Specimens from 10 cases of second-generation anticoagulant rodenticide poisoning in dogs and cats were submitted to the Texas Veterinary Medical Diagnostic Laboratory during 1986 and 1987. The clinical signs most frequently observed were lethargy, dyspnea, and ventral hematomas; common necropsy findings included hemoperitoneum, hemothorax, and pulmonary hemorrhage. In the instances when histopathological examination of the tissue was done, it supported a diagnosis of coagulopathy. The presence of anticoagulants in serum or liver was confirmed by high pressure liquid chromatography, gas chromatography/mass spectrometry, or a combination of the two. Five cases of brodifacoum poisoning, 2 of bromadiolone, and 3 of diphacinone toxicity were verified. Concentrations of these rodenticides ranged from approximately 0.001 to 12 ppm.

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...

Tremetone, the major toxic component in white snakeroot (Eupatorium rugosum Houtt) extracts, was isolated following an in vitro bioactivity assay. Microsomal activation was required to produce a product toxic to murine melanoma (B16F1) cells as well as five other mammalian cell cultures. The metabolic activation product(s) of tremetone is suspected to be responsible for the toxic activity of the plant. Tremetone is also smoothly converted to dehydrotremetone in the plant and cell free homogenates, and readily decomposes to dehydrotremetone in extracts. Dehydrotremetone is not toxic even after microsomal activation. The efficient conversion of tremetone to dehydrotremetone may explain why white snakeroot plant material and extracts have varied activities, and why a previous claim that tremetone was responsible for the toxic activity of white snakeroot was withdrawn. Rayless goldenrod extracts show the same toxic activity as white snakeroot and the toxic activity of rayless goldenrod is most likely due to tremetone.

Brunfelsia calcyina var. floribunda is an ornamental evergreen shrub found in the United States. A diagnosis of the fatal intoxication of a canine due to consumption of plant material (primarily berries) was made. The significant features of the clinical constellation were similar to those seen with substances interfering with the neurotransmission process, such as lathyrus or strychnine. Necropsy findings on the canine were unrevealing. Toxicologic studies performed on mice and rats with ground shrub material demonstrated that all parts of this plant are toxic, but unequally so. All plant preparations produced signs similar to those of a spinal convulsant. There were no distinguishing gross pathologic or histopathologic findings associated with the toxicoses induced in the laboratory animals with preparations from this plant. The toxic principles from this shrub are water soluble and very stable. The ability of aqueous extracts stored at 4 C to produce the clinical syndrome and subsequent lethality remained unchanged over a period of 4 months. Exposures are not always fatal. They most often occur in the canine and there is a significant hazard for small children.

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