Page 1155 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition
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Ionophores Chapter | 78  1087




  VetBooks.ir  myopathic conditions should be considered first. In cattle,  interlobular emphysema or pneumonia or both rather than
                                                                edema. The incoordination, stiff wobbly gait, and loss of
             these would include (1) ionophore toxicoses, (2) vitamin
                                                                visual reflexes may lead one to suspect polioencephaloma-
             E and selenium deficiencies, (3) poisonous plant inges-
             tion, e.g., senna, coyotillo, white snakeroot, vetch, and  lacia and thromboembolic meningoencephalitis. But in
             (4) the common, yet puzzling, sudden death syndrome  these conditions histologic lesions present in the brain are
             with myocardial necrosis. Ionophore toxicosis usually  confirmatory. Unequivocal central nervous system lesions
             involves an accompanying history of feed supplementa-  have not been found in cases of monensin toxicity in any
             tion or feed change and usually involves many animals.  species. However, lesions in the spinal cord and peripheral
             Clinical signs are anorexia, diarrhea, lethargy, ataxia, and  nerves occurred with lasalocid toxicosis in chickens
             the suggestion of damage to striated muscles. Vitamin E  (Shlosberg et al., 1985). Peripheral neuropathic changes
             and selenium deficiency occurs sporadically and produces  have also been reported in cats exposed to salinomycin-
             prominent degeneration and necrosis with calcification of  contaminated feed (Van der Linde-Sipman et al., 1999)and
             cardiac and skeletal muscles. Plant poisonings are usually  in dogs given narasin (Novilla et al., 1994). Salt poisoning
             localized to areas where the toxic plants are indigenous.  will cause nervous signs, paralysis, and diarrhea, but knowl-
             For instance, coffee senna (Cassia occidentalis) poisoning  edge that insufficient amounts of water were available to
             occurs in the southeastern United States. It may cause  the animals will also point to this problem. Eosinophilic
             anorexia, diarrhea, and the production of dark urine but  meningoencephalitis is pathognomonic for salt poisoning in
             generally causes more pronounced lesions in skeletal  pigs, but this lesion does not occur in other species.
             muscles than in the heart. The coyotillo plant (Karwinskia  Laboratory procedures used to confirm a diagnosis include
             huntholdtiana)  in  southwest  Texas  and  Mexico  assays of serum, cerebrospinal fluid and brain tissue for
             produces limberleg in sheep and goats characterized by  sodium concentrations (Buck et al., 1976). In cattle, urea
             progressive weakness of the legs, muscular incoordina-  toxicosis must be considered when sudden collapse, bloat,
             tion, recumbency, respiratory distress, and death. Lesions  violent convulsions, terminal tetanic spasms, and high death
             are observed both in cardiac and skeletal muscles as well  losses occur within 10 min to 4 h from exposure to newly
             as peripheral nerves and the liver. White snakeroot  formulated feed. Deaths occurring earlier than 72 h have
             (Eupatorium rugosum), a plant indigenous to much of  not been reported in cattle gavaged with high doses of mon-
             eastern Canada and the United States, causes “trembles”  ensin (Potter et al., 1984).
             in goats, sheep, cattle, horses, and swine. Cardiac and  In poultry, differential diagnoses should include nutri-
             skeletal muscle lesions may be present in animals that  tional (focal) myopathy, coffee senna toxicity, botulism,
             ingested this plant. However, with trembles there is con-  sodium chloride (salt) toxicity, mycotoxicosis by cyclo-
             stipation, blood in feces, an odor of acetone in the breath  piazonic acid and other myopathic mycotoxins, round
             and severe fatty degeneration in the liver and kidney that  heart disease and, in the turkey, the knockdown (downer)
             are not seen in ionophore toxicities. Hairy vetch (Vicia  syndrome. Although no striated muscle lesions are pro-
             villosa) also produces myocardial necrosis but, unlike  duced in botulism and sodium chloride toxicity, clinical
             monensin toxicosis, it produces dermatitis, conjunctivitis  signs of limber neck and lesions of “water belly” may be
             and abortion as well as lesions in the kidneys, adrenal  confused with ionophore toxicoses. On the other hand,
             glands, lymph nodes, and thyroid gland. The syndrome of  birds affected with salt poisoning may have enlarged
             sudden death with myocardial necrosis in cattle, espe-  hearts or have enlarged pale kidneys from urate nephrosis.
             cially calves, is common but sporadic in occurrence and  Monensin per se does not produce “barebacks” in broiler
             is associated with lesions in cardiac but not skeletal mus-  chickens, and downers among replacement birds may be
             cle (Bradley et al., 1981). Hence, clinical history and  suffering from viral arthritis. Therefore, this common reo-
             detailed pathologic studies will help distinguish among  virus infection must be excluded as a cause of the prob-
             ionophore toxicosis, acute infectious diseases, deficien-  lem in chicken flocks. In commercial turkeys reared in
             cies, and other intoxications.                     confinement, focal myopathy has been attributed to defi-
                From a clinical standpoint, respiratory diseases, particu-  ciencies in vitamin E or selenium associated with rapid
             larly infectious bovine rhinotracheitis and the shipping fever  growth (Wilson et al., 1990). Nutritional myopathy may
             complex, are initially considered in the differential diagno-  mimic skeletal muscle lesions induced by ionophore toxi-
             sis for cattle because of the respiratory difficulties that occur  coses;  but  unlike  those  of  nutritional  myopathy,
             with ionophore toxicosis. At necropsy, however, pneumonic  ionophore-induced lesions are monophasic and polyfocal
             lesions are consistent with these diseases. Animals with  with little or no mineralization. Muscle lesions also occur
             acute bovine pulmonary edema and emphysema or fog  in deep pectoral myopathy, coffee senna toxicity and toxi-
             fever, nitrogen dioxide intoxication, or rape, turnip, or kale  coses from the mold toxins, cyclopiazonic acid and moni-
             poisoning also exhibit respiratory difficulties. But in these  liformin. Their clinical presentation and presence of other
             conditions gross lesions will include severe interstitial and  lesions will help distinguish these conditions.
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