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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 60C for 30 minutes. At 80C 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



    See Also:
       Toxicological Abbreviations