Appearance and disappearance of swainsonine in serum and milk of lactating ruminants with nursing young following a single dose exposure to swainsonine (locoweed; Oxytropis sericea).
(9/214)
A series of experiments were conducted to investigate the elimination of swainsonine in the milk of lactating ruminants following a single dose oral exposure to swainsonine (locoweed; Oxytropis sericea) and to assess subsequent subclinical effects on the mothers and their nursing young. In a preliminary experiment, lactating ewes were gavaged with locoweed providing 0.8 mg swainsonine/kg BW (n = 4; BW = 75.8 +/- 3.6 kg; lactation = d 45) and lactating cows were offered up to 2.0 mg swainsonine/kg BW free choice (n = 16; BW = 389.6 +/- 20.9 kg; lactation = d 90). Serum and milk were collected at h 0 (before treatment), 3, 6, 12, and 24 for ewes, and h 0 (before treatment), 6, 12, 18, and 24 for cows. Swainsonine was highest (P < 0.05) by h 6 in the serum and milk of ewes. Consumption of at least 0.61 mg swainsonine/kg BW induced consistent (> 0.025 microg/mL) appearance of swainsonine in cow serum and milk. In response to the results obtained in the preliminary experiment, a subsequent experiment utilizing lactating ewes (n = 13; BW = 74.8 +/- 6.4 kg; lactation = d 30) and cows (n = 13; BW = 460.8 +/- 51.9 kg; lactation = d 90) was conducted. Each lactating ruminant was gavaged with a locoweed extract to provide 0 (control), 0.2, or 0.8 mg swainsonine/kg BW and individually penned with her nursing young. Serum and milk from the mothers and serum from the nursing young were collected at h 0 (before treatment), 3, 6, 9, 12, 24 and 48 (an additional sample was obtained at h 72 for ewes and lambs). Serum and milk swainsonine was higher (P < 0.05) in the 0.8 mg treated groups and maximal (P < 0.05) concentrations occurred from h 3 to 6 for ewes and h 6 to 12 h for cows (P < 0.05). Rises in alkaline phosphatase activity indicated subclinical toxicity in the treated ewes (P < 0.05). Following a single dose oral exposure to 0.2 and 0.8 mg swainsonine/kg BW provided by a locoweed extract, swainsonine was detected in the serum and milk of lactating ewes and cows, and rises in serum alkaline phosphatase activity were observed in the ewes. Neither swainsonine nor changes in alkaline phosphatase activity was detected in the serum of the lambs and calves nursing the ewes and cows dosed with swainsonine. (+info)
Evaluation of vaccination against methyllycaconitine toxicity in mice.
(10/214)
The purpose of this study was to determine whether larkspur toxins conjugated to protein carriers would promote active immunity in mice. Mice were injected with several larkspur toxin-protein conjugates or adjuvant alone to determine whether the resulting immunological response altered animal susceptibility to methyllycaconitine, the major toxic larkspur alkaloid. Although vaccinations increased the calculated lethal dose 50% (LD50) for intravenous methyllycaconitine toxicity, overlapping confidence intervals did not provide evidence of differences between the vaccinated and control groups. In the lycoctonine conjugate (LYC)-vaccinated group, mouse survival was related (P = 0.001) to serum titers for methyllycaconitine doses up to 4.5 mg/kg of body weight. When mice withlow antibody titers were removed from the vaccinated groups in which titer was related to survival, the recalculated LD50 estimates were 20% greater than the LD50 of the control group. However, the 95% confidence intervals of the recalculated LD50 groups overlapped with the control groups. Overall, these results suggest that vaccination altered methyllycaconitine toxicity in mice and that vaccination may be useful in decreasing the effects of larkspur toxins in animals. Additional studies are warranted to continue development of potential larkspur vaccines for livestock. (+info)
Toad venom poisoning: resemblance to digoxin toxicity and therapeutic implications.
(11/214)
A healthy man developed gastrointestinal symptoms after ingesting purported aphrodisiac pills. He had severe unrelenting bradycardia, hyperkalaemia, and acidosis. He rapidly developed severe life threatening cardiac arrhythmias and died after a few hours. He was found to have positive serum digoxin concentrations, although he was not taking digoxin. Toad venom poisoning is similar to digitalis toxicity and carries a high mortality. Cardiac glycoside poisoning can occur from ingestion of various plants and animal toxins, and the venom gland of cane toad (Bufo marinus) contains large quantities of cardiac glycosides. Toad venom, a constituent of an aphrodisiac, was considered responsible for the development of clinical manifestations and death in this patient. Digoxin specific Fab fragment has been reported to be beneficial in the treatment of toad venom poisoning. This report alerts physicians to the need to be aware of a new community toxic exposure, as prompt treatment with digoxin specific Fab fragment may be life saving. The treatment approach to patients with suspected toad venom poisoning is described. (+info)
A pulmonary hypertension-producing plant from Tanzania.
(12/214)
An African youth who had died from primary pulmonary hypertension was suspected of having ingested a herbal remedy containing the seeds of the local plant Crotalaria laburnoides. Consequently powdered seeds of this plant were fed to 20 Wistar albino rats for 60 dyas to see if this would induce ventricular hypertrophy and associated hypertensive pulmonary vascular disease. At the end of the experimental period right ventricular hypertrophy, medial hypertrophy of the pulmonary trunk and 'muscular pulmonary arteries', and muscularization of the pulmonary arterioles had developed in a proportion of the test animals. These are the morbid anatomical features pathognomonic of a raised pulmonary arterial pressure and show that the seeds of Crotalaria laburnoides contain an agent capable of inducing pulmonary hypertension in rats. This study suggests the value of seeking a history of ingestion of herbal remedies and drugs in cases of unexplained pulmonary hypertension in man. (+info)
Veno-occlusive lesions in the liver of rats after prolonged feeding with palmyrah (Borassus flabellifer) flour.
(13/214)
Flour from the young shoot of the palmyrah palm (Borassus flabellifer) which is consumed by people in certain tropical countries, when fed for prolonged periods to adult male rats produced chronic hepatic lesions which included intraluminal fibrosis of the centrilobular and portal veins, bile duct proliferation, increase of reticulin and fibrosis. Thromboses of the hepatic veins was not seen. The vascular lesions commenced as a subendothelial swelling which projected into the lumen and in which collagen deposition ended in almost total obliteration of the lumen. No hepatic megalocytosis was seen. It is suggested that the toxic factor(s) responsible are different from the pyrrolizidine alkaloids and dimethylnitrosamine which have been well documented to produce similar lesions. (+info)
Symmetric focal degeneration in the cerebellar and vestibular nuclei in swine caused by ingestion of Aeschynomene indica seeds.
(14/214)
A vestibulocerebellar disorder was observed in 2- to 4-month-old swine after consumption of broken rice contaminated with 13% Aeschynomene indica seeds. Affected animals recovered in 2-14 days after removal of the contaminated food. To reproduce the syndrome, 10 pigs were fed 13% A. indica seeds in commercial pig ration or rice. They showed clinical signs similar to those observed in the spontaneous cases, 1 hour to 6 days after ingestion. Three pigs recovered after the withdrawal of the contaminated food. The others were killed. Two pigs that were fed for 25 days with food containing 3% and 6% seeds and two control pigs did not show clinical signs. Histologic lesions were characterized by symmetric focal degeneration in the cerebellar and vestibular nuclei. The initial lesion, observed 24 hours after the first ingestion, was characterized by vacuolation of the neuropil. Subsequently, there was progressive loss of parenchyma, vascular reaction, a few small spheroids, astrocytosis, and accumulation of gitter cells. The brains from four pigs were perfused with a buffered solution of glutaraldehyde-paraformaldehyde 12-48 hours after they started to ingest the seeds. No ultrastructural lesions were observed in the cerebellar nuclei after 12 hours of seed consumption. At 24 hours, endothelial cells and pericytes were separated by empty spaces from astrocyte foot processes, suggesting perivascular edema. The astrocytes were enlarged, consistent with intracellular fluid accumulation. These results suggest that A. indica seeds are toxic, causing functional derangement of the vestibulocerebellar system, followed by alterations in the microvasculature in the cerebellar and vestibular nuclei. (+info)
Narthecium ossifragum (L.) huds. causes kidney damage in goats: morphologic and functional effects.
(15/214)
We studied the effects of Narthecium ossifragum on goat kidneys. Twenty-five Norwegian dairy goats, 5 weeks to 4 months of age, were orally dosed with an aqueous extract from N. ossifragum. In experiment 1, we studied microscopic and functional changes in 12 animals that were euthanatized 2, 3, 4, 5, and 6 days after treatment. In experiment 2, we included ultrastructural studies on serial renal biopsies and urine analysis from five extract-treated animals and two controls. In addition, urine samples were collected from four dosed and two control goats. Ultrasonography revealed perirenal and retroperitoneal fluids. Microscopic changes were observed after 6 hours. The findings, most obvious in the inner cortex and the outer medulla, consisted of cytoplasmic vacuolization, interstitial edema, and focal necrosis of tubular epithelial cells. Ultrastructurally, the tubules had loss of microvilli, irregular cytoplasmic vacuolization, mitochondrial swelling with loss of cristae, and irregular but continuous basement membranes even with necrosis. In the glomeruli, there were occasional endothelial damage and shortening and swelling of the foot processes. Peritubular capillaries had breaks in the vessel walls and irregular endothelial cell edema, and the interstitium had marked edema. The functional lesions included elevated serum urea, creatinine, and magnesium concentrations, a slight decrease in serum calcium concentration, elevated urine protein and urine protein-creatinine ratio, and increased activities of urine alkaline phosphatase and gamma glutamyl transferase. Our findings indicate a fast-acting toxic principle inducing damage by both direct toxic and secondary ischemic effects. (+info)
Acute plant poisoning and antitoxin antibodies.
(16/214)
Plant poisoning is normally a problem of young children who unintentionally ingest small quantities of toxic plants with little resulting morbidity and few deaths. In some regions of the world, however, plant poisonings are important clinical problems causing much morbidity and mortality. While deaths do occur after unintentional poisoning with plants such as Atractylis gummifera (bird-lime or blue thistle) and Blighia sapida (ackee tree), the majority of deaths globally occur following intentional self-poisoning with plants such as Thevetia peruviana (yellow oleander) and Cerbera manghas (pink-eyed cerbera or sea mango). Antitoxins developed against colchicine and cardiac glycosides would be useful for plant poisonings--anti-digoxin Fab fragments have been shown to be highly effective in T. peruviana poisoning. Unfortunately, their great cost limits their use in the developing world where they would make a major difference in patient management. Therapy for some other plant poisonings might also benefit from the development of antitoxins. However, until issues of cost and supply are worked out, plant antitoxins are going to remain a dream in many of the areas where they are now urgently required. (+info)