly lost weight and were killed (11/12) or died (1/12) between 22 and 50 days of dietary exposure. In addition to emaciation, six of 12 birds (50%) fed the 60-microg/g diet developed mild to moderate generalized hepatopathy with single-cell necrosis, karyomegaly of hepatocytes, hyperplastic bile duct epithelium, and/or iron accumulation in Kupffer cells. The principal lesions in birds exposed to other dietary concentrations of selenium involved integumentary structures containing hard keratin. Gross lesions developed after 76 days of dietary exposure and consisted of bilaterally symmetrical alopecia of the scalp and dorsal cervical midline, broken or lost digital nails, and necrosis of the tip of the beak (maxillary nail). One or more of these three lesions were present in 0/12 birds (0%) fed 10 ppm selenium, 5/12 birds (42%) fed 25 ppm selenium, and 4/9 (44%) birds fed a split-feed diet containing 120 ppm selenium. Controls were unaffected. Histologic lesions in digital and maxillary nails consisted of single-cell to full-thickness necrosis of keratinocytes and multifocal parakeratosis in stratum corneum. Histologic lesions in alopecic skin (necrosis of the epidermal collar, inflammation of the feather pulp, and follicular keratosis) were mild. Some birds with alopecia had no detectable lesions in feather follicles from affected areas of skin. The highest tissue concentrations of selenium were in liver, kidney, and feathers, respectively. Mean hepatic tissue concentrations were 14.5 microg/g (10 ppm group), 29.6 microg/g (25 ppm group), 60.6 microg/g (60 ppm group), 13.0 microg/g (120 ppm split-feed group), and 2.0 microg/g (controls). Integumentary and hepatic lesions may be of value in corroborating a diagnosis of selenosis based on chemical analysis of tissues from naturally intoxicated waterfowl. Some birds with fatal selenosis may have no morphologic lesions other than emaciation.
Toxicity following ingestion of the vagrant, foliose lichen Xanthoparmelia chlorochroa was identi... more Toxicity following ingestion of the vagrant, foliose lichen Xanthoparmelia chlorochroa was identified as the putative etiology in the death of an estimated 400-500 elk on the Red Rim-Daley Wildlife Habitat Management Area in Wyoming during the winter of 2004. A single, unsubstantiated report in 1939 attributed toxicity of X. chlorochroa in cattle and sheep to usnic acid, a common lichen secondary metabolite. To test the hypothesis that usnic acid is the proximate cause of death in animals poisoned by lichen, domestic sheep were dosed PO with (+)-usnic acid. Clinical signs in symptomatic ewes included lethargy, anorexia, and signs indicative of abdominal discomfort. Serum creatine kinase, aspartate aminotransferase, and lactate dehydrogenase activities were considerably elevated in symptomatic sheep. Similarly, only symptomatic ewes exhibited appreciable postmortem lesions consisting of severe degenerative appendicular skeletal myopathy. The median toxic dose (ED(50)) of (+)-usnic acid in domestic sheep was estimated to be between 485 and 647 mg/kg/day for 7 days.
Histologic, histochemical and atomic absorption studies on liver tissue from 71 West Highland whi... more Histologic, histochemical and atomic absorption studies on liver tissue from 71 West Highland white terriers are reported. Twenty-seven dogs had histologically normal liver and copper concentration comparable to mongrel control dogs. Forty-four dogs had hepatic copper concentrations up to 22 times the mean copper concentration found in clinically normal mongrel dogs. Hepatitis, hepatic necrosis and cirrhosis were associated with the increased copper concentration in some dogs. Matings between dogs with high liver copper concentration produced pups with high liver concentration. The copper storage defect is inherited.
Journal of Veterinary Diagnostic Investigation, 1995
Prolonged oral exposure of cattle to elevated dietary selenium (Se) in forage and seleniferous pl... more Prolonged oral exposure of cattle to elevated dietary selenium (Se) in forage and seleniferous plants in seleniferous areas of the western United States is associated historically with 2 clinical syndromes: alkali disease and &quot;blind staggers.&quot; The potential for Se-induced disease in cattle and other species is considerable in areas with seleniferous shales, Se-accumulating plants, arid climates, and alkaline soils. These 2 Se-associated conditions were defined in the 1930s and 1940s, and the nosology of blind staggers is questionable. Seventeen yearling steers fed 0.15, 0.28, and 0.8 mg Se/kg body weight as selenomethionine or selenite for 120 days were euthanized and examined postmortem. Significant lesions were confined to 4 steers in the medium- and high-dose selenomethionine group and to 1 steer in the high-dose selenite group. Grossly, dystrophic hoof lesions developed in 2 steers, 1 of which had extensive separation of horn from lamellar and coronary epidermis and also lost hair from the tail switch. Histologically, tubules in the stratum medium of hooves from these 5 steers were replaced by islands of parakeratotic cellular debris, separated by more normal hoof matrix. Two of the 5 steers also had hyperplasia, acanthosis, parakeratosis, and disorganized germinal epithelium of varying severity in hoof epithelium, particularly at the tips of epidermal lamellae. These changes may distinguish the hoof lesions of chronic selenosis from those of chronic laminitis in cattle, in which dermal (chorial) changes predominate. In skin from the distal part of the tail of the animal that lost its switch, most follicles were atrophic and devoid of hairshafts and displayed dyskeratosis and mild superficial follicular keratosis. No significant lesions developed in tissues other than integument. Autometallographic staining for catalytic Se bonds in various tissues, including skin, liver, and kidney, revealed no positive staining of hair shafts; the correlation between stain intensity and dose group was poor. These findings indicate that dietary exposure for 4 months to 0.28 and 0.8 mg Se/kg in the form of selenomethionine and to 0.8 mg Se/kg in the form of sodium selenite reproduces in some cattle mild (subclinical) to severe (clinical) forms of alkali disease. No significant neurological, renal, or hepatic lesions developed, supporting the contention that blind staggers is caused by factors other than excessive dietary selenium.
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Papers by M. Raisbeck