POISONOUS PLANT WE RECOMMEND NOT TO HANDLE
BELOW ARE RECOMMENDATIONS IN CASE OF TAMPERING.
POISONOUS PLANT WE RECOMMEND NOT TO HANDLE
BELOW ARE RECOMMENDATIONS IN CASE OF TAMPERING.
It grows in moist and cool environments (riverbanks, streams, roadsides and crop fields); it is native to Europe and North Africa. This invasive species, which can grow up to 2 meters in height, contains toxic substances such as cycutin, which inhibits the functioning of the central nervous system producing the so-called “cycoutism” (cyanosis, mydriasis, convulsions and coma) that begins with vertigo, headaches, drop in body temperature and reduction of muscle strength, ending in paralysis. Only a few grams of its green fruits are needed to kill a human being. The most famous historical figure who died after being condemned in a trial to drink a cup of hemlock was the philosopher Socrates in 399 BC..
The whole plant contains piperidinic alkaloids, including flavone and coumarin glycosides and an essential oil, as well as conycein and coniin (also called conine, conicine or cicutin), a neurotoxin that inhibits the functioning of the central nervous system producing the so-called “cicutism”.
Ingestion may pose a health risk.The effect of this toxin is similar to curare. Its concentration varies according to the stage of ripening and climatic conditions, being found mainly in green fruits (0.73-0.98 %), followed by ripe fruits (0.50 %) and in smaller proportion in flowers (0.09-0.24 %).
Although alkaloids are found throughout the plant, the highest concentration occurs in the fruits.A few grams of green fruits would be enough to cause the death of a human being.
Ruminants, horses, donkeys and birds are not very sensitive, but it is a violent poison for rabbits and carnivores. In humans, its ingestion causes digestive disorders (especially when the root is used), dizziness and headache, paresthesia, lowering of body temperature, reduction of muscle strength, and finally an ascending paralysis during the following hour. Death may occur due to seizures and muscle destruction leading to renal failure, or due to alterations in breathing (accelerating it at first and then depressing it), which would lead to death by asphyxia.
Generally, intoxications are caused by confusion with other edible umbelliferae (carrot, parsley, anise) or by the consumption of animals that have fed on this plant.
Generally, the morphological examination is conclusive: purplish spots on the ribbed stem, and odor (when it is worn, the plant gives off an unpleasant odor that is also perceptible in the urine and ruminant fluid of intoxicated animals). When the fruit is available, the two mericarps, each with five protruding primary ribs, are examined. The absence of vitas and external albumen is noted. The endocarp is surrounded by a row of horseshoe-shaped sclerified cells. The research and the amount of alkaloids can be done by classical procedures but taking into account the volatility of these simple piperidines (coniine is extractable by steam current). Gas chromatography and mass spectrometry are generally used to determine these molecules in plants or biological media. The consumption of 6-8 g of leaves can cause the death of an adult in a few hours.
The symptomatology can be established from the descriptions in classic treatises on toxicology. The first symptoms appear quickly: salivation, nausea, vomiting, pharyngeal irritation, intestinal pain. The intoxicated person is thirsty, swallows and speaks with difficulty and has dilated pupils. The lower limbs weaken, renal failure is added and a progressive muscular paralysis begins, ultimately affecting the respiratory muscles, and the patient dies of asphyxia. Consciousness is not altered at any time, although vision and hearing disorders are noted. Convulsive tremors and disordered movements of the limbs may occur. Whatever the small differences reported by the various authors, this symptomatology differs significantly from that which preceded the death of Socrates, only ascending paralysis that led to a peaceful and dignified death. Some hypothesize to explain these divergences that the cup presented to the philosopher contained a mixture of hemlock and opium and the latter attenuated some of the effects of the coniine.
The most recent observations indicate a dominant “lethargic” component in the symptomatology. In the first case, in a 4-year-old boy who had consumed leaves containing 0.85 mg/g of γ-conicein, rapid numbness was recorded, 30 minutes. Two hours later the child vomited in bed and continued to sleep. Stimulation of his lower limbs elicited only a very small response; after digestive decontamination, nociceptive sensitivity continued to decrease for 90 minutes, after which the child progressively recovered. In the same year a second observation reports the “numbness” of a three year old boy and his death two hours and forty minutes after ingestion at autopsy, his stomach contained 142 g of plant material. Another study carried out at the toxicological center of Angers, has recorded a beginning of intoxication caused by the ingestion of a teaspoon of coffee of green fruits of hemlock. The patient, a psychopath, presented with visual disturbances, limb ataxia, difficulty walking and muscle weakness in the hands. He was subjected to respiratory ventilation and extubated after 48 hours.
There are no specific antidotes against coniine. Gastric emptying is performed with subsequent administration of activated charcoal. If seizures occur, a benzodiazepine will be administered. Forced diuresis is recommended and renal function will be monitored. Assisted ventilation and oxygen therapy are also usually necessary. The prognosis is very serious if the patient is not treated quickly. If the critical phase is overcome, improvement is rapid and complete, although myasthenia persists for a few weeks.
Cases of poisoning, often severe, have been reported for most animal species: pigs, cows, horses, sheep, goats, rabbits, turkeys, elk. Intoxicated animals insalivate abundantly. After a transient phase of excitement, they become apathetic and non-toxic, their pupils dilate, they urinate and defecate frequently, they have a weak pulse, their membranes become cyanotic and breathing is difficult. They have great muscular weakness: the animal lies down altered and cannot get up, and also shows tremors and tearing. Death, due to respiratory paralysis, is not preceded by convulsions. The sensitivity of the species to coniine is very variable: severe symptoms appear with 3.3 mg/kg of alkaloids in cows and with 15.5 mg/kg in donkeys, while in sheep 44 mg/kg do not cause more than mild intoxication. Depressions and flaccid paralysis have also been observed in birds such as chickens, turkeys and quails. In the case of females eating hemlock, it can cause congenital malformations, especially in calves and piglets. This toxicity of hemlock and coniin to fetuses has been studied experimentally in sheep (in which minor effects are rapidly reversed), sows and cows. Without going into details, it is pointed out that these malformations, as a consequence of the reduction of fetal movements, are only induced when the repeated ingestion of the plant takes place during a certain period of gestation (from 55 to 75 days in the cow and from 43-53 days in the sow). The malformations observed are mainly joint malformations such as scoliosis, arthrogryposis (making it impossible to stand upright). Early administration to sows (3 to 45 days) causes cleft palate in piglets. Finally it is important to note that teratogenicity depends on total alkaloid content and composition with an important role of γ-conicein.
Accidental poisoning may occur because of its resemblance to celery, parsley and other plants that serve as food or condiment, although there are differences between these plants and hemlock, such as size, distinctly unpleasant odor (parsley has a characteristic pleasant odor) and red spots on the stems, always absent in parsley.
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