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S2 L78 Poisonous plants of Sri Lanka


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Title: S2 L78 Poisonous plants of Sri Lanka

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,

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

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
  • Lethal dose kernel of one fruit (or 2 leaves for
    a child)
  • Main toxic constituent/s thevetin A, thevetin B
  • Constituent type cardiac glycosides

Voltage dependent L-type Ca2 channel
Na channel
Na/K ATPase

K channel(s)
3 Na
ß-adrenergic receptor
Na/Ca2 exchanger
Heart muscle
Representative Cardiac Cell
Phase 2

3 Na
Cell Electrophysiology
2 K
Phase 2

3 Na
Therapeutic Toxic MoA
  • Clinical features of poisoning digoxin-like
  • Early on burning sensation in mouth, tingling of
    tongue, dry throat, giddiness, nausea vomiting,
  • Cardiovascular sinus bradycardia, first and
    second degree heart block, junctional rhythms,
    atrial and ventricular extrasystoles, ventricular
  • Other yellow vision, anxiety, convulsions, coma
  • Diagnosis
  • cardiac glycoside blood levels
  • seed remnants, vomitus, gastric aspirate may help
  • monitor serum potassium and electrolytes
  • Treatment of poisoning
  • induce emesis at home (ipecac)
  • gastric lavage within 1 hour or activated
  • 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
Datura metel


Scientific name Datura metelSynonyms Datura
fastuosa (L.) Datura
alba (Nees.) Family Solanaceae Sinhala
name Ela-attanaTamil name AyigamCommon
names Devil's trumpet,
downy thorn-apple,
black datura, angel's

  • 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
  • Traditional use Leaves/dried flowers are used
    to relieve asthma or wheezing like symptoms in
    many cultures eg Chinese herbal medicine (yáng
    jin hua).
  • 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 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.

  • 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
  • Treatment of poisoning
  • Ipecac to induce emesis or gastric lavage.
  • Activated charcoal to reduce absorption of toxic
  • 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/tropane20alkaloids.pd
  • waynesword.palomar.edu/ww0703.htm
  • DMA Jayaweera. Medicinal plants used in Ceylon
    Parts 1-5. Colombo National Science Foundation,
  • Lucas GN, De Silva TUN. Poisonous plants of Sri
    Lanka. Colombo Sri Lankan College of
    Paediatricians, 2006

Abrus precatorius

D. Niyangoda T.A. Ekanayaka
  • 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

  • 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)

  • 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

Myristica fragrans
  • M. Jayasinghe
  • C.M.C. Indrajith

  • Scientific name Myristica fragrans
  • Family Myristicaceae
  • Sinhala name Sadikka, Wasawasi (aril)
  • Tamil name Adipam, Attigam, Kasam, Sadi,
  • 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)

  • 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
  • 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
  • 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/pim
s/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,
  • Alocasia macrorrhiza

U.G.W.L.Jayeweera C.Premely
  • 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

Flower of the Alocasia plant
Taro corms
  • 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,
  • 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

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
Nicotiana tabacum
Sanduni Sudusinge Uthpala Siriwardhane Mano
  • Scientific name Nicotiana tabacum
  • Family Solanceae
  • Sinhalese name Dum kola
  • Tamil name Phaielai
  • English name Tobacco
  • Plant habitat native of tropical and
    subtropical America but it is
    now commercially cultivated worldwide
  • Traditional use - as an insecticide
  • - intestinal worms or constipation
  • - dried tobacco leaves for chewing,
    snuffing or smoking
  • Toxic part of the plant leaves, stems, roots and
  • Main toxic constituents nicotine

  • Mode of action
  • Nicotine binds stereo specifically to
    acetylcholine receptors at autonomic ganglia, the
    adrenal medulla, the neuromuscular junction and
    the brain
  • This evokes the release of catecholamine
  • nicotine produces ganglionic blockade, vagal
    afferent nerve stimulation, or direct depressor
    effects mediated by action on the brain
  • Clinical features of poisoning
  • Mild salivation, nausea, dizziness, drowsiness,
    headache, vomiting, diarrhoea, hand tremor
  • Serious mental confusion, circulatory collapse
    (shallow rapid pulse, cold sweating),
    convulsions, loss of consciousness, cardiac
    arrest, respiratory paralysis
  • Diagnosis
  • Blood monitoring (blood gases) and urinanalysis
  • Treatment of poisoning
  • induced emesis (ipecac) or gastric lavage and
    activated charcoal
  • supportive therapy directed towards maintaining
    respiration and blood pressure (IV fluids) and
    controlling convulsions

References www.wikipedia.com www.inchem.org
Lucas GN, De Silva TUN. Poisonous plants of Sri
Lanka. Colombo Sri Lankan College of
Paediatricians, 2006
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
  • Main toxic constituents strychnine,
  • 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
  • - 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.

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/docume
nts/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
Glorisa superba
as a Poisonus Plant in Sri Lanka
Presented by
V.N.Dissanayaka V.Ajeethan
  • 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

  • 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 -gt 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
  • burning pain, numbness, itching and tingling
    around the mouth and throat with thirst
  • nausea, intense vomiting
  • abdominal pain, severe diarrhoea with blood and
  • 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 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,
Poisonus plants of Sri lanka Ricinus communis
  • A.D.Wickramasooriya
  • S.S.Wijerama

  • 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
  • Africans use the bark for stitching up wounds
    as a dressing for 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
  • 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
  • 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

  • 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
  • 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
  • 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
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 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

  • 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 72C 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.

  • 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
  • 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
Paediatricians, 2006
(No Transcript)
Peganum harmala
  • Presented by



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
Plant habitat
  • US states of
  • Arizona,California
  • Montana, Texas - grows in salt deserts and shrub
  • Grows in India, Persia,
  • Mediterranean region, Central Asia, Arabia,
    North Africa

Multibranched, leafy, perennial,bright green,
succulent herb.Leaves divided, seed
angled,Flowers white, single.
  • Constituent type alkaloids
  • Harmaline
  • Harmine
  • Harmalol
  • Tetrahydroharmine
  • Vasicine
  • Mode of action
  • Harmaline is a reversible monoamine oxidase
    inhibitor found especially in higher quatities in
    ripe seeds
  • The plant also has antibacterial, antioxidant,
    anti-inflammatory and antitumour activity

  • Overdose is potentially comprised of
    hallucinations and neurosensorial syndromes,
    bradycardia, low blood pressure, raised body
    temperature and gastrointestinal disturbances
    such as nausea and vomiting
  • Physical examination
  • Supportive therapy
  • IV fluids
  • 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

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 -gt accidental
    ingestion by children)
  • Lethal dose ?

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  • 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 -gt diarrhoea
    with blood and mucus, abdominal colic and right
    iliac fossa tenderness after a variable period of
  • 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
  • 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

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