Abstract. During the fall of 1989 and winter of 1990, numerous reports of equine leukoencephalomalacia (ELEM) occurred from many regions of the United States. Typically, horses were consuming feed partially or entirely composed of corn and/or corn screenings. From October 1989 through May 1990, samples from 55 confirmed or suspected ELEM cases were received at the National Veterinary Services Laboratories, Ames, Iowa, for fumonisin B 1 analysis. Samples from 9 cases in 1984-1985 were also obtained. Fumonisin B 1 , a mycotoxin produced by Fusarium moniliforme, causes ELEM, but little is known of naturally occurring toxic or safe levels in feeds. To determine what levels of fumonisin B 1 in feeds are associated with ELEM, 45 selected cases were studied. The fumonisin B 1 concentrations ranged from <1 ppm to 126 ppm, with the majority of the samples above 10 ppm. All types of feeds were included: corn, screenings, sweet feeds, and commercially pelleted rations. The length of exposure varied from 7 to >35 days. Horse feed samples not associated with ELEM were also collected and analyzed. None of the nonproblem feed samples contained fumonisin B, levels >8 ppm.Equine leukoencephalomalacia (ELEM) is a neuro-ported 1,2,9 The length of exposure to the contaminated l toxic disease of equids that has been reported in China, feed in field cases has been quite variable, the morEgypt, New Caledonia, the United States, and South bidity rarely exceeds 50%, and the mortality is usually Africa . [2][3][4][5]8,14 The disease has been associated with Fu-high 2 , 1 5 sarium moniliforme -infected corn and has been ex-The diagnosis of ELEM is based exclusively on gross perimentally reproduced with F. moniliforme culture and/or histopathologic findings. With the implication material. 1,14 Recently, workers in South Africa char-of fumonisins and the evolution of analytical methods, acterized the fumonisin mycotoxins from cultures of criteria establishing the cause of the syndrome are im-F. moniliforme and induced ELEM in a horse by in-proving; feed levels of FB 1 appear to be directly related travenous injection and oral dosing of pure fumonisin to the occurrence of the disease. B 1 (FB 1 ).6,7 Recently, we reported on an ELEM field During the fall of 1989 and winter of 1990, the Naoutbreak and identified FB 1 in the feed. 16 tional Veterinary Services Laboratories (NVSL) reTypically, ELEM is characterized by sudden onset ceived numerous reports of ELEM from many regions of 1 or more of the following: frenzy, aimless circling, of the United States, and suspect feed samples were head pressing, paresis, ataxia, blindness, depression, collected and submitted to the NVSL for FB 1 deterand hyperexcitability. The primary pathologic feature mination. To gain insight into what levels of FB 1 occur of ELEM is liquefactive necrosis of the white matter in feeds associated with ELEM, selected [1989][1990] of the cerebral hemispheres. In some field and exper-cases were studied along with cases from 1984-1985 imental cases, liver involvement has als...
Dogs given a single oral dose of bromethalin at 6.25 mg/kg developed a toxic syndrome characterized by hyperexcitability, tremors, seizures, depression, and death within 15-63 hours after bromethalin administration. Gross lesions included mild cerebral edema (2/5) and mild pulmonary congestion (2/5). Histologic lesions included diffuse white matter spongiosis (5/5), mild microgliosis (3/5), optic nerve vacuolization (3/5), mild thickening of Bowman's capsule (2/5), and occasional splenic megakaryocytes (2/5). Ultramicroscopic examination of midbrain stem revealed occasional swollen axons, intramyelinic vacuolization, and myelin splitting at the intraperiod line. Bromethalin was detected in kidney, liver, fat, and brain tissues, using gas chromatography with electron capture detection. Photodegradation of extracted bromethalin may limit accurate quantification of tissue residues.
Abstract. Abstract. Aldicarb toxicosis was diagnosed in 200 sheep that died suddenly. Carbamate insecticide toxicosis Aldicarb toxicosis was diagnosed in 200 sheep that died suddenly. Carbamate insecticide toxicosis was suspected based on observed clinical signs (hypersalivation, diarrhea, urination, paddling, seizures, miosis, was suspected based on observed clinical signs (hypersalivation, diarrhea, urination, paddling, seizures, miosis, and deaths occurring within 1 hour). Tissue samples were submitted from 4 Columbian ewes for pathologic and deaths occurring within 1 hour). Tissue samples were submitted from 4 Columbian ewes for pathologic and analytical evaluation. Severe diffuse pulmonary edema was observed on gross and histologic examination. and analytical evaluation. Severe diffuse pulmonary edema was observed on gross and histologic examination. Inhibition of cholinesterase activity in retina (21.2-68.1% of normal activity, n = 3), brain (40.6-45.6% of normal activity, n = 3), and whole blood (27% of normal activity, n = 3), and whole blood (27% of normal activity, n = 1) supported a diagnosis of carbamate 1) supported a diagnosis of carbamate toxicosis. Reversal of brain and whole blood cholinesterase activities (reactivation factor > 1.4) following an toxicosis. Reversal of brain and whole blood cholinesterase activities (reactivation factor > 1.4) following an in vitro 1 hour incubation at 37 C was also consistent with carbamate poisoning. Aldicarb toxicosis was confirmed following its detection in rumen contents at 1.5, 5.5, and 334 ppm using both high-pressure liquid chromatography with UV detection and gas chromatography with nitrogen/phosphorus detection. raphy with UV detection and gas chromatography with nitrogen/phosphorus detection.Aldicarb (2-methyl-2[methylthio]propionaldehyde O-[methylcarbamoyl]-oxime) (Temik®) is a highly toxic carbamate insecticide. Carbamate insecticides are potent reversible inhibitors of acetylcholinesterase activity. A toxic dose of aldicarb produces severe cholinergic signs including salivation, urination, defecation, ataxia, dyspnea, seizures, and death. The onset of clinical signs is rapid, and the severity is dependent on the dose, route of exposure, and species involved.
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