Abstract. 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 B 1 per gram. Screenings containing 92 µg fumonisin B 1 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 B 1 intravenously at 0.8 mg/kg body weight for 14 days.Previous experimental work established the chemical structure, toxic potential, and probable carcinogenic nature of Fusarium moniliforme and the associated toxin fumonisin B 1 (FB 1 ) in several animal speciesl-4,6,7,11 Previous experimental feeding of F. moniliforme culture material to swine resulted in pulmonary edema, 5 and pulmonary edema in swine was recently reported from natural exposure to the fungus and the associated toxin fumonisin B 1 via corn screenings.3 However, except for equine leukoencephalomalacia (ELEM), large outbreaks of toxicosis associated with F. moniliforme in other species have not been reported. This report describes fumonisin associated toxicosis in swine herds in Iowa and Illinois.During October and November 1989, the Iowa State University Veterinary Diagnostic Laboratory received numerous reports of an acute fatal porcine pulmonary edema (PPE) syndrome. Each instance was associated with feeding corn screenings from the 1989 harvest, and most deaths occurred in mature animals. Reports were primarily from the southeast quadrant of Iowa and the northwest corner of Illinois. Clinical course described by referring veterinarians included acute onset of dyspnea, weakness, cyanosis, and death. Abortions were observed from 1 to 4 days after the onset of acute signs. Pathologic findings included concurrent pulmonary edema and hydrothorax but no lesions of cardiac hemorrhage or necrosis. Deaths occurred with- Received for publication May 20, 1991. in 4-10 days after the first feeding of corn screenings. The epizootiologic, clinical, and pathologic features of 16 PPE cases in Iowa and Illinois are described. In addition, the experimental confirmation of PPE and the association of FB 1 with hepatotoxicosis is reported. Materials and methodsField investigation. Clinical and epizootiologic information for 16 PPE cases was associated with the 1989 corn crop. Clinical signs and gross lesions were observed and described, and where available, corn or feed samples were collected for fumonisin analysis and fungal culture. Nine herds were visited by veterinarians from the Iowa State University Diagnostic Laboratory, and attending veterinarians and owners provid...
Abstract. Twenty mixed-breed adult laying hens from a small farm flock in Iowa were clinically normal but had been exposed to chips of lead-based paint in their environment. These chickens were brought to the Iowa State University Veterinary Diagnostic Laboratory, Ames, Iowa, where the concentration of lead in blood, eggs (yolk, albumen, and shell), and tissues (liver, kidney, muscle, and ovary) from 5 selected chickens was determined over a period of 9 days. Blood lead levels ranged from less than 50 to 760 ppb. Lead contamination of the yolks varied from less than 20 to 400 ppb, and shells were found to contain up to 450 ppb lead. Albumen contained no detectable amount. Lead content of the egg yolks strongly correlated with blood lead levels. Deposition of lead in the shells did not correlate well with blood lead levels. Mean tissue lead accumulation was highest in kidneys (1,360 ppb), with livers ranking second (500 ppb) and ovarian tissue third (320 ppb). Muscle contained the lowest level of lead (280 ppb). Lead contamination of egg yolks and edible chicken tissues represents a potential public health hazard, especially to children repeatedly consuming eggs from contaminated family-owned flocks.
costs and benefits, ethics, Federal False Claims Act, qui tam , whistle-blowing,
In this report, we describe the natural intoxication of 2 dogs that consumed moldy dairy products found in the household garbage and the procedures used to identify and quantify the tremorgenic mycotoxins, roquefortine and penitrem A, in the remaining portions of ingested materials. Following the ingestion of mycotoxins, the dogs of our report developed muscle tremors or seizures that resembled clinical signs of strychnine poisoning. Roquefortine was the predominant mycotoxin in a moldy cream cheese wrapper that was found among scattered garbage consumed by the first dog. Penitrem A was the only mycotoxin detected in discarded moldy macaroni and cheese that was consumed by the second dog. Treatment of dogs with tremorgenic mycotoxin intoxication involves supportive care. Close monitoring is important because the development of aspiration pneumonia is common and has been reported as the cause of death. Clinical signs of intoxication gradually resolve within 24 to 48 hours.
This book addresses questions in ethical theory and practical questions about lying, deception, and information disclosure in public affairs, business and professional ethics, and personal relationships. Part I is a conceptual map for the rest of the book. It proposes an analysis of the concepts of lying and deception and related concepts such as withholding information, “keeping someone in the dark,” and “half-truths.” Part II addresses questions in ethical theory. The book examines the implications of Kant's theory, act-utilitarianism, Ross's theory, and rule-consequentialism for moral questions about lying and deception. The book argues that Kant's absolutism about lying is untenable and that his moral theory doesn't commit him to being an absolutist. It also argues that the standard debates about lying and deception between act-utilitarians and their critics are inconclusive because they rest on appeals to disputed intuitions. The book defends a version of the golden rule and a theory of moral reasoning. The book's theory implies that there is a moral presumption against lying and deception that cause harm — a presumption that is at least as strong as that endorsed by act-utilitarianism. The book uses this theory to justify its claims about the issues it addresses in Part III: deception and withholding information in sales, deception in advertising, bluffing and deception in negotiations, the duty of professionals to inform their clients, lying and deception by leaders as a pretext for fighting wars (or avoiding wars), lying and deception about history (with special attention to the Holocaust), and cases of distorting the historical record by telling half truths. The book concludes with a qualified defense of the view that honesty is a virtue.
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