Gary D. Osweiler

Concentrations of fumonisin B1 in feeds associated with animal health problems

Ninety-eight samples of feeds associated with 44 cases of equine leukoencephalomalacia (ELEM) and 83 samples of feed associated with 42 cases of a porcine pulmonary edema syndrome (PPE) were analyzed for fumonisin B1 (FB1). For comparison purposes, 51 feed samples not associated with PPE or ELEM were also analyzed. Feed associated with ELEM contained FB1 ranging from less than 1 μg/g to 126 μg/g with 75% of the cases having at least 1 sample above 10 μg/g. Feeds associated with PPE ranged from less than 1 μg/g to 330 μg/g with 71% of the cases having at least 1 sample greater than 10 μg/g. Quantitation was by high performance liquid chromatography (HPLC)/fluorescence using the fluorescamine derivative with confirmation by thin layer chromatography (TLC) and/or gas chromatography/mass spectroscopy (GC/MS).

Fumonisin B1 Levels Associated with an Epizootic of Equine Leukoencephalomalacia

During the fall of 1989, an episode of equine leukoencephalomalacia involved 18 of 66 purebred Arabian horses at a breeding/training stable in Arizona. Of the 18 horses affected, the condition was fatal in 14. These horses, as well as 48 unaffected horses, had been fed a diet containing a substantial amount of white corn screenings. Gross pathologic findings included liquefactive necrosis in parts of the cerebral white matter and hemorrhagic foci of various sizes in the brain stem. Histopathologic findings included rarefied white matter with pyknotic nuclei and eosinophilic cytoplasm. Thin-layer chromatography, high-performance liquid chromatography, and gas chromatography/mass spectroscopy were utilized to identify and quantitate fumonisin B1 in 3 samples of corn from the farm. Concentrations of fumonisin B1 range from 37 to 122 ppm. Fumonisin B1 was also detected. Using information on diet, animal weights, and feeding practices, estimates of total fumonisin B1 dosage were determined. This is the first definitive report on equine leukoencephalomalacia and associated fumonisin B1 concentrations.

Characterization of an Epizootic of Pulmonary Edema in Swine Associated with Fumonisin in Corn Screenings

In 1989, corn screenings were associated with acute interstitial pulmonary edema, hydrothorax, and death in swine. Attack rate was 5–50%, case fatality rate was 50–90%, and clinical course was 1–2 days. Screenings from farms with pigs affected with pulmonary edema contained 20–330 μg fumonisin B1 per gram. Screenings containing 92 μg fumonisin B1 per gram fed to weanling pigs caused pulmonary edema and death. Sterilized corn inoculated with Fusarium moniliforme and diluted 1:1 with clean corn contained fumonisin B, (17 μg/g) and caused acute pulmonary edema when fed for 5 days. Survivors developed subacute hepatotoxicosis with individual hepatocellular necrosis, hepatomegalocytosis, and increased numbers of mitotic figures. Similar liver lesions occurred in pigs given fumonisin B1 intravenously at 0.8 mg/kg body weight for 14 days.

Experimental Equine Leukoencephalomalacia, Toxic Hepatosis, and Encephalopathy Caused by Corn Naturally Contaminated with Fumonisins

A study to evaluate the effects of dietary fumonisin B, was conducted using 6 ponies (4 test and 2 control). A ration naturally contaminated with fumonisin B, was fed in 3 phases: 1) 44 ppm fumonisin B1, 2) less than 1 ppm fumonisin B1, and 3) 88 ppm fumonisin B,. All ponies were monitored daily, weighed weekly, and limit fed at a rate of 0.8% body weight plus hay. Feed intake was measured daily, and a serum chemistry panel was completed once or twice weekly. Four to 7 days after initiation of the trial (Phase 1), all 4 test ponies had decreased feed consumption, and selected serum chemistry parameters were markedly elevated. On day 9, 1 pony died acutely with mild encephalopathy and hepatic necrosis. Another pony, euthanized on day 45, also had mild encephalopathy and hepatic necrosis. The remaining 2 test ponies continued the 44 ppm fumonisin B, diet for 98 days. Phase 2 consisted of a diet with < 1 ppm fumonisin B, for 120 days. During this phase, the serum chemistry values of the 2 ponies returned to normal. Following Phase 2, the 2 ponies were fed a diet containing 88 ppm fumonisin B1. After 75 days, 1 animal died of equine leukoencephalomalacia with mild hepatic necrosis. On day 78, the remaining pony was euthanized after showing distress; it also had leukoencephalomalacia and hepatic lesions.

Mycotoxins: Contemporary Issues of Food Animal Health and Productivity

Modern agriculture and production animal medicine require attention to high-quality feeds that are free from mycotoxin contamination that can cause economically important decreases in productivity. Maintaining current information about effects of mycotoxins on feed intake and growth, reproductive efficiency, and possible immunosuppression aid in effective consultation with livestock producers. Investigation and determination of potential production losses related to mycotoxins should use historical, clinical, laboratory, and experimental information to objectively evaluate whether mycotoxin contamination is clinically relevant. The practicing veterinarian or veterinary consultant can provide valuable clinical and interpretive assistance to producers who may have a real or potential mycotoxin contamination. Thorough diagnostic evaluation of animals, appropriate testing of feeds and forages, and rational consideration of differential diagnoses help to put mycotoxins in the proper perspective as a production-related management problem.

Cocklebur Toxicosis in Cattle Associated with the Consumption of Mature Xanthium Strumarium

Cockleburs (Xanthium spp.) are herbaceous annuals with worldwide distribution. Toxicoses are usually associated with the consumption of the seedlings in the cotyledon stage, which contain a high concentration of the toxic principle, carboxyatractyloside. The seeds are also known to contain the toxin, but it has long been assumed that the spiny capsule would deter their consumption. Six of 70 yearling calves died while being fed round bale hay composed predominately of foxtail and mature cocklebur plants with burs. Clinical signs ranged from acute death to hyperexcitability, blindness, tense musculature, and spastic gaits with heads held high and ears erect. Some symptomatic calves would stumble, fall to lateral recumbency, convulse, and later recover. Overall, the herd was very uneasy. Prominent gross lesions were ascites and a firm, pale liver with a mottled hemorrhagic pattern on cut surface. The rumen contained numerous intact burs and well-ruminated grass. Histological examination of the liver revealed marked centrolobular degeneration and necrosis with associated hemorrhage and congestion. Brain lesions were present. Plant and tissue samples were analyzed for carboxyatractyloside with various results. Samples of rumen contents, urine, and burs contained 100–200 ppm, 0.1–0.05 ppm, and 0.1 ppm, respectively. Based on the history, clinical signs, pathological lesions, and chemical analyses, cocklebur toxicosis associated with consumption of mature Xanthium strumarium in hay was confirmed.

Hypericin-Induced Phototoxicity in Cultured Fibroblasts and Swine Erythrocytes

Hypericin is a naturally occurring photosensitizer, whose presence in plants has been responsible for cutaneous phototoxicity in grazing animals. The photosensitizing properties of this agent have recently been exploited in models for anti‐tumor and anti‐viral activity. The cytotoxicity of hypericin and light was assessed in 3T3 mouse fibroblasts using the MTT [3‐(4, 5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyl tetrazolium bromide)] assay and the lactate dehydrogenase (LDH) leakage assay. Membrane damage was assessed in swine erythrocytes using hemolysis, potassium (K+) leakage and formation of lipid hydroperoxides. Concentration‐ and light‐dependent decreases in fibroblast viability were seen starting at hypericin concentrations of 1.25 μM and light power flux levels of 24 J/cm2 using a visible light source and at 0.417 μM hypericin and a similar light dose using a solar simulator, No LDH leakage was observed at hypericin concentrations up to 30 μM and visible light up to 144 J/cm2. Light‐and/or concentration‐dependent increases in hemolysis, K+ leakage and formation of lipid hydroperoxides in red blood cell (RBC) membranes were observed, but at concentrations and light doses much greater than those required to induce cytotoxicity in fibroblasts. Lipid peroxidation and hemolysis occurred at 15 μM hypericin and 24 J/cm2 (visible light source). Potassium ion leakage occurred at concentrations and light levels as low as 5 μM and 12 J/cm2 or 15 μM and 4.8 J/cm2 (visible light source) but was still a less sensitive indicator than fibroblast cytotoxicity. Evidence for both type I and type II reactions was shown in RBC membranes by TLC analysis of cholesterol products. In the absence of light, hypericin appears to be relatively nontoxic in the models tested.

Epidemiology of Lead Poisoning in Cattle– A Five-Year Study in Iowa

AbstractLead poisoning has been increasingly recognized as a significant and major cause of bovine poisoning in Iowa during recent years [3, 4]. Data from the Iowa Veterinary Diagnostic Laboratory for the years 1965 through 1971 indicate an increasing number of lead poisoning cases in cattle, with 1970 as the peak year. From January, 1967, through June 30, 1971, 80 episodes of bovine lead poisoning have been confirmed by the Veterinary Diagnostic Laboratory. Of this number, 28 were recognized in 1970 alone. Lead poisoning is the single most common toxicosis in cattle in Iowa. In order to further delineate the incidence, clinical severity, sources, seasonal occurrence, and chemical results of affected and non-affected animals, this study was undertaken.

Arsenic Concentrations in Tissues and Body Fluids of Dogs on Chronic Low-Level Dietary Sodium Arsenite

Twenty-four female Beagle dogs, 7–8 months old, were assigned to 4 groups. Control, low-dosage, medium-dosage, and high-dosage groups were offered 0, 1, 2, and 4 mg of sodium arsenite per kilogram of body weight per day (mg/kg/day), respectively, in their feed (equivalent to 0.0, 33.4, 66.7, and 133.4 μg/g in feed). On day 59, the dosage was doubled for the rest of the experiment, which ended on day 183. In general, arsenic concentrations in tissues and body fluids reflected arsenic levels in feed. Arsenic caused a dose-related decrease in food intake. Statistically significant differences in blood, liver, and kidney arsenic were detected, in most cases, between the 2 higher dosage groups and controls. The greatest differences in arsenic concentrations between groups were present in urine and hair. Results indicate that urine and hair would be the most useful specimens for chemical analysis when attempting to confirm low-level dietary inorganic arsenic exposure or poisoning.

Relationship of Mycotoxins to Swine Reproductive Failure

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