Surtos de fotossensibilização primária em equídeos causados por Froelichia humboldtiana / Outbreaks of primary photosensitization in equidae caused by Froelichia humboldtiana

The study was conducted in order to report outbreaks of photosensitization caused by Froelichia humboldtiana in equidae in the state of Rio Grande do Norte, Brazil. Animals from three farms and donkeys found abandoned in roads were examined. Peripheral blood samples were collected from five donkeys and two horses for analysis of serum activities of liver enzymes and concentrations of total, direct and indirect bilirubin...

O presente trabalho foi conduzido com o objetivo de relatar surtos de fotossensibilização causados por Froelichia humboldtiana em equídeos no Estado do Rio Grande do Norte, Brasil. Foram examinados animais de três propriedades rurais, além de asininos abandonados nas estradas. Procedeu-se a coleta de amostras de sangue periférico de cinco jumentos e dois equinos para análise das atividades das enzimas hepáticas e concentrações de bilirrubina total, direta e indireta...

The ocular disease of Aristodemus and Eurytus 480 BC: diagnostic considerations.

OBJECTIVE: In the historic description of Herodotus on the battle of Thermopylae at 480 BC two formerly healthy warriors suffer from "ophthalmia". The purpose of this study is to assess the possible aetiologies of this disease. DESIGN: We studied Herodotus' description in translation and offer a differential diagnosis. RESULTS: From the text we deduced that the "ophthalmia" was a condition in two physically fit males with a bilateral decreased or distorted vision, lasting longer than an hour, with an acute or subacute onset in Ancient Greece. The condition ultimately went into remission in one of the two patients, whereas the other subject deceased in combat not long after the onset of the disease, still suffering from the disease. The differential diagnosis consists of (1) anticholinergic syndrome secondary to an intoxication with the berries of the plant Atropa belladonna, (2) automutilation and (3) psychogenic loss of visual acuity. CONCLUSION: It is impossible to assess the ultimate cause of the "opthalmia" after 2500 years, but we suggest the anticholinergic syndrome by intoxication with Atropa belladonna is the most likely.

What killed Socrates? Toxicological considerations and questions.

The death of Socrates in 399 BCE, as reported by Plato in the Phaedo, is usually attributed to poisoning with common hemlock. His progressive centripetal paralysis is characteristic of that poison. Socrates is said to have had a prominent loss of sensation extending centrally from his legs, which is not a feature of hemlock poisoning, and he seems not to have had the unpleasant taste or common gastrointestinal effects of that poison. It is suggested that Plato gave a modified account of the death of Socrates for political and other reasons by describing a more "noble" death.

The biogeochemistry of selenium in Sunan grassland, Gansu, Northwest China, casts doubt on the belief that Marco Polo reported selenosis for the first time in history.

In order to clarify the historic academic problem of whether or not livestock poisoning in ancient Suzhou of Northwest China, recorded by Marco Polo in 1295, was selenosis, this study deals with the biogeochemistry of selenium in Sunan County in the Hexi Corridor, which is part of ancient Suzhou in China. It was found that quite a number of farm animals had suffered from intoxication and died as a result of grazing poisonous grasses, mostly Oxytropis DC, Stellera chamaejasme, and Achnatheru inebrians. Toxic symptoms of livestock grazing on Oxytropis DC are similar to those of selenium toxicity, for instance, hair loss and hoof lesions as described by Marco Polo. Therefore, we thought that toxic grass, probably Oxytropis DC, led to the intoxication of livestock recorded by Marco Polo. Average Se concentrations in two members of this species were 0.112 +/- 0.038 mg/kg for the root of Oxytropis glabra, 0.102 +/- 0.027 mg/kg for the stem and leaf of Oxytropis glabra, and 0.066 +/- 0.009 mg/kg for Oxytropis ochrocephala. The average soil selenium concentration was 0.205 +/- 0.127 mg/kg on grassland producing Oxytropis glabra and 0.152 +/- 0.024 mg/kg on grassland producing Oxytropis ochrocephala. The average Se concentration in other plants was 0.076 mg/kg in the root of Ephedra monosperma Mey, 0.029 mg/kg in the root of Rheum palmatum, 0.031 mg/kg in the root of Stellera chamaejasme, 0.037 mg/kg in Achnatherum inebrians, and 0.067 mg/kg in forage grass (Achnatherum splendens ohwi). Selenium concentrations in soils and plants in Sunan County are far less than the thresholds causing selenium toxicity in livestock. As a result, this study concludes that the livestock poisoning recorded by Marco Polo in 1295 might not have been selenosis.

"Poorly co-ordinated structures for public science that failed us in the past"? Applying science to agriculture: a New Zealand case study.

This paper examines the effectiveness of applied science in a case study of two aspects of livestock and human poisoning in New Zealand, from the earliest European contact in the 1770s through to the 1950s. It considers the role and value of government science first in attempting to solve a problem that continues to affect New Zealand farmers, killing according to one estimate between 10 and 15 percent of their stock annually. Second, it addresses a related problem that has a much longer history of human poisoning, but that turned out to have quite unexpected causes in New Zealand. From this analysis, the historic bases on which present-day science funding policies were "reformed" in the 1990s are questioned.

[Suicidal yew poisoning--from Caesar to today--or suicide instructions on the internet]. / Suizidale Eibenintoxikationen--von Cäsar bis heute--oder: Suizidanleitung im Internet.

Already the Celts and ancient Germanic peoples knew about the poisonousness of the yew, which played an important part in the mythology of these civilizations. For hunting, the arrows were made poisonous with yew juice, and yew leaves were used for homicide and suicide. In modern times taxine is rarely used with suicidal intent, although this method is actually recommended on the respective Websites. After a 14-year-old boy had intensively studied poisonous plants and methods of suicide on various Websites, he cut leaves from a yew tree (taxus baccata) in his parents' garden, crushed and ingested them and died soon afterwards. At the forensic autopsy pieces of the partially crushed, partially completely preserved yew leaves were found in the stomach. The histological findings were unspecific, e.g. marked general blood congestion of the internal organs and pronounced cerebral and pulmonary edema. When the tree leaves found in the stomach were viewed under the light microscope, a stoma typical of taxus was observed; chemical-toxicological investigations revealed 3,5-dimethoxyphenol in the gastric content, which is considered a marker for the ingestion of taxus.

History of USDA poisonous plant research.

Research on poisonous plants was instituted by the United States Department of Agriculture (USDA) as a result of serious livestock poisoning by plants as the pioneers moved west in the mid-to-late 1800s and early 1900s. Historical records indicate the USDA began poisonous plant research in 1894 under the direction of Mr. V. K. Chestnut, a botanist (Table 1 briefly summarizes those who have directed poisonous plant research from the inception to the present). Mr. Chestnut's responsibility (1894-1904) was primarily administrative, although he did extensive field work in Washington and Montana. Temporary field stations were set up to study specific poisonous plant problems. These included field stations at Hugo and Woodland Park, Colorado, and Imperial, Nebraska (1905-1909), to study locoweed; Gunnison, Colorado (1910-1912), to primarily study larkspur; and Greycliff, Montana (1912-1915), to study the poisonous plants of the Yellowstone Valley. Dr. Rodney True replaced Mr. Chestnut in 1904 and in 1905 hired Dr. C. D. Marsh (1905-1930) to establish the temporary field stations listed above. In 1915 a permanent facility was established at Salina, Utah, under the direction of C. D. Marsh who remained in charge until 1930 when he retired; he was followed by A. B. Clawson until 1937 when Dr. Ward Huffman was placed in charge. Research on poisonous plants was located at the Salina Experiment Station until 1955 when the station was closed and the laboratory moved to the campus of Utah State Agricultural College at Logan, Utah, where it is currently located. Dr. Wayne Binns was hired as the director of the laboratory in 1954 and retired in 1972. In 1972 Dr. Lynn F. James, who joined the PRPL staff in July 1957, was appointed as Research Leader and presently directs the research at the Poisonous Plant Research Laboratory.

Teratological research at the USDA-ARS poisonous plant research laboratory.

Research on teratogenic plants started at the USDA-Agricultural Research Service-Poisonous Plant Research Laboratory in the mid 1950s when Dr. Wayne Binns, Director of the laboratory, was asked to investigate the cause of a cyclopian facial/skeletal birth defect in lambs. Dr. Lynn F. James joined the staff shortly after. These two people worked as a team wherein most planning was done jointly with Binns supervising most of the laboratory work and James the field studies. It was determined that when pregnant ewes grazed Veratrum californicum on day 14 of gestation a significant number of lambs had the cyclopic defect. Skeletal and cleft palate birth defects in calves was associated with pregnant cows grazing certain lupine species during 40-70 days of gestation. Shortly thereafter research work was initiated on locoweed which caused abortions, wasting, right heart failure, skeletal birth defects, and fetal right heart failure. Dr. Richard F. Keeler, a chemist who joined the staff in the early 1960s, isolated and characterized the teratogens in V. californicum as the steroidal alkaloids cyclopamine, jervine, and cycloposine. He also described the teratogen in lupines as the quinolizidine alkaloid anagyrine and the piperidine alkaloid ammodendrine. Drs. Russell Molyneux and James identified the toxin in locoweed as the indolizidine alkaloid swainsonine. In 1974 the editor of Nutrition Today (Vols. 9 and 4) wrote "The idea that birth defects occurring in humans may be in some way related to diet is not widely held ..." Dr. Lynn James pointed out in this issue that such defects in animals can be produced with absolute predictability and regularity by foods ordinarily beneficial to livestock. Management strategies have been developed to prevent or minimize the economic impact of the cyclopian lamb and the crooked calf condition on livestock producers and well on the way to doing the same with locoweed. It is of interest to note that livestock research on Veratrum, lupines and locoweed and toxins therefrom are now significant research tools for specific human health problems.

[Poisoning with toxic plants in Curacao in 1766]. / Vergiftiging met toxische planten op Curaçao in 1766.

In the spring of 1766 a black supervisor in Curaçao was the victim of attempted poisoning by a black practitioner or curador, engaged by two persons caught stealing by the supervisor. Data on the case were preserved in a letter from the Curaçao director to the managers of the West-Indian Company in Amsterdam. In retrospect, the symptoms of the intoxication indicate that a similar mixture of toxic plants was used as described in 890 A.D. by the Arabic medical writer Wahshiya in his 'Book of Poisons': Calotropis procera and Pithecellobium unguis cati.

The toxic factor in white snakeroot: identity, analysis and prevention.

White snakeroot (Eupatorium rugosum Houtt) has been known to cause trembles in animals and milk sickness in humans since the American Revolution. It still continues to poison animals. Horses and goats are particularly sensitive to white snakeroot poisoning. Resurgence of livestock production on small farm units, and utilization of fresh raw milk may result in milk sickness; if the animals have white snakeroot exposure. The goat is the only animal with good toxicity threshold data. In other animals and humans the toxicity thresholds of white snakeroot are not known, and that until responsible toxic principles are identified and their fate in animals and milk studied, such an assessment will not be possible. The toxic component(s) in white snakeroot has not been identified. The mechanism of action of the toxin in animals or humans remains unknown. However, metabolic studies in chicks initially suggest that a specific metabolic enzyme may be the target of the toxic principle. Components of white snakeroot that are toxic after microsomal activation have been isolated. Cytochrome P-450 is responsible for this activation. Activation in vitro can be totally inhibited by the cytochrome P-450 specific autocatalytic inhibitor, 1-aminobenzotriazole. In view of the importance of white snakeroot in the history of the United States and the ongoing problems today, it would be most unfortunate if studies were not pursued expeditiously to identify the toxicant(s) responsible, and to understand the mechanism(s) of action and toxicity thresholds.

Cycad (zamia) poisoning in Australia.

The Cycads belong to an ancient family of plants and were the cause of the first well documented plant poisoning in Australia when Captain Cook's men and their pigs were affected by eating them. Subsequent reports particularly by early explorers refer to toxicity of the seeds to man. One reason for this was the evidence that the natives ate them. Subsequent reports and experimental work established the toxicity to sheep and cattle. In sheep and cattle 2 syndromes occur, ataxia and liver damage. In cattle the former is the better known, the spinal cord lesion being mainly a demyelination of the sensory pathways. The liver damage is necrosis and fibrosis.