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Other DiseasesLast updated on 05/11/02 ToxicologySalt poisoningSodium chloride toxicity (although it can be caused by any sodium salt) or water deprivation syndrome occurs most often in swine and poultry, although almost any species can be affected. The typical history is of animals on a high-salt diet (2-13% of the ration) that are deprived of water. Hypernatremia causes the brain to shrink. Eventually the plasma sodium returns to normal (because they get water, or sodium is eliminated by the kidneys), the blood becomes hypotonic relative to the brain, and osmotic cerebral edema occurs because the equilibration of NaCl between plasma and the extracellular space in the CNS takes 36-48 hours.{4105} OrganophosphatesOrganophosphorus nerve agents, pesticides, fungicides, herbicides and rodenticides bind to acetylcholinesterase, causing acute buildup up of the neurotransmitter acetylcholine (ACh). Signs include miosis, hypersecretion, muscular fasciculations, tremors, seizures, convulsions and death in NHPs and small animals such as dogs and cats. In food animals, CNS depression is more common than hyperactivity{4105}. The immediate cause of death is respiratory failure with bronchoconstriction, increased secretions, and muscle paralysis.{4105} Treatment currently includes atropine, 2-PAM (pralidoxime chloride, which reactivates acetylcholinesterase), and diazepam to control seizures. Some seizures, however, are refractory to anticholinergic treatment.{4084} Research indicates that the damage induced by the nerve agent soman exceeds the time right after injection, indicating that other mechanisms of ongoing toxicity may be involved. In particular, macaques given soman show lesions in the hippocampus and amygdala, myocardial degeneration and necrosis, and myofiber degeneration in some skeletal muscles. Hypoxia may be one cause. Another may be that non-cholinergic neurotransmitters such as glutamate may be recruited and are directly neurotoxic. The pathophysiology of the heart and skeletal muscle lesions is unclear.{4084} A different presentation, delayed neurotoxicity, is caused by other groups of organophosphates (those found in lubricants, hydraulic fluid, plasticizers and flame retardants). Young animals are more resistant because they can adapt better. Species that are susceptible include cats, cattle, sheep, goats, water buffalo, chickens, pheasants, and mallard ducks. Rats, mice, hamsters, gerbils, guinea pigs, rabbits, dogs and some NHPs are less sensitive. While there are no gross lesions, microscopically there is distal axonopathy of sensory and motor neurons. The nerves, particularly the larger ones, die back from the periphery to the cell body. The responsible compounds apparently interfere with a target enzyme called neuropathy target esterase.{4105} Toxic plants (Astragalus, Oxytropis, and Swainsona) {4105}Astragalus is the largest genus of legumes in North America, with at least 300 species. They cause three different types of toxicity: nitro-containing, selenium-accumulating, or locoweed type. Locoweeds are considered to be Astragalus, Oxytropis, and in Australia, Swainsona. The toxic principle, swainsonine, inhibits lysosomal a-mannosidase and thus causes a syndrome similar to genetically-acquired a-mannosidosis. Degenerative diseasesNeurodegenerative diseasesThe cells of the CNS include neurons, oligodendroglia, astrocytes, microglia, and blood vessels. These cells taken together are called the neuropil, which stains as an eosinophilic meshwork with H&E. The cells differ in their susceptibility to different kinds of insult. Neurons are the most sensitive to ischemia. Glial cells such as astrocytes and microglia respond to injury by increasing in size and/or number.{4105} Neuron cell bodies vary considerably in size and shape. Nissl substance is composed of arrays of endoplasmic reticulum and polysomes responsible for important activities such as production of cytoskeletal components and regeneration of damaged nerves. When damaged, neurons take on a variety of appearances depending on the cause of the damage:
Astrocytes have several functions:
Oligodendroglia are found in both white and gray matter of the CNS. In white matter, they form and maintain myelin sheaths. When they degenerate, which can be caused by ischemia, viral infection or immune processes, the myelin sheaths undergo primary demyelination. Microglia may be monocytes that enter the CNS during embryogenesis and become resident at perineuronal, perivascular and interfascicular sites mostly in gray matter. They have a role in development, remodeling, homeostasis of neurotransmitters and hormones, lipid turnover, inflammation, repair, and immune functions (antigen processing and macrophage activation). When tissue necrosis occurs, they phagocytize debris and become gitter cells.{4105} Disorders of myelinationThe Bouncer Long Evans ratThis is caused by a spontaneous autosomal recessive mutation in Long Evans rats. Rats develop whole body tremor which progresses to severe ataxia and seizures induced by such minor stimuli as activity in the room. Lifespan is fairly long, >45 weeks, although some die acutely with spinal cord necrosis due to vertebral fractures caused by the seizuring spinal muscles. There is severe global dysmyelination, with thin, uncompacted myelin sheaths in the spinal cord and optic nerve. The myelin sheaths in the adjacent peripheral nerves are normal. The defect is probably an inability of the oligodendrocytes to form myelin sheaths normally, possibly involving the myelin basic protein gene. The rat is similar to the Long Evans shaker (les) rat, but les rats never have normal weight gain and they develop histopathologic signs later than these LE-bo rats.{4104} Nutritional diseasesZinc deficiencyGoats can become zinc-deficient if fed too much alfalfa, which is high in calcium. Signs of zinc deficiency include symmetrical alopecia, hyperkeratosis, weight loss, anorexia, matted and rough hair, sensitivity in the coronary band, flaky skin, and hair that is easily epilated. In non-ruminants, cereal grains with high phytate or phytic acid (inositol hexaphosphate), are known to chelate zinc or calcium to block absorption. Normal serum levels of zinc in the goat are 0.65-2.5mg/dl.{4295} |
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©1999, Janet Becker Rodgers, DVM, MS All rights reserved. Comments? Send an email to rodgers@uky.edu |