Abrus precatorius L.
| 1. NAME |
| 1.1 Scientific name |
| 1.2 Family |
| 1.3 Common name(s) |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First-aid measures and management principles |
| 2.5 Poisonous parts |
| 2.6 Main toxins |
| 3. CHARACTERISTICS |
| 3.1 Description of the plant |
| 3.1.1 Special identification features |
| 3.1.2 Habitat |
| 3.1.3 Distribution |
| 3.2 Poisonous parts of the plant |
| 3.3 The toxin(s) |
| 3.3.1 Name(s) |
| 3.3.2 Description, chemical structure, stability |
| 3.3.3 Other physico-chemical characteristics |
| 3.4 Other chemical contents of the plant |
| 4. USES/CIRCUMSTANCES OF POISONING |
| 4.1 Uses |
| 4.2 High risk circumstances |
| 4.3 High risk geographical areas |
| 5. ROUTES OF ENTRY |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination by route of exposure |
| 7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY |
| 7.1 Mode of action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Animal data |
| 7.2.3 Relevant in vitro data |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 8.1 Material sampling plan |
| 8.1.1 Sampling and specimen collection |
| 8.1.1.1 Toxicological analyses |
| 8.1.1.2 Biomedical analyses |
| 8.1.1.3 Arterial blood gas analysis |
| 8.1.1.4 Haematological analyses |
| 8.1.1.5 Other (unspecified) analyses |
| 8.1.2 Storage of laboratory samples and specimens |
| 8.1.2.1 Toxicological analyses |
| 8.1.2.2 Biomedical analyses |
| 8.1.2.3 Arterial blood gas analysis |
| 8.1.2.4 Haematological analyses |
| 8.1.2.5 Other (unspecified) analyses |
| 8.1.3 Transport of laboratory samples and specimens |
| 8.1.3.1 Toxicological analyses |
| 8.1.3.2 Biomedical analyses |
| 8.1.3.3 Arterial blood gas analysis |
| 8.1.3.4 Haematological analyses |
| 8.1.3.5 Other (unspecified) analyses |
| 8.2 Toxicological Analyses and Their Interpretation |
| 8.2.1 Tests on toxic ingredient(s) of material |
| 8.2.1.1 Simple Qualitative Test(s) |
| 8.2.1.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.1.3 Simple Quantitative Method(s) |
| 8.2.1.4 Advanced Quantitative Method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple Qualitative Test(s) |
| 8.2.2.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.2.3 Simple Quantitative Method(s) |
| 8.2.2.4 Advanced Quantitative Method(s) |
| 8.2.2.5 Other Dedicated Method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 CNS |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Others |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ears, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Others |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Relevant laboratory analyses and other investigations |
| 10.2.1 Sample collection |
| 10.2.2 Biomedical analysis |
| 10.2.3 Toxicological/toxinological analysis |
| 10.2.4 Other investigations |
| 10.3 Life supportive procedures and symptomatic treatment |
| 10.4 Decontamination |
| 10.5 Elimination |
| 10.6 Antidote/antitoxin treatment |
| 10.6.1 Adults |
| 10.6.2 Children |
| 10.7 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 11.2 Internally extracted data on cases |
| 11.3 Internal cases |
| 12. ADDITIONAL INFORMATION |
| 12.1 Availability of antidotes/antitoxins |
| 12.2 Specific preventive measures |
| 12.3 Other |
| 13. REFERENCES |
| 13.1 Clinical and toxicological |
| 13.2 Botanical |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
POISONOUS PLANTS
1. NAME
1.1 Scientific name
Abrus precatorius L.
1.2 Family
Leguminosae
1.3 Common name(s)
Abrus seed
Aivoeiro
Arraccu-mitim
Buddhist rosary bead
Carolina muida
Crabs eye
Deadly crab's eye
Indian bead
Indian liquorice
Jequirite
Jequirity Bean
Jumble beads
Juquiriti
Lucky bean
Prayer beads
Precatory bean
Rosary beads
Rosary Pea
Ruti
Tentos da America
Tentos dos mundos
Weather plant
Wild liquorice
2. SUMMARY
2.1 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. Infusion of
seed extracts can cause eye damage after contact.
2.2 Summary of clinical effects
The early features of toxicity are burning of the mouth and
oesophagus, and severe gastroenteritis with vomiting,
haematemesis, diarrhoea, melaena, and abdominal pain. Later,
drowsiness, disorientation, weakness, stupor, convulsions,
shock, cyanosis, retinal haemorrhages, haematuria, and
oliguria can occur. Contact with the eyes can cause
conjunctivitis and even blindness.
2.3 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.
2.4 First-aid measures and management principles
First-aid measures: Remove all seed particles from the mouth.
Induce vomiting and save it for identification. Ensure that
the patient's airway is clear and that there is adequate
ventilation.
Do not induce vomiting if the patient is semi-conscious or is
at risk of having convulsions. If the eyes are contaminated,
wash eyes with running water for ten minutes. Medical
attention is essential if the seeds were ingested, or if the
eyes were contaminated. Collect remaining seeds or plant
material or remnants of seeds for identification.
Management principles: induce emesis or perform gastric
lavage. Supportive measures include parenteral fluids and
electrolytes. Keep the patient in hospital for several days
because severe symptoms can develop some time after ingestion.
2.5 Poisonous parts
The most poisonous parts of the plant involved in poisoning
are the small, scarlet seeds, that have a black eye at the
hilum.
2.6 Main toxins
The main toxin is abrin, which is concentrated in the seeds.
3. CHARACTERISTICS
3.1 Description of the plant
3.1.1 Special identification features
Abrus precatorius is a slender, perennial climber that
twines around trees, shrubs, and hedges. It has no
special organs of attachment. Leaves are glabrous with
long internodes. It has a slender branch and a
cylindrical wrinkled stem with a smooth-textured brown
bark. Leaves alternate compound paripinnate with
stipules. Each leaf has a midrib from 5 to 10 cm long.
It bears from 20 to 24 or more leaflets, each of which
is about 1.2 to 1.8 cm long, oblong and obtuse. It is
blunt at both ends, glabrous on top and slightly hairy
below. Flowers are small and pale violet in colour with
a short stalk, arranged in clusters. The ovary has a
marginal placentation.
The fruit, which is a pod, is flat, oblong and truncate-
shaped with a sharp deflexed beak is about 3 to 4.5 cm
long, 1.2 cm wide, and silky-textured. The pod curls
back when opened to reveal pendulous seeds. Each fruit
contains from 3 to 5 oval-shaped seeds, about 0.6 cm.
They are usually bright scarlet in colour with a smooth,
glossy texture, and a black patch on top.
3.1.2 Habitat
Abrus precatorius is a wild plant that grows best in
fairly dry regions at low elevations.
3.1.3 Distribution
It grows in tropical climates such as India, Sri Lanka,
Thailand, the Philippine Islands, South China, tropical
Africa and the West Indies. It also grows in all
tropical or subtropical areas.
3.2 Poisonous parts of the plant
The most poisonous part of the plant is the seed. It is 0.6 cm
long (although length may vary), and oval-shaped. It is
usually bright scarlet, and has a jet-black spot surrounding
the hilum which is the point of attachment. The seed coat, or
testa, is smooth and glossy and becomes hard when the seed
matures.
3.3 The toxin(s)
3.3.1 Name(s)
Abrin, which consists of abrus agglutinin, and toxic
lectins abrins [a] to [d] are the five toxic
glycoproteins found in the seeds (Budavari, 1989).
3.3.2 Description, chemical structure, stability
Five glycoproteins have been purified from the seeds.
They are abrus agglutinin (a haemagglutinin) and the
toxic principles abrins [a] to [d].
Abrus agglutinin is a tetramer with a molecular weight
of 134,900. It is non-toxic to animal cells and a potent
haemagglutinator.
Abrins a through d (molecular weight: 63,000 - 67,000)
are composed of two disulphide-linked polypeptide
chains. The larger sub-unit, which is the neutral B-
chain has a molecular weight of approximately 35,000.
The other sub-unit an acidic A-chain has a molecular
weight of approximately 30,000 (Windholz, 1983; Budavari,
1989).
Stability: Pure abrin is a yellowish-white amorphous
powder. The toxic portion is heat-stable to incubation
at 60°C for 30 minutes. At 80°C most of the toxicity is
lost in 30 minutes (Budavari, 1989).
3.3.3 Other physico-chemical characteristics
Pure abrin is a yellowish-white amorphous powder. Abrin
is soluble in sodium chloride solutions, usually with
turbidity (Budavari, 1989).
3.4 Other chemical contents of the plant
The seeds also contain an amino acid known as abrine (N-methyl-
L-tryptophan), glycyrrhizin and a lipolytic enzyme.
The roots, stems, and leaves also contain glycyrrhizin
(Windholz, 1983).
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
Children are attracted by the brightly-coloured seeds.
In some countries theyplay with them and in school use
them in their handiwork and to count. Necklaces and
other ornaments made from the seeds are worn by both
children and adults.
The seeds were also used to treat diabetes and chronic
nephritis.
The plant is also used in some traditional medicine to
treat scratches and sores, and wounds caused by dogs,
cats, and mice, and is also used with other ingredients
to treat leucoderma. The leaves are used for their anti-
suppurative properties. They are ground with lime and
applied on acne sores, boils, and abscesses. The plant
is also traditionally used to treat tetanus, and to
prevent rabies. Various African tribes use powdered
seeds as oral contraceptives (Watt & Breyer, 1962).
Boiled seeds of Abrus precatorius are eaten in certain
parts of India (Rajaram& Janardhanan, 1992).
4.2 High risk circumstances
Children are attracted to the brightly-coloured seeds and may
chew, suck, or swallow them. Because of the hard and
relatively impermeable coat of the mature seeds, they are
considerably less toxic if swallowed whole. They are more
dangerous when the seeds are chewed or sucked because the
toxic elements in the seeds are extracted and mixed with
enzymes. Immature seeds are also poisonous if ingested
because of their soft and easily broken coat. When the seeds
are used as ornaments, such as necklaces, holes are drilled in
the seeds, which allows contact between the intestinal
secretions and the core of the seed resulting in absorption of
the toxic ingredients.
Another reported circumstance is the drinking of beverages
where seeds from a necklace have been soaked (Jouglard, 1977).
If swallowed, these seeds easily cause poisoning.
4.3 High risk geographical areas
The high-risk areas are the dry regions and lowland tropical
areas although necklaces are sold in many countries.
5. ROUTES OF ENTRY
5.1 Oral
Abrus precatorius mature or immature seeds are chewed or
ingested.
5.2 Inhalation
Unknown.
5.3 Dermal
Unknown.
5.4 Eye
Cold preparations made from soaking the seeds have been used
to treat trachoma and corneal opacities (Hart, 1963).
5.5 Parenteral
Subcutaneous injections from dried infusions made from the
seeds have been used to poison livestock and human beings in
India (Hart, 1963).
5.6 Others
Unknown.
6. KINETICS
6.1 Absorption by route of exposure
Abrin is very stable in the gastrointestinal tract, from where
it is slowly absorbed. It is considerably less toxic after
oral administration than after parenteral injection Gunsolus,
1955).
6.2 Distribution by route of exposure
Abrin is widely distributed in tissues.
6.3 Biological half-life by route of exposure
Unknown.
6.4 Metabolism
Unknown.
6.5 Elimination by route of exposure
Unknown.
7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY
7.1 Mode of action
Abrin exerts its toxic action by attaching itself to the cell
membranes. Abrin's toxic effect is due to its direct action
on the parenchymal cells (e.g., liver and kidney cells) and
red blood cells (Hart, 1963).
Both subunits from which abrins [a] through [d] are made up
are required for its toxic effects.
The larger subunit, the B chain (haptomere) binds to the
galactosyl-terminated receptors on the cell membrane, which is
a prerequisite for the entry of the other subunit, the A chain
(effectomere). This inactivates the ribosomes, arrests
protein synthesis, and causes cell death (Stirpe & Barbieri,
1986). The A-chain attacks the 60S subunit of the ribosomes
and by cutting out elongation factor EF2, stops protein
synthesis (Frahne & Pfander, 1983).
Abrus agglutinin agglutinates the red blood cells by combining
with the cell stroma (Hart, 1963).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
One seed well masticated can cause fatal
poisoning (Budavari, 1989).
7.2.1.2 Children
One seed well masticated can cause fatal
poisoning (Budavari, 1989).
7.2.2 Animal data
Abrin's toxicity has been tested in different animals
with widely divergent results. The lethal dose for
animals is about 0.01 mg/kg body weight (Gunsolus,
1955). The intra-peritoneal LD50 value in mice is 0.02
mg/kg body weight (Budavari, 1983). The intravenous
minimal lethal dose of abrin in mice is 0.7
micrograms/kg (Ellenhorn, 1988). Simpson et al. report
that 2 ounces of seeds are fatal to horses, but that
cows, goats and dogs are more resistant. The symptoms
reported are anorexia, violent vomiting, lassitude,
chills, and incoordination. Severe gastroenteritis is
also common in animals (Gosselin, 1984).
7.2.3 Relevant in vitro data
No data available.
7.3 Carcinogenicity
Unknown.
7.4 Teratogenicity
Unknown.
7.5 Mutagenicity
Unknown.
7.6 Interactions
Unknown.
8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
8.3.1.2 Urine
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Symptoms and signs can occur after a latent period that
ranges from a few hours to several days. They include a
burning sensation in the mouth, dysphagia, nausea,
vomiting, bloody diarrhoea, and abdominal cramps.
Drowsiness, disorientation, convulsions, cyanosis,
stupor, circulatory failure, retinal haemorrhages,
haematuria and oliguria may occur.
9.1.2 Inhalation
Unknown.
9.1.3 Skin exposure
Unknown.
9.1.4 Eye contact
Eye irritation leads to a dose-related reaction ranging
from mild conjunctivitis to a severe damage (Hart,
1963).
9.1.5 Parenteral exposure
The clinical effects after intravenous and subcutaneous
administration are similar to ingestion but
gastrointestinal symptoms are lesser. There is severe
inflammation at the injection site.
9.1.6 Other
Unknown.
9.2 Chronic poisoning
9.2.1 Ingestion
Unknown.
9.2.2 Inhalation
Unknown.
9.2.3 Skin exposure
Unknown.
9.2.4 Eye contact
Unknown.
9.2.5 Parenteral exposure
Unknown.
9.2.6 Other
Unknown.
9.3 Course, prognosis, cause of death
The major symptoms of poisoning are acute gastroenteritis with
nausea, vomiting and diarrhoea leading to dehydration,
convulsions, and shock. Dehydration, as well as direct
toxicity on the kidneys, could result in oliguria that might
progress to death in uraemia.
The fatality rate is approximately 5%.
Reported fatalities occurred after a 3 to 4 day course
characterized by persistent gastroenteritis (Ellenhorn, 1988).
Death may occur up to 14 days after poisoning from uraemia
(Dreisbach & Robertson, 1987).
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
There is no direct effect on the heart.
Shock, hypotension, and tachycardia may occur after
prolonged vomiting and diarrhoea.
9.4.2 Respiratory
Cyanosis secondary to hypotension and shock may be seen.
9.4.3 Neurological
9.4.3.1 CNS
Drowsiness, convulsions, hallucinations, and
trembling of the hands.
9.4.3.2 Peripheral nervous system
Unknown.
9.4.3.3 Autonomic nervous system
Unknown.
9.4.3.4 Skeletal and smooth muscle
Unknown.
9.4.4 Gastrointestinal
Because of abrin's irritant action, severe
gastroenteritis with nausea, vomiting, diarrhoea,
dysphagia and abdominal cramps may occur. Nausea and
vomiting are due to direct irritation of the gastric
mucosa. Erosion of the intestinal mucosa can cause
haematemesis and melaena.
9.4.5 Hepatic
The necrotizing action of the toxin causes liver damage.
Serum levels of liver cell enzymes, i.e., aspartate-
transferase (AST), alanine-transferase (ALT), and lactic
dehydrogenase (LDH) are markedly increased. The serum
bilirubin level is elevated indicating progression of
the lesions. Hypoglycaemia may occur.
9.4.6 Urinary
9.4.6.1 Renal
Oliguria and anuria may result from prolonged
hypotension, but may also be due to acute renal
failure as a result of focal degeneration of the
tubular cells. Blocking of the tubules with
haemoglobin from haemolysed red cells may also
contribute to renal failure.
9.4.6.2 Others
Unknown.
9.4.7 Endocrine and reproductive systems
Unknown.
9.4.8 Dermatological
Skin contact may cause irritation and dermatitis.
9.4.9 Eye, ears, nose, throat: local effects
Eye: Retinal haemorrhages can appear early in the course
of intoxication. The patient may complain of impaired
vision that is caused by changes in the retina. Eye
contact can cause severe swelling and reddening of the
ocular conjunctiva.
Ear, nose, throat: Irritation of the throat may occur
after ingestion.
9.4.10 Haematological
Abrus agglutinin causes haemagglutination and
haemolysis by its direct effect on red cells. Blood
loss may also occur because of haemorrhages in the
gastrointestinal tract.
9.4.11 Immunological
Unknown.
9.4.12 Metabolic
9.4.12.1 Acid base disturbances
Prolonged vomiting may cause alkalosis. Shock
is likely to lead to acidosis. Acidosis can
also occur from renal failure.
9.4.12.2 Fluid and electrolyte disturbances
Vomiting, diarrhoea, and haemorrhages lead to
loss of fluids and electrolytes, thus causing
lethargy, muscle weakness, cardiac
dysrhythmias, and muscle cramps.
9.4.12.3 Others
Liver damage may cause hypoglycaemia.
9.4.13 Allergic reactions
Unknown.
9.4.14 Other clinical effects
Unknown.
9.4.15 Special risks
Unknown.
9.5 Others
9.6 Summary
10. MANAGEMENT
10.1 General principles
The management of poisoning cases is mainly symptomatic and
supportive. Induced emesis or gastric lavage are usually
indicated (if the conditions of the patient allow the
procedures) to remove the seeds from the stomach. Fluid and
electrolyte imbalances should be carefully monitored and
corrected.
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
Collect the seeds or any other plant material for
identification, also collect the vomitus or gastric
contents in a clean jar. Seeds may be identified if
vomitus is put inside a transparent plastic bag.
10.2.2 Biomedical analysis
Full blood count, liver profile, serum electrolytes
blood gases, blood urea and creatinine are the
essential analyses. Urinalysis may reveal the
presence of protein, red blood cells, haemoglobin,
and casts.
10.2.3 Toxicological/toxinological analysis
No simple analyses are available in practice.
10.2.4 Other investigations
May be indicated according to the patient's
condition.
10.3 Life supportive procedures and symptomatic treatment
Make a proper assessment of airway, breathing, circulation
and neurological status of the patient.
Monitor vital signs.
Maintain a clear airway. Administer oxygen if the patient is
in shock.
Monitor acid base balance, and fluid and electrolyte
balance.
Give adequate oral fluids by mouth, if possible. If the
patient is unable to swallow, administer intravenous fluids
and electrolytes, according to the severity of the symptoms
and the results of serum electrolyte analysis. Correct
metabolic acidosis if present.
Fluid loss may lead to hypovolaemic shock with hypotension.
If the intravenous fluid therapy does not raise the blood
pressure, insert a central venous pressure line and give
plasma or dextran to expand the intravascular volume. If
hypotension still persists consider administration of
dopamine or dobutamine in a continuous infusion.
No cases of severe haemolysis have been reported. However,
if significant haemolysis occurs, and if kidney function is
normal, maintain the urine output at over 100 ml/hour with
alkaline fluids.
If anuria persists after receiving fluid replacement,
consider the possibility of dialysis.
If convulsions occur, administer anti-convulsant drugs
(diazepam, intravenously or intrarectally in paediatric
emergencies).
Demulcents may relieve oropharyngeal and gastric irritation.
10.4 Decontamination
Emesis with syrup of ipecacuanha is the best way to remove
the seeds or pieces of plant from the stomach unless
contraindications to induced emesis exist or orpharyngeal
oedema is present.
If emesis induction is not possible, gastric lavage may be
performed if the condition of the patient allows it. If the
patient is obtunded, convulsing or comatose, insert an oro-
or naso-gastric tube and lavage after endotracheal
intubation.
Cathartics should not be used because they can aggravate
diarrhoea and fluid loss.
In case of eye exposure, irrigate eyes with copious amounts
of water or saline.
10.5 Elimination
No method has proved to be beneficial.
10.6 Antidote/antitoxin treatment
10.6.1 Adults
There is no specific antidote available.
An anti-serum used to be supplied under the name of
"anti-abrin" or "jequiritol" (Gunsolus, 1955) but is
no longer available.
10.6.2 Children
There is no specific antidote available.
An anti-serum used to be supplied under the name of
"anti-abrin" or "jequiritol" (Gunsolus, 1955) but is
no longer available.
10.7 Management discussion
Gastric lavage may be difficult to perform and may not be
successful if the size of the seeds is large. Induction of
emesis may be preferred.
A cathartic can be administered to accelerate intestinal
transit in cases where entire seeds have been recently
ingested and no clinical features of poisoning are present.
Cathartics are contraindicated in the symptomatic patient.
Magnesium sulphate should be avoided when gastrointestinal
irritation is present because it may be absorbed
systemically.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Adults: Some investigators have reported that abrin is
poorly absorbed from the intestine. However, there have
been reports of severe, sublethal toxicity in adults after
ingestion of only one-half to two seeds (Hart, 1963).
A 37-year-old man was severely poisoned after ingesting half
a seed (Gunsolus, 1955).
A 19-year-old girl died after she was treated for trachoma
with jequirity infusions (Gunsolus, 1955).
An adult, who homogenized 20 seeds in a blender and a
portion of the mixture died (Davis, 1978).
Children: Deaths in children have been reported in Florida,
USA, in 1949, 1958 and 1962 after ingestion of one or more
seeds. In 1955, two seeds caused severe but non-fatal
poisoning (Hart, 1963). In Missouri, USA, a child who
ingested exactly one-half seed was immediately made forced
to vomit. The remainder of the swallowed half seed, whose
coat was broken, was found in the vomitus. He was treated
immediately and did not develop any symptoms (Kinamore,
1980). In most of the cases, the quantity of the seed
ingested has been described as the potentially lethal dose
in children.
11.2 Internally extracted data on cases
To be added by the centre.
11.3 Internal cases
To be added by the centre.
12. ADDITIONAL INFORMATION
12.1 Availability of antidotes/antitoxins
No antidotes are available at present.
12.2 Specific preventive measures
Do not allow children to play with seeds of Abrus
precatorius.
Keep seeds or ornaments made out of seeds away from
children.
Do not grow Abrus precatorius plants in home gardens.
Educate older children and the public of the dangers of
ingesting seeds.
12.3 Other
No data available.
13. REFERENCES
13.1 Clinical and toxicological
Budavari S ed. (1989) The Merck Index: an encyclopedia of
chemicals, drugs, and biologicals, 10th ed. Rahway, New
Jersey, Merck and Co., Inc.
Davis JH (1978) Abrus precatorius (rosary pea). The most
common lethal plant poison. Journal of Florida Medical
Association, 65: 189-191.
Dreisbach RH & Robinson WO eds. (1987) Handbook of
Poisoning: Prevention, Diagnosis & Treatment, Los Altos,
California, Appleton and Lange. p 497.
Ellenhorn MJ & Barceloux DG. eds (1988). Medical Toxicology.
New York, Elsevier Science Publishing Company, Inc. 1224-
1225.
Gosselin RE, Smith RP, & Hodge HC (1984) ed. Clinical
Toxicology of Commercial Products, Baltimore/London,
Williams & Wilkins.
Gunsolus JM (1955). Toxicity of Jequirity beans. J Amer
Med Assoc, 157: 779.
Hart M (1963). Jequirity bean Poisoning. N Engl J Med,
268: 885-886.
Hoehne FC (1978). Plantaxe substancias vegetais toxicase
medicinais. Sao Paulo, Novos Horizontes, 355p
Jouglard J (1977). Intoxications d'origine vegetale In:
Encycl. Med. Chir.; Intoxication Paris, Editions Techniques,
16065 A-10-A-20.
Kinamore PA, Jager RW, De Castro FJ, & Peck KO (1980).
Abrus & Ricinus Ingestion: Management of three cases.
Clinical Toxicology, 17(3): 401-405.
Kunkel DB (1983). Poisonous Plants in: Haddad LM &
Winchester JF. ed. Clinical Management of Poisoning & Drug
Overdosage, Canada, W.B. Saunders Company. pp 1012.
Lampe KF (1976). Changes in therapy in Abrus precatorius &
Ricinus communis poisoning suggested by recent studies in
their mechanism of Toxicity. Clinical Toxicology, 9(1): 21.
Lin JY, Tserng, KY, Chen CC, Lin LT, & Tung TC (1970).
Abrin & Ricin: New Anti-tumour Substances. Nature, 227:
292 - 293.
Reynolds JEF, ed (1982) Martindale, The Extra Pharmacopoeia,
28th ed. London, Pharmaceutical Press, p 2025
Rajaram N & Janardhanan K (1992) The chemical composition
and nutritional potential of the tribal pulse, Abrus
precatorius L. Plant Foods Hum Nutr, 42(4): 285-290.
Schvartsman S (1979) Plantas venenosas. Sao Paulo, Sarvier.
Stripe F & Barbieri L (1986). Symposium: Molecular
Mechanisms of Toxicity, Toxic Lectins from Plants. Human
Toxicology, 5(2): 108-109.
Windholz M. ed (1983) The Merck Index: an encyclopedia of
chemicals, drugs, and biologicals, 10th ed. Rahway, New
Jersey, Merck and Co., Inc.
13.2 Botanical
Frohne D & Pfander HJ (1983) ed. A Colour Atlas of Poisonous
Plants, Germany, Wolfe Publishing Ltd. pp 291.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Dr Ravindra Fernando
National Poisons Information Centre
Faculty of Medicine
Kynsey Road
Colombo 8
Sri Lanka
Tel: 94-1-94016
Fax: 94-1-599231
Date: September 1988
Reviewer: Dr A. Furtado Rahde
Poisons Control Centre
Rua Riachuelo 677/201
90100 Porto Alegre
Brazil
Tel: 55-512-275419
Fax: 55-512-391564
Date: November 1988
Peer Review: London, United Kingdom, March 1990
Update: Dr R. Fernando, London, United Kingdom, June 1993
Review: IPCS, May 1994