Definition• A substance which• when taken or• administered into body in whatever manner or• form other than therapeutic amounts,• causes disturbances of function• which may result in illness or death.
Thevetia peruviana Yellow Oleander KaneruNerium oleander Pink Oleander Kaneru White OleanderStrychnos nux vomica Bitter Nut Goda KaduruPagiantha dichotoma Eve‟s Apple Divi KaduruCerbera manghas Sea Mango Diya kaduruRicinus communis Castor bean Thel / Beheth Endaru Weta EndaruDatura stramonium Thorn Apple / Angels Kalu Aththana TrumpetAdenia palmata HondalaGloriosa superba Glory Lily NiyangalaAbrus precatorius Black-eyed Susan / Rosary Olinda pea / Precatory bean
Scientific name: Gloriosa superbaSinhala name: NiyangalaTamil: Karththigaikkilangu, IllangalliEnglish/common names: • flame lily, glory lily, tiger clawPlant habitat: • native of tropical Africa, India, Malaya, etc • found in low country Sri LankaTraditional use: • tuber – bruises and sprainsPoisonous parts of the plant: • The entire plant, especially the tubers, are extremely poisonous
Main toxic constituents: – colchicine (+ „gloriosine‟ in tubers)Constituent type: alkaloidMode of action: • Colchicine has an antimitotic effect – It stops cell division by disrupting the spindle apparatus during the metaphase – Cells with rapid turnover are affected (bone marrow, intestinal epithelium, hair-producing cells -> hair loss) – It can alter neuromuscular function – (It can withstand drying, storage and boiling - tubers not a foodsource!)Clinical features of poisoning: • Initial symptoms develop within 6-12 hours of ingestion – burning pain, numbness, itching and tingling around the mouth and throat with thirst – nausea, intense vomiting – abdominal pain, severe diarrhoea with blood and mucus • These lead to – electrolyte imbalance, dehydration, hypovolaemic shock manifested hypotension and tachycardia
• After 24 hours patients develop – Muscle weakness, myoglobinuria, bronchial constriction, leucopenia, thrombocytopenia, clotting defects with bleeding, polyneuropathy cardiac arrhythmias, hepatic insufficiency, acute renal failure • In severe cases there may be – Respiratory depression, confusion, delirium, convulsions, coma • Death occurs due to shock or respiratory failureDiagnosis: • Toxicological, biomedical, blood gas, haematological analysesTreatment of poisoning: • hospitalize the patient immediately • induce vomiting (ipecac) / gastric lavage • give repeated activated charcoal • supportive care eg IV fluid, assisted ventilation may be neededReferences: Jayaweera DMA. Medicinal plant use in Ceylon - Part 3.Colombo: The National Science Foundation, 2006;http://www.inchem.org/documents/pims/plant (Accessed 4 July 2008];Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: SriLankan College of Paediatricians, 2006
Thevetia peruvianaFamily: ApocyanaceaeSinhala name/s: kaneruTamil name/s: manjal alariEnglish/common name/s: yellow oleander, lucky nutPlant habitat: • often used for hedging in Sri Lanka • native of Central & S.America but now grown throughout tropical and subtropical regionsToxic part of the plant: seed (although all parts toxic)Lethal dose: kernel of one fruit (or 2 leaves for a child)Main toxic constituent/s: thevetin A, thevetin BConstituent type: cardiac glycosidesMode of action: inhibit sodium-potassium ATPase • increased intracellular sodium and serum potassium • negative chronotropic, positive inotropic effects
= DigoxinDigoxin K+ 2 [K+]Phase 2 3 [Na+] Na+ Ca2+ Ca2+ 2+ Ca Ca2+2+ Ca2+ SR (Mitochondria) Ca 2+ 2+ 2+2+ 2+ Ca Ca Ca Ca2+ 2+ Ca2+ 2+ Ca Ca Ca 2+ Ca 2+ Ca Ca Ca2+ Ca2+ Ca2+2+ Ca2+ Ca2+ Ca2+ Ca 2+ 2+ Ca 2+ Ca 2+ Ca Ca2+ Ca 2+ Ca Therapeutic & Toxic MoA
Clinical features of poisoning: “digoxin-like” • Early on: burning sensation in mouth, tingling of tongue, dry throat, giddiness, nausea vomiting, diarrhoea • Cardiovascular: sinus bradycardia, first and second degree heart block, junctional rhythms, atrial and ventricular extrasystoles, ventricular fibrillation • Other: yellow vision, anxiety, convulsions, coma Diagnosis: • cardiac glycoside blood levels • seed remnants, vomitus, gastric aspirate may help identify • monitor serum potassium and electrolytes Treatment of poisoning: • induce emesis at home (ipecac) • gastric lavage within 1 hour or activated charcoal • atropine 0.5mg IV for bradycardia, repeated • cardiac pacing for third degree heart block • anti-digoxin Fab antibodies in severe casesReferences: Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College ofPaediatricians, 2006; IPCS Inchem. Thevetia peruviana. Dated March 1990 [Accessed athttp://www.inchem.org/documents/pims/plant on 29 June 2008]; www.wikitox.org
Scientific name : Strychnos nux-vomicaSinhala name : Godakaduru, Visha kaduruTamil name : Eddi, Etti, KagodiEnglish/common name : Poison nut, Nux vomica, bitter nutPlant habitat dry forests of Ceylon, flowers in August A moderate sized or large tree with an erect trunk, Slide 5 Bark Wood Leaves Flowers FruitTraditional use : Root - cures fever and bites of venomous snakes Used for preparation of homeopathic medicineToxic part of the plant : seed (although all parts toxics)
Main toxic constituents : strychnine, (brucine)Constituent type : alkaloids.Lethal dose : plant poisoning is rare possibly due to bitter taste The quantity of strychnine in one seed could be fatal If seeds are swallowed uncrushed they are not poisonousMode of action : Strychnine is a potent convulsant. It causes increased reflex excitability in the spinal cord Brucine – resembles strychnine activity but it is less potentClinical features of poisonings : Symptoms appear within 15 - 30 min of ingestion - Initial symptoms – bitter taste in mouth, feeling of suffocation - Twitching of the muscles in neck, body and limbs - Extreme contractions affecting all muscles in the body - The patient is conscious and has intense pain. - Complications - lactic acidosis, rhabdomyolysis, acute renal failure - Death is caused by asphyxia or muscular paralysis
Diagnosis : Based on history of ingestion and development of muscular stiffness Strychnine (and brucine) can be measured chemically but there is no time to perform this procedure before treatment Measure acidosis, serum potassium, SGOT, LDH, CPK etcTreatment of poisonings : Activated charcoal Support respiratory and cardiovascular functions If convulsions cannot be controlled with diazepam (IV or rectal), or if they recur, administer phenobarbitone or phenytoin. Intubation with suxamethonium chloride may be necessary When convulsions and hyperactivity are completely controlled, gastric lavage can be performed safelyReferences : http://www.inchem.org/documents/pims/plant [accessed 29 June2008]; Jayaweera DMA. Medicinal plant use in Ceylon - Part 3. Colombo: TheNational Science Foundation, 2006; Lucas GN, De Silva TUN. Poisonousplants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006
Scientific name: Ricinus communis Linn.Synonyms: Ricinus africanus Willd., Ricinus communis L. var. viridis (Willd.) Müll. Arg., Ricinus inermis Jacq., Ricinus lividus Jacq., Ricinus macrocarpus G. Popova, Ricinus microcarpus G. Popova, Ricinus persicus G. Popova, Ricinus speciosus Burm., Ricinus viridis Willd., Ricinus vulgaris Mill., Ricinus zanzibaricus G. Popova, Croton spinosusFamily: Euphorbiaceae (spurge family)Sinhala name/s: Erandu, Tel-erandu, beheth endaru, thel endaruTamil name/s: Amanakku, Muttu-kottai, AndagamEnglish/common name/s: castor bean, castor-oil plant, Palma ChristiiPlant habitat: Cultivated as a decorative plant in village gardens in Sri lanka Probably of African origin but now grows in tropical, subtropical and temperate areas Commercially cultivated mainly in Brazil, India, Italy, etc.Traditional use: In Sri lanka the root of the plant is used in pleurodynia (muscular rheumatism) and rheumatic pains while seeds are used for lumbago and sciatica Africans use the bark for stitching up wounds & as a dressing for sores Local application of fresh leaves to the lactating breast is said to produce a powerful galactogogic action. They are also used headaches The root is a remedy for abdominal pains and diarrhoea while root bark (and seed oil) is a purgative also used for skin diseases and sores
Toxic part of the plant: seeds are the most toxic part (leaves are also poisonous)Lethal dose: 1mg/kg pure ricin in man • Ingestion of a single well chewed bean has caused death • 1-3 seeds can be fatal to a child • 2-4 seeds cause severe poisoning in an adult • poisoning is unlikely if seeds are swallowed without chewingMain toxic constituent/s: RicinConstituent type: Glycoprotein or a toxalbumin • member of a class of plant toxins known as type 2 ribosome inactivating proteinsMode of action: Ricin impairs chain elongation in protein synthesis, causing cell death and tissue damageClinical features of poisoning: Early on - burning sensation of the mouth and throat occurs After 3-6 hrs - nausea, vomiting, severe abdominal pain and diarrhoea resulting in dehydration electrolyte imbalance and shock Cardiovascular - hypotention, tachycardia, ECG changes and circulatory failure Other - prostration, blurring of vision, loss of consciousness, convulsions, haemolysis, uraemia and liver necrosis
Diagnosis: Blood gases and electrolytes analysis Close monitoring of renal, hepatic hematological systems & blood clotting. Botanical & pharmacognostical identification of a sample of the plant or vomitus Radioimmunoassay with antiricin antibodies labeled with iodine 125 for ricin in plasma or urineTreatment of poisoning: Induce emesis at home (ipecac) Immediate gastric lavage or activated charcoal Correct fluid & electrolyte imbalance immediately In case of bronchial asthma, oxygen, B2-agonist eg salbutamol and corticosteroids may be necessary (if acute poisoning occurred by inhalation) Antihistamines or corticosteroids may be beneficial in treating skin lesions (if acute poisoning occurred by skin exposure) References: Jayaweera DMA. Medicinal plants used in Ceylon. Part 2. Colombo: The National Science Foundation, 2006 http://www.inchem.org/documents/pims/plant.htm www.wikipedia.org Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006
Plant habitat:Native to China, India and South East Asia. It is a common weed in waste and cultivated land in Sri-lanka and now it is used in landscaping and gardening .Plant description: Shrub-like annual herb with large flowers, typically white or yellow with deep purple accents. Leaves are alternate and simple.Traditional use: Leaves/dried flowers are used to relieve asthma or wheezing like symptoms in many cultures eg Chinese herbal medicine (yáng jīn huā). Leaf poultices are applied to engorged breasts to relief excess milk production, rheumatic swelling of joints and lumbago. Powdered root is rubbed into gums or stuffed into cavities for toothache.Toxic part of the plant : all parts.Main toxic constituents : tropane alkaloids
Leaves/flowers - mainly atropine Seeds/roots - mainly hyoscyamine Fruits – scopolamineDose: Accidentally (or intentionally) ingesting even a single leaf could lead to severe side effectsSymptoms: anticholinergic Thirst, dry mouth, blurred vision, photophobia, urinary retention occur soon after ingestion. Skin is hot, dry and flushed. Pupils are dilated and fixed. Cardiovascular effects are sinus tachycarida, hypertension, supra/ventricular arrhythmias, orthostatic hypertension. Severe poisoning causes disorientation, agitation, violent behaviour, convulsions, delirium, visual and auditory hallucinations, ataxia, respiratory depression, coma.
Mode of action: It stimulates the central nervous system and simultaneously depresses peripheral nerves and dilates the pupils by peripheral action. The most probable action in this case is paralysis of the occulomotor nerve ending or its myoneural junction.Treatment of poisoning: Ipecac to induce emesis or gastric lavage. Activated charcoal to reduce absorption of toxic substances. Catheterization to empty bladder if necessary Diazepam for hallucinations and delirium.References:• www.wikipedia.org/wiki/Datura_metel• www.ces.ncsu.edu/depts/hort/consumer/ poison/Daturme.htm• www.people.vcu.edu/~asneden/tropane%20alkaloids. pdf• waynesword.palomar.edu/ww0703.htm• DMA Jayaweera. Medicinal plants used in Ceylon Parts 1-5. Colombo: National Science Foundation, 2006• Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians,
Adenia palmata• Synonyms: Adenia hondala, Granadilla hondala, Modecca palmata• Family: Passifloraceae• Sinhala name/s: hondala• Tamil name/s: kondala• English/common name/s: ?• Plant habitat: • large aerial plant climbing by tendrils attached to large trees growing in the wet and dry zones along forest edges• Traditional use: ?• Toxic part of the plant: fruit (which closely resembles passion fruit -> accidental ingestion by children)• Lethal dose: ?• Main toxic constituent/s: a cyanogenic glycoside, a toxalbumin and emulsin (an enzyme)• Constituent type: cyanogenic glycoside
• Mode of action: • 1st phase – hydrocyanic acid • 2nd phase – local toxalbumin effects • 3rd phase - hypersensitivity reaction • Clinical features of poisoning: • 1st phase – vomiting, fever, restlessness, dizziness, disorientation, abdominal pain and diarrhoea within one hour • 2nd phase – necrotising enteritis -> diarrhoea with blood and mucus, abdominal colic and right iliac fossa tenderness after a variable period of time • 3rd phase – myocarditis with ECG changes, tender hepatomegaly, retinopathy with papilloedema, exudates and haemorrhages may be seen 2- 3 weeks after ingestion – all transient • Diagnosis: • cardiac glycoside blood levels • seed remnants, vomitus, gastric aspirate may help identify • monitor serum potassium and electrolytes • Treatment of poisoning: • if no vomiting occurs induce emesis with ipecac syrup or perform gastric lavage • activated charcoal will help with the absorption of toxic substances • IV fluid therapy may be needed • antidotes for cyanide poisoning not usually necessary • blood transfusion may be necessary in the 2nd phaseReference: Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006
Abrus precatoriusBlack-eyed Susan / Rosary pea / Precatory bean [Olinda]
Manihot utilissima• Scientific name: Manihot utilissima•Synonyms: Jatropha manihot (Kunth), Manihot manihot (Cockerell), Manihot melanobasis (Muell)•Family: Euphhorbiaceae•Sinhala name: "Manyokka"•Tamil names: “Maravalli” “Alavalli”•English /common name: cassava, manioc, tapioca•Plant description: shrub with a big tuberous root•Plant habitat: The sweet and bitter cassava plants are indigenous toSouthern and Central America but have been introduced to almostall tropical countries•Traditional use : Used as a food source. American Indians use thebrown juice for burns By : J.S.R.Sherif E.M.A.K.Ekanayaka
Toxicity of the plant : The leaves and roots contain free and bound forms of thecyanogenic glycoside linamarin, which is converted to cyanide in the presence oflinamarinase, a naturally occurring enzyme in cassava or via exposure to theatmosphere. (Slide 5)Two varietiesSweet - contains as little as 20 milligrams of cyanide (CN) per kilogram of freshrootsBitter - may produce more than 50 times as much (1 g/kg)The paralytic neurological disease caused by long-term consumption of cassava iscalled mantakassa. Yam that is cut, washed and boiled in an open container at72°C for long enough will destroy the enzyme and any hydrocyanic acid formed willevaporate.•Lethal dose : One dose of pure cassava cyanogenic glucoside (40mg) issufficient to kill even a cow. Hence about 300 grams of fresh root is enough to killan adult human and about 125 grams of fresh root would be enough to kill a child•Mode of action :A "large" sudden dose (HCN) is highly poisonous to all humans and animalsbecause it rapidly inactivates cellular respiration thereby causing death. This meansthat it stops cells from being able to use oxygen. The heart, respiratory system andcentral nervous system are most susceptible to cyanide poisoning and cease tofunction as a result of lack of oxygen.
Clinical features of poisoning : Acute: Within 3-6 hours of ingestion burning epigastric pain, vomiting, flushing of skin, dry mouth, tachycardia, pupil constriction, restlessness, giddiness and hallucinations occur. Chronic: initial symptoms are described as tremor, cramps, a heavy feeling and/or weakness in the legs, a tendency to fall down and difficulty remaining upright There is a visible hypertonic gait when walking or running Occasionally there will be lower back pain, blurred vision, speech difficulties and/or paresthesia of the legs, but they disappear within a month, later some people will develop dysarthria, abnormalities of eye movement, hypertonicity of the arms •Diagnosis Acute poisoning: signs of extreme metabolic acidosis Chronic poisoning: a visible hypertonic gait when walking or running, bilateral brisk knee and Achilles tendon reflexes without signs of vertebral lesions The onset of the disease takes less than one week and then remains stable Urinary concentrations of (thiocyanate and linamarin are elevated) (Cyanide (CN-) is normally converted thiocyanate (SCN-) by the enzyme rhodanase) •Treatment of poisoning There is no known treatment for cyanide poisoning . Treatment with sodium thiosulphate (Na2S2O3), a cyanide antidote, gave disappointing results. A good and varied diet, high dose multivitamins (specially B12 ,it detoxifies the HCN) and physical rehabilitation are advised.References Affran DK. Cassava and its economic importance. Ghana Farmer 1968; 12(4): 172-178; Bellotti AC et al. Recent advances in cassavapest management. Ann Rev Entomol 1999; 44: 343-370; Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of