1. S2 L7-8 Poisonous plants of
Sri Lanka
Anna Drew
& Peradeniya University BPharm Batch 2005/6
(8 July 2008)
with slide contribution from: Ruben Thanacoody, www.wikitox.org

2. Paracelcus 1493-1541
“All substances
are poisons; there
is none which is
not a poison. The
right dose
differentiates a
poison from a
remedy.”

3. Thevetia peruviana
Family: Apocyanaceae
Sinhala name/s: kaneru
Tamil name/s: manjal alari
English/common name/s: yellow oleander, lucky nut
Plant habitat:
• often used for hedging in Sri Lanka
• native of Central & S.America but now grown throughout tropical and
subtropical regions
Toxic 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 B
Constituent type: cardiac glycosides
Mode of action: inhibit sodium-potassium ATPase
• increased intracellular sodium and serum potassium
• negative chronotropic, positive inotropic effects

4. Na+
/K+
ATPase
3 Na3 Na++
2 K2 K++
Representative Cardiac CellRepresentative Cardiac Cell
NaNa++
channelchannelNaNa++
channelchannel
Voltage dependentVoltage dependent
L-typeL-type CaCa2+2+
channelchannel
Voltage dependentVoltage dependent
L-typeL-type CaCa2+2+
channelchannel NaNa++
/K/K++
ATPaseATPaseNaNa++
/K/K++
ATPaseATPase
NaNa++
/Ca/Ca2+2+
exchangerexchangerNaNa++
/Ca/Ca2+2+
exchangerexchanger
SR (Mitochondria)SR (Mitochondria)
Heart muscleHeart muscleHeart muscleHeart muscle
KK++
channel(s)channel(s)KK++
channel(s)channel(s)
Na+
/Ca2+
Antiporter
Ryanodine receptorRyanodine receptorRyanodine receptorRyanodine receptor
3 Na3 Na++
CaCa2+2+
ββ-adrenergic receptor-adrenergic receptorββ-adrenergic receptor-adrenergic receptor

5. 3 Na3 Na++
2 K2 K++
Cell ElectrophysiologyCell Electrophysiology
SR (Mitochondria)SR (Mitochondria)
CaCa2+2+
Phase 2Phase 2
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
3 Na3 Na++
CaCa2+2+

6. 3 [Na3 [Na++
]]
2 [K2 [K++
]]
Therapeutic & Toxic MoATherapeutic & Toxic MoA
SR (Mitochondria)SR (Mitochondria)
CaCa2+2+
Phase 2Phase 2
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
= Digoxin= Digoxin
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
CaCa2+2+
Digoxin
NaNa++
K+K+

7. 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 cases
References: Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of
Paediatricians, 2006; IPCS Inchem. Thevetia peruviana. Dated March 1990 [Accessed at
http://www.inchem.org/documents/pims/plant on 29 June 2008]; www.wikitox.org

8. Datura metel
S.H.T. SUDESHIKA
T.A.D. SANJEEWA

9. Scientific name: Datura metel
Synonyms: Datura fastuosa (L.)
Datura alba (Nees.)
Family: Solanaceae
Sinhala name: Ela-attana
Tamil name: Ayigam
Common names: Devil's trumpet,
downy thorn-apple,
black datura,
angel's trumpet

10. 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 j n hu ).ī ā
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

11. Leaves/flowers - mainly atropine
Seeds/roots - mainly hyoscyamine
Fruits – scopolamine
Dose: Accidentally (or intentionally)
ingesting even a single leaf could
lead to severe side effects
Symptoms: 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.

12. 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, 2006

13. D. Niyangoda
T.A. Ekanayaka

14. Scientific name: Abrus precatorius L.
Synonyms: A.minor, A.pauciflorus
Family: Leguminosae
Sinhala name: Olinda
Tamil name: Adisamiyai
Common names:
• Abrus seed, crabs eye, Indian bead, Indian liquorice, wild liquorice,
lucky bean, prayer or rosary beads, precatory bean, weather plant,
jumble beads, jequirity bean
Plant description: slender perennial twiner
Habitat: grows wild in dry regions of Sri Lanka at low elevations
Traditional use:
• To cure itch, sores and wounds due to bites of dogs, cats and rats
• Leaves: conjunctivitis, painful swellings; ground with lime for acne,
boils, abscesses and tetanus
• Seeds: diabetes, Bright’s disease

15. Toxic part of the plant: seed
• The most poisonous parts of the plant involved in poisoning are the small, scarlet
seeds, that have a black eye at the hilum
Toxicity: One seed well masticated can cause fatal poisoning (adults and
children)
Main toxins: Abrin - concentrated in seeds
Mode of action:
– Abrin exerts its toxic action by attaching itself to the cell membranes
– It has a direct action on parenchymal cells (eg liver and kidney cells) and red
blood cells
Clinical effects:
– Early features of toxicity - burning of the mouth and oesophagus, and
severe gastroenteritis with vomiting, diarrhoea and abdominal pain.
Haematemesis and melaena are less common
– Later - drowsiness, disorientation, weakness, stupor, convulsions, shock,
hepatotoxicity, cyanosis, retinal haemorrhages, haematuria, and acute renal
failure (oliguria) can occur
– (Contact with the eyes can cause conjunctivitis and even blindness)

16. Diagnosis:
– Diagnosis is made by the presence of the typical manifestations following
ingestion: gastroenteritis with risk of dehydration, haematemesis and
melaena. Drowsiness and convulsions may occur.
– Toxicological analysis of body fluids for the poison is not helpful.
– Plant material, seeds or remnants of seeds, vomitus and gastric aspirate
should be collected in clean bottles for identification.
Main risks and target organs:
– The main risk is the severe gastroenteritis leading to dehydration and shock.
Ingested seeds can affect the gastrointestinal tract, the liver, spleen, kidney,
and the lymphatic system.
Treatment:
– Administration of fluids and electrolytes will alleviate dehydration.
References:
Jayaweera DMA. Medicinal plant use in Ceylon - Part 3. Colombo: The National Science
Foundation, 2006
http://www.inchem.org/documents/pims/plant/abruspre.htm [accessed 03/07/2008]

17. Myristica fragrans
M. Jayasinghe
C.M.C. Indrajith

18. Scientific name: Myristica fragrans
Family: Myristicaceae
Sinhala name: Sadikka, Wasawasi (aril)
Tamil name: Adipam, Attigam, Kasam, Sadi, Sadikkay
English/common names: Nutmeg, Mace tree
Plant habitat:
– A native of E.Moluccas and other Indian Islands
– Now cultivated in Sri Lanka, Malaya, Philippines, W.Indies & South America
Traditional use:
– As a spice in foods
– As a traditional medicine for diarrhoea
Toxic part of the plant: seeds (nutmeg) and, to a lesser extent, the aril (mace)
Lethal dose: Humans: 1-3 nutmegs (5-15g) for adults, 2 nutmegs for children
Animals: oral dose of 24mg nutmeg oil per kg body weight
Main toxins: myristicin & elemicin
myristicin

19. Mode of action:
• Elemicin undergoes oxidation of its oleficin side chain to produce TMA
(3,4,5-trimethoxyamphetamine), a psychotropic drug agent
• Myristicin produces MMDA which is metabolised to form TMA. MMDA has a
higher potency than TMA
• Nutmeg has monoamineoxidase inhibition properties and anti-prostaglandin
synthesis effects
Clinical features of poisoning:
• symptoms are usually seen within 3-6 hours after ingestion and vary
according to the dose taken and the variability between different samples of
nutmegs
• intoxication resembles anti-cholinergic intoxication ie profuse sweating,
flushed face, dry mouth, burning epigastric pain, tachycardia, restlessness,
giddiness, hallucinations
• unlike anti-cholinergic symptoms pupils constrict
Diagnosis:
• Blood monitoring (electrolytes, liver enzymes, renal function) and urinalysis
Treatment of poisoning: symptomatic and supportive
• Induce emesis (with ipecac) or gastric lavage
• Activated charcoal
• Diazepam for restlessness or hallucinations
References: http://www.rain tree nutmeg.com/plant images/myristica pic.htm [01.07.2008];
http://www.inchem.org/documents/pims/plants/pim335.htm [1.07.2008]; http://en.wikipedia.org/wiki/ [1 July 2008]
; Jayaweera DMA. Medicinal plant use in Ceylon - Part 3. Colombo: The National Science Foundation, 2006

20. Alocasia macrorrhiza
U.G.W.L.Jayeweera
C.Premely

21. Scientific name: Alocasia macrorrhiza
Synonyms: A.odora, A.commutata, Colocasia
macrorrhiza, Caladium glycyrrhizum,
Philodendron peregrinum, Arum grandiflorum
Family: Araceae (Magnoliophyta)
Sinhala name: Habarala
Tamil name: Parum sembu
English/common names:
giant taro, elephant ear, ape flower
Plant habitat:
• grows in all tropical countries including India,
Sri Lanka, Malaya & Philippines
Traditional use:
• Acrid juice of the leaf gives instant relief to
stings of the giant nettle
• Chopped leaves & roots used as an application
on painful joints
• Cut stem + lime/water applied to dogs bites
• Dried stems for haemorrhoids & chronic fevers
• Crystals destroyed on boiling or roasting so
starch in stem can be used as a foodsource
Flower of the
Alocasia plant
Taro corms

22. • Toxic part of the plant: all parts
• Main toxic constituent/s:
• all parts of the plant contain specialized cells containing bundles of needle-
like calcium oxalate crystals and toxic proteins
• Mode of action:
• When the plant is chewed the sharp crystals injure the mucous membrane
allowing toxic proteins to penetrate
• Lethal dose:
• The extreme oropharyngeal response generally limits the amount of plant
ingested and oxalate absorbed through the oral mucosa is unlikely to cause
systemic poisoning
• Symptoms:
• Eating parts of the plant causes a severe burning in mouth and throat. Other
symptoms may include:
– Redness, swelling, pain, burning pain of the tongue and mucous membranes,
profuse salivation, dysphagia
– Swelling can rarely cause obstruction and respiratory compromise
– Loss of speech may last several days and swelling more than a week
• Treatment of poisoning:
• wipe out the mouth with a cold, wet cloth and give milk to drink
• antihistamines, mouthwashes, antiseptics and steroids may be used
References: http://en.wikipedia.org/wiki/Alocasia [3 July 2008]; Jayaweera DMA. Medicinal plants used in
Ceylon. Part 1. Colombo: The National Science Foundation, 2006; Lucas GN, De Silva TUN. Poisonous plants of
Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

23. NicotianaNicotiana
tabacumtabacum
Sanduni Sudusinge
Uthpala Siriwardhane
Mano Wickramarathne

24. Scientific nameScientific name Nicotiana tabacumNicotiana tabacum
FamilyFamily SolanceaeSolanceae
Sinhalese nameSinhalese name Dum kolaDum kola
Tamil nameTamil name Phaielai
English nameEnglish name TobaccoTobacco
Plant habitatPlant habitat native of tropical and subtropicalnative of tropical and subtropical
America but it is now commerciallyAmerica but it is now commercially
cultivated worldwidecultivated worldwide
Traditional useTraditional use - as an insecticide- as an insecticide
- intestinal worms or constipation- intestinal worms or constipation
- dried tobacco leaves for chewing,- dried tobacco leaves for chewing,
snuffing or smokingsnuffing or smoking
Toxic part of the plantToxic part of the plant leaves, stems, roots and flowersleaves, stems, roots and flowers
Main toxic constituentsMain toxic constituents nicotinenicotine
Constituent typeConstituent type alkaloidalkaloid
Lethal doseLethal dose 0.5-1 mg/kg body weight nicotine (~ 40 - 60 mg)0.5-1 mg/kg body weight nicotine (~ 40 - 60 mg)

25. Mode of actionMode of action
 Nicotine binds stereo specifically to acetylcholine receptors atNicotine binds stereo specifically to acetylcholine receptors at
autonomic ganglia, the adrenal medulla, the neuromuscular junctionautonomic ganglia, the adrenal medulla, the neuromuscular junction
and the brainand the brain
 This evokes the release of catecholamineThis evokes the release of catecholamine
 nicotine produces ganglionic blockade, vagal afferent nervenicotine produces ganglionic blockade, vagal afferent nerve
stimulation, or direct depressor effects mediated by action on thestimulation, or direct depressor effects mediated by action on the
brainbrain
Clinical features of poisoningClinical features of poisoning
 Mild: salivation, nausea, dizziness, drowsiness, headache, vomiting,Mild: salivation, nausea, dizziness, drowsiness, headache, vomiting,
diarrhoea, hand tremordiarrhoea, hand tremor
 Serious: mental confusion, circulatory collapse (shallow rapid pulse,Serious: mental confusion, circulatory collapse (shallow rapid pulse,
‘cold sweating’), convulsions, loss of consciousness, cardiac arrest,‘cold sweating’), convulsions, loss of consciousness, cardiac arrest,
respiratory paralysisrespiratory paralysis
DiagnosisDiagnosis
 Blood monitoring (blood gases) and urinanalysisBlood monitoring (blood gases) and urinanalysis
Treatment of poisoningTreatment of poisoning
 induced emesis (ipecac) or gastric lavage and activated charcoalinduced emesis (ipecac) or gastric lavage and activated charcoal
 supportive therapy directed towards maintaining respiration andsupportive therapy directed towards maintaining respiration and
blood pressure (IV fluids) and controlling convulsionsblood pressure (IV fluids) and controlling convulsions
References:References: www.wikipedia.com; www.inchem.org;www.wikipedia.com; www.inchem.org; Lucas GN, De Silva TUN.
Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians,
2006

26. Scientific name : Strychnos nux-vomica
Synonyms : S.lucida, S.colbrina, S.aromatica
Family : Loganiaceae
Sinhala name : Godakaduru, Visha kaduru
Tamil name : Eddi, Etti, Kagodi
English/common name : Poison nut, Nux vomica, Quaker buttons
Plant habitat :
♣ dry forests of Ceylon, flowers in August
♣ A moderate sized or large tree with an erect trunk, Slide 5
♣ Bark ♣ Wood ♣ Leaves ♣ Flowers ♣ Fruit
Traditional use : Root - cures fever and bites of venomous snakes
Used for preparation of homeopathic medicine
Toxic part of the plant : seed (although all parts toxics) Wathsala Wimalasena
Kanishka Jayaweera

27. 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 poisonous
Mode of action :
♣ Strychnine is a potent convulsant. It causes increased reflex
excitability in the spinal cord
♣ Brucine – resembles strychnine activity but it is less potent
Clinical 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

28. 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 etc
Treatment 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 safely
References : http://www.inchem.org/documents/pims/plant [accessed 29 June
2008]; Jayaweera DMA. Medicinal plant use in Ceylon - Part 3. Colombo: The
National Science Foundation, 2006; Lucas GN, De Silva TUN. Poisonous
plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

30. Scientific name: Gloriosa superba
Synonyms: G.simplex, Methonica
doniana, Eugonia superba
Family: Colchicaceae, Liliaceae
Sinhala name: Niyangala
Tamil: Karththigaikkilangu, Illangalli
English/common names:
• flame lily, glory lily, tiger claw
Plant habitat:
• native of tropical Africa, India, Malaya, etc
• found in low country Sri Lanka
Traditional use:
• tuber – bruises and sprains
Poisonous parts of the plant:
• The entire plant, especially the tubers, are extremely poisonous

31. Main toxic constituents:
– colchicine (+ ‘gloriosine’ in tubers)
Constituent type: alkaloid
Mode 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

32. • 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 failure
Diagnosis:
• Toxicological, biomedical, blood gas, haematological analyses
Treatment of poisoning:
• hospitalize the patient immediately
• induce vomiting (ipecac) / gastric lavage
• give repeated activated charcoal
• supportive care eg IV fluid, assisted
ventilation may be needed
References: 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: Sri
Lankan College of Paediatricians, 2006

33. Poisonus plants of Sri lankaPoisonus plants of Sri lanka
RicinusRicinus communiscommunis
A.D.WickramasooriyaA.D.Wickramasooriya
S.S.WijeramaS.S.Wijerama

34. 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 spinosus
Family: Euphorbiaceae (spurge family)
Sinhala name/s: Erandu, Tel-erandu,
beheth endaru, thel endaru
Tamil name/s: Amanakku, Muttu-kottai, Andagam
English/common name/s: castor bean, castor-oil
plant, Palma Christii
Plant 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

35. 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 chewing
Main toxic constituent/s: Ricin
Constituent type: Glycoprotein or a toxalbumin
• member of a class of plant toxins known as type 2 ribosome
inactivating proteins
Mode of action: Ricin impairs chain elongation in
protein synthesis, causing cell death and tissue
damage
Clinical 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

36. 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 urine
Treatment 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

37. • 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 to Southern
and Central America but have been introduced to almost all tropical countries
•Traditional use : Used as a food source. American Indians use the brown juice
for burns
By : J.S.R.Sherif
E.M.A.K.Ekanayaka
Manihot utilissimaManihot utilissima

38. Toxicity of the plant : The leaves and roots contain free and bound forms of the
cyanogenic glycoside linamarin, which is converted to cyanide in the presence of
linamarinase, a naturally occurring enzyme in cassava or via exposure to the atmosphere. (
Slide 5)
Two varieties
Sweet - contains as little as 20 milligrams of cyanide (CN) per kilogram of fresh roots
Bitter - may produce more than 50 times as much (1 g/kg)
The paralytic neurological disease caused by long-term consumption of cassava is called
mantakassa. Yam that is cut, washed and boiled in an open container at 72°C for long
enough will destroy the enzyme and any hydrocyanic acid formed will evaporate.
•Lethal dose : One dose of pure cassava cyanogenic glucoside (40mg) is sufficient to kill
even a cow. Hence about 300 grams of fresh root is enough to kill an 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 animals because it
rapidly inactivates cellular respiration thereby causing death. This means that it stops cells
from being able to use oxygen. The heart, respiratory system and central nervous system
are most susceptible to cyanide poisoning and cease to function as a result of lack of
oxygen.

39. 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 cassava
pest management. Ann Rev Entomol 1999; 44: 343-370; Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of

41. Presented by:
► M.M.JAYARATHNA
► H.V.N.LAKMALI
Botanical Name:
Peganum harmala
FamilyName:
Zygophyllaceae
Local Name: Ispandur
Urdu Name: Harmal
Sinhala name: Rata aruda
English name: Wild Rue
Tamil name: Simaiyarawandi
Part used: Whole plant
Flowering: May - June

42. Plant habitatPlant habitatUS states ofUS states of
Arizona,CaliforniaArizona,California
Montana, Texas -Montana, Texas -
grows in salt desertsgrows in salt deserts
and shrub lands.and shrub lands.
Grows in India, Persia,Grows in India, Persia,
MediterraneanMediterranean
region, Central Asia,region, Central Asia,
Arabia, North AfricaArabia, North Africa

43. Multibranched, leafy, perennial,Multibranched, leafy, perennial,
bright green, succulent herb.bright green, succulent herb.
Leaves divided, seed angled,Leaves divided, seed angled,
Flowers white, single.Flowers white, single.
 Constituent type:Constituent type:
alkaloidsalkaloids
 HarmalineHarmaline
 HarmineHarmine
 HarmalolHarmalol
 TetrahydroharmineTetrahydroharmine
 VasicineVasicine
Mode of action:Mode of action:
 Harmaline is a reversibleHarmaline is a reversible
monoamine oxidase inhibitor foundmonoamine oxidase inhibitor found
especially in higher quatities in ripeespecially in higher quatities in ripe
seedsseeds
 The plant also has antibacterial,The plant also has antibacterial,
antioxidant, anti-inflammatory andantioxidant, anti-inflammatory and
antitumour activityantitumour activity

44. CLINICAL FEATURESCLINICAL FEATURES
Overdose is potentially comprised of hallucinations andOverdose is potentially comprised of hallucinations and
neurosensorial syndromes, bradycardia, low blood pressure,neurosensorial syndromes, bradycardia, low blood pressure,
raised body temperature and gastrointestinal disturbancesraised body temperature and gastrointestinal disturbances
such as nausea and vomitingsuch as nausea and vomiting
DIAGNOSIS ONDIAGNOSIS ON
Physical examinationPhysical examination
TREATMENTSTREATMENTS
Supportive therapySupportive therapy
IV fluidsIV fluids
Antacids (or H2 antagonists)Antacids (or H2 antagonists)
References:
•IPCS Inchem.Peganum harmala [Accessed at
http://www.inchem.org/documents/pims/plant 04 July 2008 ]
•Massoud M et al. Toxicity of Peganum harmala: Review and a Case
Report. Iranian Journal of Pharmacology & Therapeutics 2002: 1(1); 1-4

45. • 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
Adenia palmata

47. • 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
phase
Reference: Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

48. Datura metel atropine, hyoscine, hyoscyamine alkaloids seed (all)
Gloriosa superba colchicine tuber
Nicotiana tabacum nicotine leaf (all)
Pagiantha dichotoma ? narcotic, datura-like seed
(Peganum harmala) harmaline seed
Strychnos nux vomica strychnine seed
Alocasia macrorrhiza calcium oxalate crystals
(needle-like), toxic
proteins
leaf/stem (all)
Anthurium sp.
Dieffenbachia sp.
Scindapsus aureus
Zantedeschia aethiopica
Cerbera manghas cerberine, odollum,thevetin cardiac glycosides fruit kernel
Thevetia peruviana thevetin A, theventin B fruit
Adenia palmata cyanogenic glycoside, toxalbumin,
emulsin enzyme
cyanogenic glycosides fruit
Manihot utilissima linamarin, (linase enzyme) tuber
Abrus precatorius abrin toxalbumins seed
Jatropha curcas curcin seed (all)
Jatropha multifida Jatrophin
Ricinus communis ricin
Eucalyptus robusta oil of eucalyptus (eugenol) volatile oils all
Myristica fragrans myristicin seed (aril)
Amanita phalloides phalloidin, phalloin, phallolysin
alpha, beta, gamma amanitin
phlallatoxins
amatoxins
aerial parts
(mushroom)