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An outbreak of neurological disorders in a flock of 20 sheep coming from a rural farm in Civitella Roveto, Italy, occurred in winter 2015. All the animals showed tonic-clonic convulsions followed by muscle paralysis associated with dilated pupils, tremor, tachycardia, tachypnea and diarrhea. The presence of bundles of dry broom of Spartium junceum L. in the feed, eaten by the animals supported the hypothesis of plant intoxication. Two animals died after worsening of clinical signs. The anatomopathological findings and the laboratory results ruled out viral or bacterial infections or accidental exposure to other toxics. Phytochemical study showed the presence of large amount of cytisine, a nicotinic acetylcholine receptor agonist, in all parts of the plant eaten by the animals. Clinical and pathological findings, the complete remission of clinical signs after the exclusion of dry broom from the diet, together with the results of phytochemical analyses results corroborated the hypothesis of S. junceum L. intoxication.

Background: Baptisia is commonly found in residential gardens as an ornamental plant, in municipal "rain gardens" for water control, as well as in native and restored prairie habitat. Cytisine, an alkaloid with nicotinic acetylcholine receptor agonist properties, is a component of Baptisia., Case Report: Two patients poisoned after simultaneously ingesting Baptisia plant material are presented. In addition to findings of generalized nicotinic agonist toxicity, including generalized weakness and gastrointestinal symptoms, profound ataxia was present in both, consistent with recently described nicotinic subunit activity in the cerebellum. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Baptisia, a native prairie plant commonly found in restored prairie habitats and public spaces, has striking "look-alike" characteristics, in its immature state, to asparagus. As future exposures by foraging citizens will be likely, awareness of this relationship and the toxic manifestations of cytisine will be useful., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Unlabelled: Serotonin syndrome is caused by excess serotonin in the central nervous system. It usually occurs as adverse drug-therapy (neuroleptic agents, monoamine oxidase inhibitors, serotonin reuptake inhibitors and others)., Case Presentation: a 50-year-old woman with a history of depression, was admitted to our hospital, due to suicidal drug poisoning (moclobemide- 4500 mg, venlafaxine 1050 mg, mianserin 300 mg and cytisine 30mg). She was also drunk. The patient was unconscious and sweaty, on the ECG tachycardia (120/min) was observed. In addition, several hours after admission, the patient developed acute respiratory failure, we observed myoclonus, lockjaw, body temperature increased to 37.3 degrees Celsius, and blood pressure was 170/80 mmHg. During the neurological examination there was a tendency to bilaterall Babinski sign and the nystagmus was present. The patient was intubated, and we started an intravenous infusion of Relanium. In laboratory studies: ethanol: 2.52 g/l, tests for benzodiazepines and tricyclic antidepressants were negative, WBC 13.1 tys/microl, CPK was elevated to 372 U/L, other parameters (electrolytes, transaminases, serum total protein, glucose, CRP, creatinine) were normal. The patient required intensive care and treatment during the next two days. The diagnosis of serotonin syndrome was based on the Hunter's criteria, which are more sensitive and more specific than Sternbach's criteria. The patient was discharged from hospital in good condition.

We report about a fatal cytisine intoxication in a 20-year-old man who, according to his mother, had drunken tea prepared from plant material of Laburnum anagyroides with the toxic pyridine-like alkaloid as ingredient, which exhibits pharmacological effects similar to nicotine. Using a liquid chromatographic-mass spectrometric (LC-MS) procedure cytisine was quantified in post-mortem specimens. By exclusion of other causes of death an intoxication was determined as the cause of death with respiratory failure as the pathophysiological mechanism.

Dolasetron (Anzemet) overdose is uncommon, and, to our knowledge, this is the only case report of an intentional overdose. Dolasetron (dolasetron mesylate) is a selective 5-hydroxytryptamine 3 antagonist derived from pseudopelletierine, and is used in the prevention and treatment of nausea and vomiting. Transient and asymptomatic ECG changes, including QRS widening and PR and QTc prolongation, have been reported in therapeutic doses. The case of a 21-year-old woman who presented after an intentional overdose of 10x200 mg dolasetron tablets resulting in prolongation of the QTc interval and severe hypotension is reported here. Management of hypotension included intravenous fluid resuscitation and norepinephrine infusion with invasive monitoring in a high dependency unit. Sodium cardiac channel block contributes to cardiotoxicity observed in dolasetron overdose. Sodium bicarbonate was used in an attempt to reduce cardiac sodium channel block, although we observed no apparent benefit. As dolasetron becomes more commonly used in the outpatient setting, both doctors and patients need to be aware of the dangers of dolasetron in toxic doses. The pharmacology and toxicology of dolasetron are discussed.

Several species of lupine (Lupinus spp.) are poisonous to livestock, producing death in sheep and "crooked calf disease" in cattle. Range livestock cope with poisonous plants through learned foraging strategies or mechanisms affecting toxicant disposition. When a toxic plant is eaten, toxicant clearance may be influenced by the animal's nutritional and/or physiological status. This research was conducted to determine whether differences in body condition or short-term nutritional supplementation of sheep altered the disposition of lupine alkaloids given as a single oral dose of ground silvery lupine (Lupinus argenteus) seed. Ewes in average body condition (ABC, n = 9) and low body condition (LBC, n = 10) received a single dose of ground lupine seeds including pods (8.5 g/kg BW) via gavage on the first day of the experiment, and were then randomly assigned to one of two nutritional supplement treatments. Blood samples were taken 0 to 60 h after dosing to compare blood alkaloid concentration and to evaluate alkaloid absorption and elimination profiles. Concentrations of total alkaloid and anagyrine, 5,6 dehydrolupanine, lupanine, and alkaloid E were measured in serum. These four alkaloids constituted 78 and 75% of the total alkaloid concentration in serum for LBC vs. ABC groups, respectively. Initial analysis indicated that short-term supplementation had no effect on alkaloid disposition, and supplementation was removed from the statistical model. The highest concentration of total alkaloids was observed 2 h after dosing. Overall, serum total alkaloid and anagyrine levels (area under the curve) were higher (P < 0.01) for sheep in the LBC group. Serum peak concentrations of total alkaloid and anagyrine were higher in LBC vs. ABC groups (P < 0.05). Serum elimination of anagyrine, unknown alkaloid E, and lupanine was decreased in LBC vs. ABC treatments (P < 0.05). These results demonstrate that body condition is important in the disposition of lupine alkaloids; however, further research is needed to determine the potential benefit, if any, that short-term nutritional supplementation might have on alkaloid disposition.

A case of Flumequine poisoning is described; a 13-year-old girl was admitted for a psychiatric syndrome. 3 hours after, seizures, coma, and metabolic disorders were observed. Infectious, encephalitic or diabetic diseases were suspected, but not confirmed. After 12 hours of a symptomatic treatment, the clinical status improved and the patient was discharged. At that time a tablet was found in her bedroom and a mas spectrographic analysis was positive for Flumequine. This case report is in agreement with previous observations and confirms the small therapeutic index of quinolone, and the absolute necessity to assess carefully a psychiatric diagnosis.