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yorkiegirl2 · 09-06-2006, 06:18 AM

Mercury Poisoning
Dogs and cats are susceptible to mercury poisoning [39,103-105] a condition that has been termed Minamata disease (methyl mercury poisoning) in people. Elemental mercury is transported in blood plasma, proteins and hemoglobin, and may be incorporated rapidly into the brain [106]. While rarely seen in clinical practice, methylmercury (MM) poisoning or methylmercurialism usually occurs after consumption of contaminated fish, especially in cats [107-109] although it has also been reported in dogs [110]. Neurologic signs in dogs and cats following oral exposure have included abnormal symmetrical use of pelvic limbs, hypermetria, ataxia, paresis, abducted pelvic limbs, loss of postural reactions, proprioceptive impairment, blindness, opisthotonus, grand mal convulsions and terminal recumbency [111]. Serum biochemical findings were limited to hypercholesterolemia in dogs. Significant species difference in susceptibility to MM-induced neuronal lesions was the relative resistance of the feline spinal cord, canine cerebellar cortex and canine peripheral nervous system. Subacute exposure produced marked cerebral cortical involvement in dogs and cats, marked cerebellar cortical lesions, marked CNS perivascular inflammatory cell cuffing in cats, marked leptomeningitis in dogs and moderate lesions in the brain stem and cerebellar roof nuclei in both species. Chronic exposure of a dog to 120.4 mg Hg/kg/day for 55 weeks produced a marked loss of neurons and reactive astrocytosis in the cerebral cortex in the absence of clinical signs of toxicity. Twice weekly exposure to 0.64 mg Hg/kg as MM for 6 to 9 weeks in 5 dogs produced milder clinical signs, hypercholesterolemia, lipoproteinemia, and hydrocephalus. Neuronal loss and gliosis were most severe in the cerebral cortex with minimal involvement of the brain stem. Cerebellar lesions observed in cats include focal atrophy of the granular layer, focal spongiosus of the molecular layer and degeneration and loss of Purkinje cells in the cerebellum [112]. Demyelination in the fiber tracts of the dorsal funiculus, mainly the fasciculus cuneatus and in the lateral and ventral corticospinal tracts were also noted [112]. Terminal blood MM levels were in excess of 18 mg/ml, while brain methylmercury levels ranged from 21.0 to 28.4 mg/g. The liver and kidney contained the highest total levels of mercury of 50 to 80 mg/g, of which 23 to 37% was inorganic [112]. Increased levels of mercury in the brain does not necessarily result in behavior abnormalities or pathology [113]. In acute exposure to ingested mercury salts, oral administration of milk and eggs to bind mercury to protein has been recommended [11].

Metaldehyde
Metaldehyde toxicosis usually follows ingestion of metaldehyde-based molluscicides [2]. The incidence of toxicosis is more common in coastal and low-lying areas. Metaldehyde is degraded to various aldehydes in the stomach which may give a formaldehyde odor to the contents [114]. Signs include tachycardia, salivation, tremors, vomiting, hyperesthesia, nystagmus (especially in cats), ataxia, opisthotonus and seizures, hyperthermia, diarrhea, and depression. Death from respiratory failure may follow from 4 to 24 hours after ingestion. Delayed deaths may follow liver failure (after 3 to 4 days). Stomach contents should be submitted in suspected poisonings. Treatment includes activated charcoal, anticonvulsants, and fluid therapy with sodium lactate to correct the severe acidosis that develops in poisoned animals [11].

Methionine
Methionine is an essential amino acid and nutrient, a lipotrope, and a urine acidifier [65]. It has been used as a nutritional supplement in food animals. Accidental ingestion may lead to neurotoxicity and metabolic acidosis. The toxicity of methionine is partially related to its metabolism to ammonia and to increased production of mercaptan-like compounds. Toxicity is especially apparent in dogs with pre-existing liver disease. Signs include excessive salivation and vomiting, ataxia, depression, lethargy, circling, head pressing, aimless pacing, aggression, somnolence, blindness, seizures, stupor and coma [1]. In experimental studies, cats given DL-methionine (0.5 to 1 g/kg of body weight/day) developed severe hemolytic anemia and excessive oxidation of hemoglobin leading to a marked increase of methemoglobin concentration and Heinz-body formation [115]. Treatment is supportive, including emetics, activated charcoal, saline cathartic, and fluids containing bicarbonate [1].

(2-Methyl-4-chloro) Phenoxyacetic Acid
Ten hours following ingestion of an accidentally spilled herbicide that contained an octanoic acid ester of bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) and an isooctyl ester of (2-methyl-4-chloro) phenoxyacetic acid (MCPA), an 8 year old Golden Retriever showed signs of vomiting, abdominal pain on palpation, ataxia, anorexia, and generalized weakness [116]. Appendicular muscles were firm on palpation and persistent muscle contraction (myotonia > 1 minute duration) was found on muscle percussion, using a reflex hammer. Electrical activity indicative of myotonia was identified on EMG evaluation. With supportive treatment, the dog eventually recovered from suspected MCPA toxicosis.

Metoclopramide
Metoclopramide, a derivative of para-aminobenzoic acid, has GI stimulatory and antiemetic properties, and has been employed clinically for gastric stasis disorders, gastroesophageal reflux, vomiting, nausea, and to allow intubation of the small intestine [117]. In the CNS, metoclopramide antagonizes dopamine at receptor sites and also sensitizes tissues to the effects of acetylcholine. Neurotoxicity may occur at therapeutic levels with dogs and cats showing signs of movement disorders such as slow to rapid twisting movements of the face, neck, trunk or limbs, as well as CNS depression, nervousness, restlessness, or frenzied behavior (especially in cats) [1]. Signs usually resolve within a few days after terminating metoclopramide medication. Diphenhydramine (2 - 4 mg/kg PO, IM, or IV, tid) may reduce the movement disorders. Most of the sign dissapear in 2 - 3 days after stopping medication [10].

09-06-2006, 06:18 AM	#7
yorkiegirl2 YT 2000 Club Member Join Date: Apr 2005 Location: Missouri Posts: 2,394	page 7 Mercury Poisoning Dogs and cats are susceptible to mercury poisoning [39,103-105] a condition that has been termed Minamata disease (methyl mercury poisoning) in people. Elemental mercury is transported in blood plasma, proteins and hemoglobin, and may be incorporated rapidly into the brain [106]. While rarely seen in clinical practice, methylmercury (MM) poisoning or methylmercurialism usually occurs after consumption of contaminated fish, especially in cats [107-109] although it has also been reported in dogs [110]. Neurologic signs in dogs and cats following oral exposure have included abnormal symmetrical use of pelvic limbs, hypermetria, ataxia, paresis, abducted pelvic limbs, loss of postural reactions, proprioceptive impairment, blindness, opisthotonus, grand mal convulsions and terminal recumbency [111]. Serum biochemical findings were limited to hypercholesterolemia in dogs. Significant species difference in susceptibility to MM-induced neuronal lesions was the relative resistance of the feline spinal cord, canine cerebellar cortex and canine peripheral nervous system. Subacute exposure produced marked cerebral cortical involvement in dogs and cats, marked cerebellar cortical lesions, marked CNS perivascular inflammatory cell cuffing in cats, marked leptomeningitis in dogs and moderate lesions in the brain stem and cerebellar roof nuclei in both species. Chronic exposure of a dog to 120.4 mg Hg/kg/day for 55 weeks produced a marked loss of neurons and reactive astrocytosis in the cerebral cortex in the absence of clinical signs of toxicity. Twice weekly exposure to 0.64 mg Hg/kg as MM for 6 to 9 weeks in 5 dogs produced milder clinical signs, hypercholesterolemia, lipoproteinemia, and hydrocephalus. Neuronal loss and gliosis were most severe in the cerebral cortex with minimal involvement of the brain stem. Cerebellar lesions observed in cats include focal atrophy of the granular layer, focal spongiosus of the molecular layer and degeneration and loss of Purkinje cells in the cerebellum [112]. Demyelination in the fiber tracts of the dorsal funiculus, mainly the fasciculus cuneatus and in the lateral and ventral corticospinal tracts were also noted [112]. Terminal blood MM levels were in excess of 18 mg/ml, while brain methylmercury levels ranged from 21.0 to 28.4 mg/g. The liver and kidney contained the highest total levels of mercury of 50 to 80 mg/g, of which 23 to 37% was inorganic [112]. Increased levels of mercury in the brain does not necessarily result in behavior abnormalities or pathology [113]. In acute exposure to ingested mercury salts, oral administration of milk and eggs to bind mercury to protein has been recommended [11]. Metaldehyde Metaldehyde toxicosis usually follows ingestion of metaldehyde-based molluscicides [2]. The incidence of toxicosis is more common in coastal and low-lying areas. Metaldehyde is degraded to various aldehydes in the stomach which may give a formaldehyde odor to the contents [114]. Signs include tachycardia, salivation, tremors, vomiting, hyperesthesia, nystagmus (especially in cats), ataxia, opisthotonus and seizures, hyperthermia, diarrhea, and depression. Death from respiratory failure may follow from 4 to 24 hours after ingestion. Delayed deaths may follow liver failure (after 3 to 4 days). Stomach contents should be submitted in suspected poisonings. Treatment includes activated charcoal, anticonvulsants, and fluid therapy with sodium lactate to correct the severe acidosis that develops in poisoned animals [11]. Methionine Methionine is an essential amino acid and nutrient, a lipotrope, and a urine acidifier [65]. It has been used as a nutritional supplement in food animals. Accidental ingestion may lead to neurotoxicity and metabolic acidosis. The toxicity of methionine is partially related to its metabolism to ammonia and to increased production of mercaptan-like compounds. Toxicity is especially apparent in dogs with pre-existing liver disease. Signs include excessive salivation and vomiting, ataxia, depression, lethargy, circling, head pressing, aimless pacing, aggression, somnolence, blindness, seizures, stupor and coma [1]. In experimental studies, cats given DL-methionine (0.5 to 1 g/kg of body weight/day) developed severe hemolytic anemia and excessive oxidation of hemoglobin leading to a marked increase of methemoglobin concentration and Heinz-body formation [115]. Treatment is supportive, including emetics, activated charcoal, saline cathartic, and fluids containing bicarbonate [1]. (2-Methyl-4-chloro) Phenoxyacetic Acid Ten hours following ingestion of an accidentally spilled herbicide that contained an octanoic acid ester of bromoxynil (3,5-dibromo-4-hydroxybenzonitrile) and an isooctyl ester of (2-methyl-4-chloro) phenoxyacetic acid (MCPA), an 8 year old Golden Retriever showed signs of vomiting, abdominal pain on palpation, ataxia, anorexia, and generalized weakness [116]. Appendicular muscles were firm on palpation and persistent muscle contraction (myotonia > 1 minute duration) was found on muscle percussion, using a reflex hammer. Electrical activity indicative of myotonia was identified on EMG evaluation. With supportive treatment, the dog eventually recovered from suspected MCPA toxicosis. Metoclopramide Metoclopramide, a derivative of para-aminobenzoic acid, has GI stimulatory and antiemetic properties, and has been employed clinically for gastric stasis disorders, gastroesophageal reflux, vomiting, nausea, and to allow intubation of the small intestine [117]. In the CNS, metoclopramide antagonizes dopamine at receptor sites and also sensitizes tissues to the effects of acetylcholine. Neurotoxicity may occur at therapeutic levels with dogs and cats showing signs of movement disorders such as slow to rapid twisting movements of the face, neck, trunk or limbs, as well as CNS depression, nervousness, restlessness, or frenzied behavior (especially in cats) [1]. Signs usually resolve within a few days after terminating metoclopramide medication. Diphenhydramine (2 - 4 mg/kg PO, IM, or IV, tid) may reduce the movement disorders. Most of the sign dissapear in 2 - 3 days after stopping medication [10].