aconitine and Plant-Poisoning

Topics: Accidents; Aconitine; Aconitum; Cicuta; Conium; Humans; Japan; Plant Poisoning; Plants, Toxic; Scopolia; Veratrum; Veratrum Alkaloids

Topics: Aconitine; Aconitum; Biomarkers; Humans; Plant Poisoning

Topics: Aconitine; Aconitum; Animals; Chemistry Techniques, Analytical; Humans; Plant Poisoning; Specimen Handling; Tandem Mass Spectrometry; Toxicology

Aconitine and related alkaloids found in the Aconitum species are highly toxic cardiotoxins and neurotoxins. The wild plant (especially the roots and root tubers) is extremely toxic. Severe aconite poisoning can occur after accidental ingestion of the wild plant or consumption of an herbal decoction made from aconite roots. In traditional Chinese medicine, aconite roots are used only after processing to reduce the toxic alkaloid content. Soaking and boiling during processing or decoction preparation will hydrolyze aconite alkaloids into less toxic and non-toxic derivatives. However, the use of a larger than recommended dose and inadequate processing increases the risk of poisoning.. A Medline search (1963-February 2009) was conducted. Key articles with information on the use of aconite roots in traditional medicine, active (toxic) ingredients, mechanisms of toxicity, toxicokinetics of Aconitum alkaloids, and clinical features and management of aconite poisoning were reviewed.. The cardiotoxicity and neurotoxicity of aconitine and related alkaloids are due to their actions on the voltage-sensitive sodium channels of the cell membranes of excitable tissues, including the myocardium, nerves, and muscles. Aconitine and mesaconitine bind with high affinity to the open state of the voltage-sensitive sodium channels at site 2, thereby causing a persistent activation of the sodium channels, which become refractory to excitation. The electrophysiological mechanism of arrhythmia induction is triggered activity due to delayed after-depolarization and early after-depolarization. The arrhythmogenic properties of aconitine are in part due to its cholinolytic (anticholinergic) effects mediated by the vagus nerve. Aconitine has a positive inotropic effect by prolonging sodium influx during the action potential. It has hypotensive and bradycardic actions due to activation of the ventromedial nucleus of the hypothalamus. Through its action on voltage-sensitive sodium channels in the axons, aconitine blocks neuromuscular transmission by decreasing the evoked quantal release of acetylcholine. Aconitine, mesaconitine, and hypaconitine can induce strong contractions of the ileum through acetylcholine release from the postganglionic cholinergic nerves.. Patients present predominantly with a combination of neurological, cardiovascular, and gastrointestinal features. The neurological features can be sensory (paresthesia and numbness of face, perioral area, and the four limbs), motor (muscle weakness in the four limbs), or both. The cardiovascular features include hypotension, chest pain, palpitations, bradycardia, sinus tachycardia, ventricular ectopics, ventricular tachycardia, and ventricular fibrillation. The gastrointestinal features include nausea, vomiting, abdominal pain, and diarrhea. The main causes of death are refractory ventricular arrhythmias and asystole and the overall in-hospital mortality is 5.5%.. Management of aconite poisoning is supportive, including immediate attention to the vital functions and close monitoring of blood pressure and cardiac rhythm. Inotropic therapy is required if hypotension persists and atropine should be used to treat bradycardia. Aconite-induced ventricular arrhythmias are often refractory to direct current cardioversion and antiarrhythmic drugs. Available clinical evidence suggests that amiodarone and flecainide are reasonable first-line treatment. In refractory cases of ventricular arrhythmias and cardiogenic shock, it is most important to maintain systemic blood flow, blood pressure, and tissue oxygenation by the early use of cardiopulmonary bypass. The role of charcoal hemoperfusion to remove circulating aconitine alkaloids is not established.. Aconite roots contain aconitine, mesaconitine, hypaconitine, and other Aconitum alkaloids, which are known cardiotoxins and neurotoxins. Patients present predominantly with neurological, cardiovascular, and gastrointestinal features. Management is supportive; the early use of cardiopulmonary bypass is recommended if ventricular arrhythmias and cardiogenic shock are refractory to first-line treatment.

Topics: Aconitine; Aconitum; Alkaloids; Animals; Dose-Response Relationship, Drug; Humans; Medicine, Chinese Traditional; Plant Poisoning; Plant Roots

Severe intoxications after ingestion of monk's hood are rare in childhood. We report a case of fatal intoxication in a 20 months old child. There is no specific therapy available. A review of the literature is added.

Topics: Aconitine; Brain; Brain Edema; Female; Gastric Mucosa; Heart Arrest; Humans; Infant; Plant Poisoning

Larkspur (Delphinium spp.) poisoning is a long-term problem for cattle grazing on rangelands of western North America. Results from preliminary experiments have suggested that differences in larkspur toxicity may exist between heifers and bulls. The objective of this study was to compare the physiological responses of yearling Angus heifers, steers, and bulls with a standardized dose of Delphinium barbeyi and to test the hypothesis that the response is sex dependent. Clinical signs of intoxication, including muscle coordination and function, were measured 24 h after oral dosing with larkspur by walking the cattle at a pace of 5 to 6 km h-1 for up to 40 min on an oval dirt track. Due to the experimental methods used, the variation in susceptibility to larkspur was not quantifiable for walking times of 0 or 40 min or more. Larkspur susceptible animals that were not able to walk (0 min; 36% of the animals) or larkspur resistant animals that walked the entire test period of 40 min (9% of the animals) resulted in censored or truncated data. The statistical methods (censReg and lmec) were used to adjust for data truncation or censoring. The heifers were only able to walk -8.9 ± 3.9 min (65.5% censored on the left) compared with 13.2 ± 3.7 min for bulls and 15.9 ± 2.7 min for steers. When heifers were compared with bulls and steers together, heifers walked 23.4 ± 4.5 min less (P < 0.0001). Serum alkaloid concentrations were measured immediately before walking, and deltaline concentrations averaged 266 ± 28, 131 ± 20, and 219 ± 28 ng mL-1 for all heifers, steers, and bulls, respectively, and serum methyllycaconitine concentrations averaged 660 ± 46, 397 ± 32, and 612 ± 34 ng mL-1 for all heifers, steers, and bulls, respectively. The relative risk of a zero walk time for yearling heifers is 330% that of yearling bulls (P = 0.0008). These results suggest that yearling Angus heifers are more susceptible to larkspur intoxication and, when possible, heifers should be kept from grazing larkspur-infested rangelands as a simple management tool to reduce the risk of fatal poisoning.

Topics: Aconitine; Alkaloids; Animal Husbandry; Animals; Cattle; Cattle Diseases; Delphinium; Diterpenes; Female; Male; North America; Plant Poisoning; Plants, Toxic; Sex Factors; Walking

Larkspurs (Delphinium spp.) are native perennial plants that have a serious toxic potential to cattle on foothill and mountain rangelands in the western United States. Livestock death due to larkspur toxicity is attributed to norditerpenoid alkaloids. Diagnosing plant poisonings in livestock is often challenging. The objective of this study was to evaluate the use of three matrices; earwax, oral fluid, and nasal mucus, as noninvasive specimens to determine livestock exposure to larkspurs. Reversed phase high performance liquid chromatography - high resolution mass spectrometry was used to analyze for norditerpene alkaloids, in all three matrices, in cattle administered a single dose of larkspur. Earwax, oral fluid, and nasal mucus were collected over 6 days post-dosing. Methyllycaconitine (MLA) and deltaline concentrations in earwax ranged from 0.4 ± 0.1 to 0.2 ± 0.06 and 0.6 ± 0.5 to 0.11 ± 0.08 ng/mg, respectively. MLA and deltaline concentrations in oral fluid ranged from 0.08 ± 0.03 to 0.01 ± 0.002 ng/mg and 0.07 ± 0.03 ng/mg to not detected (ND), respectively. MLA and deltaline concentrations in nasal mucus ranged from 0.2 ± 0.13 to 0.03 ± 0.01 ng/mg and 0.2 ± 0.12 ng/mg to ND, respectively. The ability to detect differing norditerpene alkaloid chemotypes from two different Delphinium spp. was also possible in the three matrices. This study demonstrates the potential of earwax, oral fluid, and nasal mucus as noninvasive specimens for chemical analyses to aid in the diagnosis of livestock that may have been exposed to and poisoned by larkspur plants.

Topics: Aconitine; Alkaloids; Animals; Cattle; Cattle Diseases; Chromatography, High Pressure Liquid; Delphinium; Diterpenes; Livestock; Male; Plant Poisoning; Plants, Toxic; Specimen Handling; United States

Poisoning of cattle by larkspur plants (Delphinium spp.) is a concern for cattle ranchers in western North America. Previous research studies have evaluated the toxicokinetic profile of multiple larkspur toxins in several livestock species. However, those studies were all performed by orally dosing plant material. Consequently some toxicokinetic parameters could not be definitively determined. In this study, we compared the serum toxicokinetic profile of the larkspur alkaloids methyllycaconitine (MLA) and deltaline in goats dosed both IV and via oral gavage. The results from this study indicate that the toxic alkaloids in larkspurs undergo flip-flop kinetics, meaning the rate of absorption of the alkaloids is slower than the rate of elimination. The implications of flip-flop kinetics in treating animals poisoned by larkspur is discussed.

Topics: Aconitine; Administration, Intravenous; Administration, Oral; Animals; Delphinium; Diterpenes; Goats; Plant Poisoning; Toxicokinetics

We report about an acute monkshood intoxication requiring acute resuscitation in suicidal intent in a 56-year-old patient. The Blue Monkshood (Aconitum napellus) is considered to be the most toxic plant in Europe. All plant parts contain the highly toxic alkonoid aconitin. The lethal dose in adults is 2 - 6 mg. Intoxications are often fatal. Asymptomatic patients with suspected monkshood intoxication should also be monitored on an ICU. First signs of intoxication are paraesthesia in the mouth and throat area, abdominal cramps, nausea, vomiting and severe pain in skeletal muscle. Affected patients die within hours after ingestion due to respiratory distress and/or cardiac arrhythmia.The most important measure after oral ingestion is to achieve a rapid primary poison elimination clearance (in the case of awareness clear patients, trigger vomiting, otherwise gastric lavage under protective intubation) and the subsequent carbonation. A specific antidote is not available. The management of an intoxication consists primarily of the therapy of the rhythm disturbances in the form of magnesium and amiodarone.Strict adherence to protective measures (gloves, masks) must be strictly observed. A direct skin contact with plant parts is to be avoided as well as the potential contact with vomit or aspirate.. Wir berichten über eine akute Eisenhutintoxikation einer 56-jährigen Patientin mit Blauem Eisenhut (Aconitum napellus) in suizidaler Absicht. Der Blaue Eisenhut gilt als die giftigste Pflanze Europas. Alle Pflanzenteile enthalten das hochgiftige Alkaloid Aconitin. Die letale Dosis beim Erwachsenen beträgt 2 – 6 mg. Intoxikationen verlaufen häufig tödlich. Auch asymptomatische Patienten mit Verdacht auf Eisenhutintoxikation sollten auf einer Intensivstation überwacht werden. Erste Intoxikationszeichen sind Parästhesien im Mund- und Rachenbereich, Bauchkrämpfe, Übelkeit, Erbrechen und starke Schmerzen der Skelettmuskulatur. Betroffene Patienten versterben innerhalb weniger Stunden nach Ingestion aufgrund von Atemlähmung und/oder Herzrhythmusstörungen.Die wichtigste Maßnahme nach oraler Ingestion besteht in einer möglichst schnellen primären Giftelimination (bei bewusstseinsklaren Patienten Erbrechen auslösen, sonst Magenspülung unter Schutzintubation) und der anschließenden Kohlegabe. Ein spezifisches Antidot steht nicht zur Verfügung. Das Management einer Intoxikation besteht vor allem aus der Therapie der Rhythmusstörungen in Form von Magnesium und Amiodaron.Auf die strikte Einhaltung von Eigenschutzmaßnahmen (Handschuhe, Mundschutz) muss unbedingt geachtet werden. Ein direkter Hautkontakt mit Pflanzenteilen ist ebenso zu vermeiden wie der potenzielle Kontakt mit Erbrochenem oder Aspirat.

Topics: Aconitine; Aconitum; Amiodarone; Anti-Arrhythmia Agents; Female; Glasgow Coma Scale; Humans; Middle Aged; Plant Poisoning; Resuscitation; Suicide, Attempted; Tachycardia; Therapeutic Irrigation

Larkspurs ( spp.) are one of the most serious toxic plant problems on foothill and mountain rangelands in the western United States. A considerable amount of research has been conducted over the years in both field and pen settings. The results of these research efforts have significantly increased our understanding of the poisoning of cattle by larkspurs. However, most of the pen studies conducted thus far have used a dosing regimen of a single bolus dose, which does not accurately mimic the manner by which cattle are poisoned by larkspur while grazing. Consequently, the objective of this study was to evaluate the acute toxicity of tall larkspur ( collected near Manti, UT) when administered in multiple doses, with the intent to identify a no observable adverse effect level (NOAEL). The adverse effect selected for this study was muscle weakness to the point the cattle could no longer remain ambulatory as would be required in a grazing environment, thus becoming sternally recumbent when exercised. Hereford steers were administered various doses of tall larkspur at 12-h intervals for 4 d or until they showed marked signs of muscle weakness. The results suggest that a dose of 2 mg kg∙d -(methylsuccinimido) anthranoyllycoctonine (MSAL)-type alkaloids is the NOAEL for a tall larkspur population with a norditerpenoid alkaloid profile containing 4 mg MSAL-type alkaloids/g plant material and 12 mg non-MSAL-type alkaloids/g plant material. Additionally, a computer model was generated to simulate multiple-dosing regimens at the various doses as well as different dosing regimens. The results from this study suggest that a 500-kg steer can consume a daily dose of 1.25 kg of fresh tall larkspur (with a similar alkaloid profile) without becoming severely poisoned (suffering from muscle weakness to the point of recumbency). Additionally, these results indicate that a serum concentration of approximately 355 ng methyllycaconitine/mL may represent a toxic threshold.

Topics: Aconitine; Alkaloids; Animals; Cattle; Cattle Diseases; Delphinium; Diterpenes; Plant Poisoning; Plants, Toxic; United States

Fatal exposure to poisonous plants in northern Europe is a rare condition. In this case report we describe an intended poisoning with Aconitum napellus (monkshood), which contains the toxin aconitine. The lethal dose in adults is 3-6 mg. The toxin affects excitable cells such as neurons and myocytes causing degrees of unconsciousness, hypotension and cardiac arrhythmias. There is no antidote and treatment is symptomatic. We describe a patient who had eaten monkshood. She was treated with infusion of lidocaine and survived. After 24 hours of treatment and monitoring she was discharged from the intensive care unit.

Topics: Aconitine; Aconitum; Anti-Arrhythmia Agents; Critical Illness; Female; Humans; Lidocaine; Middle Aged; Plant Poisoning; Suicide, Attempted; Treatment Outcome

Cattle are poisoned by N-(methylsuccinimido) anthranoyllycoctonine type (MSAL-type) and 7,8-methylenedioxylycoctonine type (MDL-type) norditerpenoid alkaloids in Delphinium spp. Alkaloids in D. glaucescens are primarily of the MSAL-type, while D. barbeyi is a mixture of MSAL and MDL-types. The objectives of this study were to determine and compare the toxicokinetics of selected alkaloids from D. glaucescens and D. barbeyi in cattle. The two species of larkspur were dosed to three groups of Angus steers via oral gavage at doses of 8 mg kg⁻¹ MSAL-type alkaloids for D. barbeyi and either 8.0 or 17.0 mg kg⁻¹ MSAL-type alkaloids for D. glaucescens. In cattle dosed with D. barbeyi, serum deltaline (MDL-type) concentrations peaked at 488 ± 272 ng ml⁻¹ at 3 h and serum methyllycaconitine (MSAL-type) concentrations peaked at 831 ± 369 ng ml⁻¹ at 6 h. Deltaline was not detected in the serum of cattle dosed with D. glaucescens. Serum methyllycaconitine concentrations peaked at 497 ± 164 ng ml⁻¹ at 18 h, and 1089 ± 649 ng ml⁻¹ at 24 h for the 8 mg kg⁻¹ and 17 mg kg⁻¹ doses of D. glaucescens respectively. There were significant differences between the maximum serum concentrations and the area under the curve for the two doses of D. glaucescens but not D. barbeyi. Results from this experiment support the recommendation that approximately 7 days are required to clear 99% of the toxic alkaloids from the serum of animals orally dosed with D. barbeyi or D. glaucescens, and that MDL-type alkaloids play an important role in the toxicity of Delphinium spp. in cattle.

Topics: Aconitine; Administration, Oral; Alkaloids; Animals; Cattle; Cattle Diseases; Delphinium; Diterpenes; Linear Models; Male; Plant Poisoning; Plants, Toxic

Death camas (Zigadenus spp.) is a common poisonous plant on foothill rangelands in western North America. The steroidal alkaloid zygacine is believed to be the primary toxic component in death camas. Poisonings on rangelands generally occur in the spring when death camas is abundant, whereas other more desirable forage species are limited in availability. In most cases where livestock are poisoned by plants in a range setting, there is more than one potential poisonous plant in that area. One common poisonous plant that is often found growing simultaneously in the same area as death camas is low larkspur (Delphinium nuttallianum). Consequently, the objectives of this study were to conduct acute toxicity studies in mice and to determine if coadministration of low larkspur will exacerbate the toxicity of death camas. We first characterized the acute toxicity of zygacine in mice. The LD(50) of zygacine administered intravenously (i.v.) and orally was 2.0 ± 0.2 and 132 ± 21 mg/kg, respectively. The rate of elimination of zygacine from whole blood was determined to be 0.06 ± 0.01/min, which corresponds to an elimination half-life of 13.0 ± 2.7 min. The i.v. LD(50) of total alkaloid extracts from a Utah and a Nevada collection were 2.8 ± 0.8 and 2.2 ± 0.3 mg/kg, respectively. The i.v. LD(50) of methyllycaconitine (MLA), a major toxic alkaloid in low larkspur, was 4.6 ± 0.5 mg/kg, whereas the i.v. LD(50) of a 1:1 mixture of MLA and zygacine was 2.9 ± 0.7 mg/kg. The clinical signs in mice treated with this mixture were very similar to those of mice treated with zygacine alone, including the time of onset and death. These results suggest that there is an additive effect of coadministering these 2 alkaloids i.v. in mice. The results from this study increase knowledge and understanding regarding the acute toxicity of death camas. As combined intoxications are most likely common, this information will be useful in further developing management recommendations for ranchers and in designing additional experiments to study the toxicity of death camas to livestock.

Topics: Aconitine; Alkaloids; Animals; Delphinium; Lethal Dose 50; Livestock; Male; Mice; Nevada; Pharmacokinetics; Plant Poisoning; Seasons; Utah; Zigadenus

This report involves a 54-year-old man who died following refractory ventricular fibrillation after ingestion of a plant in a suicide attempt. Repeated direct-current cardioversions were unsuccessful and no single anti-arrhythmic agent was effective for arrhythmia control. The routine blood toxicological screening was negative. Aconitine, the main toxin of Aconitum napellus was identified using a specific liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. The whole blood concentration (24 microg/l) was higher than those reported in other aconitine-related deaths. The patient had found information about the life-threatening nature of such a toxic herb intake on a free medical encyclopedia online.

Topics: Aconitine; Aconitum; Chromatography, High Pressure Liquid; Fatal Outcome; Forensic Toxicology; Humans; Male; Middle Aged; Plant Poisoning; Plant Preparations; Plants, Toxic; Suicide; Tandem Mass Spectrometry; Ventricular Fibrillation

To describe the simple elimination kinetics of methyllycaconitine (MLA) and deltaline and evaluate the heart rate response in cattle following oral administration of larkspur.. 5 healthy Angus steers that were habituated to metabolism crates.. Tall larkspur (Delphinium barbeyi) in the early flowering stage was collected, dried, and ground. Each steer received a single dose of larkspur that was equivalent to 10.4 mg of MLA/kg and 11.0 mg of deltaline/kg via oral administration. Steers were housed in metabolism crates during a 96-hour period following larkspur administration; heart rate was monitored continuously, and blood samples were collected periodically for analysis of serum MLA and deltaline concentrations as well as assessment of pharmacokinetic parameters.. No overt clinical signs of poisoning developed in any steer during the experiment. Mean +/- SE heart rate reached a maximum of 79.0 +/- 5.0 beats/min at 17 hours after larkspur administration. Serum MLA concentration was correlated directly with heart rate. Mean times to maximal serum concentration of MLA and deltaline were 8.8 +/- 1.2 hours and 5.0 +/- 0.6 hours, respectively. Mean elimination half-life values for MLA and deltaline were 20.5 +/- 4.1 hours and 8.2 +/- 0.6 hours, respectively.. Following larkspur administration in 5 healthy steers, maximum serum concentrations of MLA and deltaline were detected within 10 hours, and changes in serum MLA concentration and heart rate were correlated. Results indicated that cattle that have consumed larkspur will eliminate 99% of MLA and deltaline from serum within 144 hours.

Topics: Aconitine; Alkaloids; Animals; Area Under Curve; Cattle; Cattle Diseases; Delphinium; Diterpenes; Half-Life; Male; Plant Poisoning; Plants, Toxic

A sensitive and specific method for aconitine extraction from biological samples was developed. Aconitine, the main toxic alkaloid from plants belonging to Aconitum species (family Ranunculaceae), was determined in plant material by an external standard method, and by a standard addition calibration method in biological fluids. Described here is one fatal case and five intoxications of accidental aconitine poisoning following the ingestion of aconite mistaken for an edible grass, Aruncus dioicus (Walt.) Fernald, "mountain asparagus", and Cicerbita alpina (L.) Wallroth. The aconitine content in urine was in the range 2.94 microg/mL (dead patient)-0.20 microg/mL (surviving patients), which was almost two to four times higher than that in plasma.

Topics: Aconitine; Aconitum; Alkaloids; Bile; Chromatography, High Pressure Liquid; Diterpenes; Fatal Outcome; Gastrointestinal Contents; Humans; Plant Poisoning; Spectrophotometry, Ultraviolet

Poisoning from aconite occurs worldwide as a result of misuse of the potent plant. Laboratory investigation into suspected intoxication cases is challenging because the content of toxic aconitum alkaloids varies depending on the plant source, market processing, dosing protocol, hydrolytic degradation, and metabolic transformation. Using a triple-quadrupole tandem mass spectrometer, a group screening method was developed based on the mass-fragmentographic scheme of common aconitum alkaloids. The precursor-ion scans of m/z 105 and 135 permitted selective profiling of 14-O-benzoyl-norditerpenoids and the 14-O-anisoyl-norditerpenoids, respectively. Gradient reversed-phase liquid chromatography minimized coelution of isobaric compounds. The screening protocol was applied to a clinical investigation of suspected herbal poisoning. In total, 15 urine samples were thus screened positive for aconitum alkaloid over 5 years. The diagnoses of aconite poisoning in 11 patients were firmly established based on the known prescription history and the positive urine finding. In four patients, without aconitum herbs being listed in the herbal prescriptions, contamination of the herbal remedies by aconite was suspected to be the hidden cause of their acute poisoning. Yunaconitne, a highly toxic aconitum alkaloid, was thus identified in human urine for the first time. The group screening method of aconitum alkaloids in urine is an important diagnostic aid for acute poisoning by aconites of an unclear origin.

Topics: Aconitine; Aconitum; Adult; Aged; Alkaloids; Chromatography, Liquid; Drugs, Chinese Herbal; Female; Gas Chromatography-Mass Spectrometry; Humans; Male; Middle Aged; Plant Poisoning; Plant Tubers; Reproducibility of Results; Retrospective Studies; Spectrometry, Mass, Electrospray Ionization; Tandem Mass Spectrometry

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.

Topics: Aconitine; Animals; Animals, Domestic; Binding, Competitive; Biological Assay; Delphinium; Dose-Response Relationship, Drug; Immunity, Active; Lethal Dose 50; Mice; Plant Extracts; Plant Poisoning; Random Allocation; Survival Analysis; Vaccination

"Torikabuto" is a kind of plant which contains deadly poison. Its ingredient is aconitine alkaloids. We report a case of aconitine poisoning with fatal arrhythmia and acute pulmonary edema who was saved with cardio pulmonary bypass. A 41-year-old male ate to mistake "Torikabuto" for wild plant. He developed symptoms of dysarthria and admitted to our hospital. He developed ventricular tachycardia and fibrillation soon after his admission. Then he developed cardiogenic shock. He was resuscitated and supported with a percutaneous cardio pulmonary bypass. Ventricular tachycardia disappeared 24 hours after admittion. About 1 week later, cardio pulmonary bypass was terminated and about 3 months later, he discharged from our hospital.

Topics: Aconitine; Acute Disease; Adult; Cardiopulmonary Bypass; Humans; Male; Plant Poisoning; Plants, Toxic; Pulmonary Edema; Tachycardia, Ventricular; Treatment Outcome

Tall larkspur poisoning of cattle is a serious problem on western US rangelands. Single oral doses of tall larkspur ranging from 1.5 to 3 g/kg body weight were administered to steers. These doses caused clinical signs of muscular tremors and collapse. Physostigmine was administered iv, ip or sc at 0.04 to 0.08 mg/kg body weight when animals were sternally or laterally recumbent. Physostigmine given iv rapidly reversed the larkspur toxicity. Serial injections of physostigmine were generally necessary to reverse acute toxicity. Administration of physostigmine to grazing animals poisoned on larkspur was also effective. Physostigmine can be effective treatment for intoxicated cattle consuming tall larkspurs.

Topics: Aconitine; Administration, Oral; Animals; Cattle; Cattle Diseases; Injections, Intraperitoneal; Injections, Intravenous; Injections, Subcutaneous; Male; Physostigmine; Plant Extracts; Plant Poisoning; United States; United States Food and Drug Administration

We determined the po toxicity of tall larkspur (Delphinium barbeyi) of known alkaloid composition to cattle. We calculated the effective dose at which the alkaloids methyllycaconitine and 14-deacetylnudicauline, collectively termed total toxic alkaloid, caused collapse and sternal recumbency. The effective dose of total toxic alkaloid that produced sternal recumbency in steers was 11.2 mg/kg bw. Based on this dose, we hypothesize that the LD50 for a po dose of total toxic alkaloids in cattle will be 25 to 40 mg/kg bw.

Topics: Aconitine; Alkaloids; Animal Feed; Animals; Cattle; Cattle Diseases; Lethal Dose 50; Male; Plant Poisoning; Plants, Toxic