Faudzil @ Ajak

Faudzil @ Ajak
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Showing posts with label HEALTH - POISON. Show all posts
Showing posts with label HEALTH - POISON. Show all posts

7 November 2014

POISONOUS PLANT - Aconitum napellus, monkshood





Summary

This popular garden plant is one of the most poisonous plants in the garden but it has such a distinctive and unpleasant taste that cases of accidental poisoning are extremely rare though not unknown.

Family

Ranunculaceae

Meaning of the Name

AconitumAccording to Theophrastus, the name comes from the village of Akonai which was part of the land occupied by the Mariandynoi people.  There is no trace of the village today but the area, which is now in Turkey, has a town called Karadeniz Ereğli near to which is a cave which was said to house the entrance to Hades and was guarded by Cerebus.

Other sources suggest the Greek word ‘akónitos’ formed from ‘ak’, ‘pointed’ and kônos, ‘cone’. The suggestion is that the name refers to the pointed leaves though some sources say a pointed cone is an arrow and refers to its use as an arrow poison.

Napellus
From the Latin 'napus', 'turnip' thus ‘like a small turnip’ referring to the shape of the root.

Common Names and Synonyms

Monkshood, European monkshood, tiger's bane, dog's bane. Many other names associated with its helmet shaped flower such as soldier's helmet, old wife's hood and October stormhatt in Scandinavia.

Mousebane is used to refer to its alleged ability to kill mice just from the smell. Also sometimes called wolfsbane, though this is mostly applied to Aconitum lycoctonum.

How Poisonous, How Harmful?

The principal alkaloids are aconite and aconitine. Of these aconitine is thought to be the key toxin. Ingestion of even a small amount results in severe gastrointestinal upset but it is the effect on the heart, where it causes slowing of the heart rate, which is often the cause of death.

The poison may be administered by absorption through broken skin or open wounds and there are reports of florists being unwell after working with the flowers but there are no documented cases.

Its distinctive taste makes it unpleasant to eat so accidental poisoning is extremely rare but not unknown. The taste is described as initially very bitter followed by a burning sensation and, then, a numbing of the mouth.

Incidents

In July 2014, I was contacted by someone whose small terrier had died after eating some of the root. The dog had buried a bone at the base of the plant and is thought to have scratched at the root when retrieving it. It is not clear whether the owner had bought the plant from somewhere other than an HTA member garden centre or whether the warning required by the HTA list of potentially harmful plants had proved inadequate.

A rising young Canadian actor, Andre Noble, accidentally ate monkshood on 30th July 2004 whilst on a camping trip. He is said to have believed he was eating wild parsnip.

Until recently, the only well established case of murder with aconitine was in 1881 when Dr. Lamson used it to poison his brother-in-law after putting it in the newly invented soluble capsules for taking medicine without having to taste it. The 'yuck' inducing details of how Dr. Lamson was convicted form one of the highlights of the Medical Murderers talk.

In February 2010, Lakhvir Singh was convicted of the murder of her lover, Lakhvinder Cheema, who died after eating a curry to which Ms Singh had added the extract of Aconitum ferox, known as Indian monkshood or Himalayan monkshood. His new fiancée, with whom he shared the meal, became very ill but recovered. Media reports have described the poisoning agent as aconitine but the primary alkaloid in Aconitum ferox is pseudoaconitine, sometimes called Indian aconite.

Gurjeet Choongh, who survived the poisoning, told the court that Mr Cheema said that he felt numb and 'everything was going dark'. Mr Choongh, who ate less of the leftover curry, later began experiencing similar feelings as well as abdominal pain. The two were treated in hospital but it was not possible to save Cheema. Both experienced severe vomiting and the tachycardia expected in Aconitum poisoning but no aconitine was found. One of those involved in the case had read an 1845 publication about Aconitum napellus that had mentioned 'far-eastern' species and noted that these might have different effects. When an herbal remedy was found in the killer's possession, tests showed that it contained pseudaconitine and this alkaloid was also found in the victims.

Aconitum napellus, monkshood

Aconitum napellus, monkshood
Again in February 2010, a case was reported from India of a 62-year old man given a herbal remedy for diarrhoea who suffered severe heart problems. Analysis showed that the remedy contained roots from an unidentified species of Aconitum.
In 1996, a 61 year old man died after eating the leaves of Aconitum thinking it was an edible grass.

The 2002 annual meeting of the North American Congress of Clinical Toxicology heard a case report of a 36-year old man who ate an estimated 30gms of crushed root, believing it would reduce his neuropathic pain. He had heart palpitations and chest discomfort but no vomiting. He recovered after 24 hours of treatment to control ventricular tachycardia. The fact that such a large dose can have such a relatively small effect illustrates the difficulty of answering the question 'How much would it take to kill?' when applied to any poisonous plant.

In 2005, a 21-year old man made up his own capsules of crushed Aconitum root which, he believed, would work as 'natural' sleeping tablets. He suffered all the classic symptoms of monkshood poisoning but recovered after two days in the hospital ICU.

A couple thought it looked so lovely they planted it to brighten up their herb garden. When the wife picked a herb leaf salad she, accidentally, included some leaves from the monkshood and both suffered severe stomach upsets lasting two days.

These last two prove a point which was contentious for a long time. Many people said that it was only the root which was poisonous and not the leaves. Even today, it is possible to find poison plant listings that say the root is the only toxic part.

William Rhind was a 19th century Scot who trained and practiced as a doctor before turning his attention to studying and writing about natural history in all its forms. In his ‘History of the Vegetable Kingdom’ he cites a case in Sweden, though without giving a date, where a man exhibited maniacal symptoms after eating fresh leaves of the monkshood. A doctor, summoned to assist him, expressed the view that the plant could not be the cause of his disorder since it was only the root which was toxic and ate freely of the leaves to prove his point. He died in dreadful agony. Rhind, sadly, does not say what became of the patient.

Folklore and Facts

The confusion which common names can cause is well illustrated by this plant. People ask if winter aconite is as poisonous as the monkshood or wolfsbane. Winter aconite is Eranthis hyemalis which, although it is member of the Ranunculaceae family and should contain protoanemonin, is not thought of as a poisonous plant.

Aconitum napellus, monkshood, foliage

Aconitum napellus, monkshood, foliage
Either this or the A. lycoctonum were used by the aboriginal peoples of the Kamchatka peninsula, Kurile, Kodiak and Aleutian islands in the far north Pacific Ocean to poison whales. They would row out in small boats and get close enough to a whale to stab it with a short harpoon. The shaft would be broken off leaving the poisoned head imbedded and the hope was that the dead whale would wash up on shore a couple of days later. The harpoon heads were carved with a 'signature' of the individual whalers so that the washed up whales could be properly attributed.

Details are limited as the use of the poison was kept a close secret. The ability to kill whales gave the hunter great status in the community and a dead whaler would often be rendered down so that his body fat could be applied to the harpoon heads to pass his skills onto his successor.

It was used to poison arrows in ancient China but not just the tips. The shafts would be smeared with a paste made from the plant in the hope that anyone attempting to remove an arrow from a wounded soldier would absorb the poison.

There are stories of its being used to poison water sources. Mostly, these were those water sources passed by a retreating army anxious to dissuade pursuit. There is no evidence of mass poisonings resulting from this use which leads me to think it may have been the taste which made it so attractive. By making it obvious that the water had been poisoned, it might be expected that a pursuing army would abandon the chase after realising that there would be no drinkable water if they continued.


Source: http://www.thepoisongarden.co.uk/atoz/aconitum_napellus.htm



ACONITE PLANT - Aconite poisoning.




Chan TY

Abstract


INTRODUCTION:

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.

METHODS:

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.

MECHANISMS OF TOXICITY:

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.

CLINICAL FEATURES:

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:

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.

CONCLUSIONS:

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.

Comment in

  • SDH, CCO and PKCα are the direct targets of aconitine? [Med Hypotheses. 2012]
  • Aconitine poisoning from leaves of aconitum pseudo-leave var. erectum, not the root in humans. [Clin Toxicol (Phila). 2009]
PMID:
 
19514874
 
[PubMed - indexed for MEDLINE]



Source: http://www.ncbi.nlm.nih.gov/pubmed/19514874


SHOCKING - Gardener, 33, died 'after brushing against highly poisonous plant' while working at businessman's £4m estate





Gardener, 33, died 'after brushing against highly poisonous plant' while working at businessman's £4m estate


  • Nathan Greenaway was the gardener at £4million estate in Alton, Hampshire 
  • The 33-year-old mysteriously fell ill and later died from multiple organ failure
  • Inquest heard death was 'more likely than not' caused by poisonous plant 
  • Poisioning from aconitum can occur if ingested or handled without gloves



A 33-year-old gardener who tended the manicured lawns and flower beds on a businessman's £4million estate died after apparently handling a highly-poisonous plant, a coroner heard.

Nathan Greenaway was one of several staff employed at Millcourt House, in the exclusive Upper Froyle near Alton, Hampshire, which is owned by former venture capitalist Christopher Ogilvie Thompson and his wife Katherine.

The groundsman, from Aldershot, was experienced at looking after the gardens at the mansion but collapsed and died after apparently brushing against the deadly flower aconitum - also known as devil's helmet and monkshood - which was growing in the grounds.


Nathan Greenaway, 33, from Aldershot, died from multiple organ failure after allegedly brushing against the poisonous aconitum plant at Millcourt House, in the  Upper Froyle near Alton, Hampshire
Nathan Greenaway, 33, from Aldershot, died from multiple organ failure after allegedly brushing 
against the poisonous aconitum plant at Millcourt House, in the Upper Froyle near Alton, Hampshire

A pre-inquest hearing in Basingstoke, Hampshire, was today told that Mr Greenaway died in hospital from multiple organ failure.

After mysteriously falling ill in September, the gardener was taken to hospital but despite frantic analysis of his blood, doctors were unable to diagnose him. He died of multiple organ failure five days later.

The coroner heard that it was only after his devastated father, Richard Greenaway, carried out hours of tireless research in an effort to find out what happened, that the link with the aconitum plant became apparent.

North Hampshire coroner Andrew Bradley heard a report from histopathologist Asmat Mustajab, who concluded it was 'more likely than not' that Mr Greenaway died after coming into contact with the deadly purple flowering plant.

Mr Greenaway was employed by South African-born Mr Ogilvie Thompson and his wife to maintain the manicured gardens of their sprawling estate.

Millionaire Mr Ogilvie Thompson is a consultant for high-end technology companies and formerly worked as venture manager for operations at Element Six Ventures, a fund focusing on early and growth phase investments in material science companies.

The inquest was told that the gardener was thought to have handled the highly-toxic plant, which is a member of the buttercup family of ranunculaceae, while working on the estate. He died on September 7.

Poisioning from the aconitum plant can occur if it is ingested or handled without gloves.

In severe cases, the poisoning causes heart arrhythmia, paralysis of the heart and respiratory problems. Other symptoms include vomiting, dizziness and diarrhoea.

Aconitum is also known as monkshood and devil's helmet due to its resemblance to a drawn hood, and is known by some as wolfsbane, because its poison is so toxic that it was once used to kill wolves.


The aconitum plant, which is also known as monkshood and devil's helmet, can cause heart arrhythmia, paralysis of the heart, vomiting, dizziness and diarrhoea if it is ingested or if it is handled without gloves
The aconitum plant, which is also known as monkshood and devil's helmet, can cause heart arrhythmia, paralysis of the heart, vomiting, dizziness and diarrhoea if it is ingested or if it is handled without gloves


The attractive plant has been responsible for several high-profile human deaths, including that of Canadian actor Andre Noble, who died on a camping trip in 2004 after accidentally consuming the plant.

In 2009 Brit Lakhvir Singh, dubbed the 'curry killer', poisoned her lover Lakhvinder Cheema with a curry dish laced with Indian aconite, from the same plant family.

Barrister Tim Sharpe, representing the Ogilvie Thompsons, told the pre-inquest that an expert on plant toxicology was needed to establish whether or not coming into contact with aconitum was the definitive reason for Mr Greenaway's death.

Coroner Mr Bradley said that, while blood samples taken after Mr Greenaway's death were still available for analysis, the sample taken at the time of his admission had since been destroyed.

Dr Maggie Bloom, representing the family of Mr Greenaway, said: 'There's even a note in the medical records where it says all samples are to be retained.'

The hearing was also told that the plant's deadly toxin works so quickly that it would have caused huge damage to Mr Greenaway's internal organs within hours and would have been out of his blood system altogether within a day.


The inquest heard  Mr Greenaway worked at the £4million estate of Christopher and Kathy Ogilvie Thompson
The inquest heard Mr Greenaway worked at the £4million estate of Christopher and Kathy Ogilvie Thompson


Nathan Greenaway worked at the £4million Millcourt House estate in Upper Froyle near Alton, Hampshire
Nathan Greenaway worked at the £4million Millcourt House estate in Upper Froyle near Alton, Hampshire



The Grade II-listed Georgian house lies at the heart of a complex of outbuildings, cottages and tennis courts


The gardener's widow, Tegan, and his parents, Richard and Marian, listened intently to the proceedings with other members of the family.

Addressing them at the end of the hearing, Mr Bradley said: 'I'm sorry that we are not progressing this today. I am acutely aware of the difficulties that go with these cases and we will achieve what we can.'

Mr and Mrs Ogilvie Thompson's Grade II-listed Georgian house lies at the heart of a complex of outbuildings, staff cottages and tennis courts at the end of a long gravel drive, next to the River Wey.

At the back there is a veranda with seating room for at least a dozen guests.

A member of staff, who asked not to be named, today described Mr Greenaway as 'a really nice guy who was really good to work with.'

Mrs Ogilvie Thompson said the couple did not wish to comment on the inquest or the circumstances leading to their gardener's death. 





Source: http://www.dailymail.co.uk/