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Jatropha podagrica

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 Biochemcial 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
   8.5 Overall Interpretation of all toxicological analyses and
   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 Hematological
      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
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
             Jatropha podagrica
    1.2      Family
             Euphorbiaceae
    1.3      Common name(s)
             Coral nut
             Guatemala rhubarb
             HOOK
             Physic nut
    2.  SUMMARY
    2.1      Main risks and target organs
             Dehydration and cardiovascular collapse as a result of 
             haemorrhagic gastro-enteritis.  Central nervous system 
             depression. 
    2.2      Summary of clinical effects
             Symptoms are largely those associated with gastro-intestinal  
             irritation.  There is acute abdominal pain and a burning 
             sensation in the throat about half an hour after ingestion 
             of the seeds, followed by nausea, vomiting and diarrhoea.  The 
             vomitus and faeces may contain blood.  In severe intoxications 
             dehydration and haemorrhagic gastroenteritis can occur. There 
             may be CNS and cardiovascular depression and collapse; 
             children are more susceptible. 
    2.3      Diagnosis
             Diagnosis by case history and presenting symptoms.  A definite  
             diagnosis can only be made if there is a  history of 
             ingestion and the ingested plant material has been positively 
             identified as Jatropha. 
    2.4      First-aid measures and management principles
             INGESTION:  Unless the patient is unconscious, convulsing, or 
             unable to swallow give fluids (milk or water) to dilute.  
             Seek medical assistance.   
             In hospital or a health care facility induce vomiting unless 
             the patient has already vomited, or perform gastric lavage.  
             Administer activated charcoal and a cathartic to hasten 
             elimination, although in the presence of diarrhoea this is 
             unecessary. 
             SKIN:  Wash the affected area well with plenty of water and 
             use a mild soap. 
             EYE:  Flush the eye with copious amounts of water for at least 
             15 minutes.  If irritation persists seek medical assistance. 

    2.5      Poisonous parts
             All parts are considered toxic but in particular the seeds.
    2.6      Main toxins
             Contains a purgative oil and a phytotoxin or toxalbumin 
             (curcin) similar to ricin in Ricinis.  
    3.  CHARACTERISTICS
    3.1      Description of the plant
             3.1.1    Special identification features
                      Jatropha podagrica is similar to J. curcas has a  
                      thick gouty stem. It has thin, often  greenish bark 
                      which exudes copious  amounts of watery sap when cut.   

                      Leaves: leaves with broad, blunt lobes and a stout  
                      stalk 
                      Flowers:  The flowers are red and similar to those of 
                      J.multifida  which are bright red and resemble a 
                      piece of coral. 
                      Fruit:  Similar to that of J. curcas, that is - small 
                      capsule-like, round fruit; about 2.5 -  4 cm (1-1.5
                      inches) in diameter.  These are green and fleshy when 
                      immature,  becoming dark  brown when ripe and 
                      splitting to release 2 or 3  black seeds each  about 
                      2 cm (3/4 inch) long.  The meat of the  seeds is 
                      white and oily in texture and are reported to have an  
                      agreeable taste. (Micromedex, 1974-1994) 

             3.1.2    Habitat
                      Widely cultivated as an ornamental.  Prefers arid   
                      environments.
             3.1.3    Distribution
                      Native to tropical America, but is now cultivated 
                      widely in  tropical countries throughout the world.  
                      It is grown occasionally in warmer parts of Australia 
                      and is naturalised in a few places in   Queensland 
                      and the Northern Territory.  In Florida it is found 
                      chiefly south of Orlando.  It is also a common plant 
                      in the   Hawaiian Islands.  Introduced to southern 
                      Africa, the plant has   spread from Mozambique 
                      through Zambia to the Transvaal and Natal.   This 
                      species is also found throughout the warmer parts of 
                      Asia. 
    3.2      Poisonous parts of the plant
    3.3      The toxin(s)
             3.3.1    Name(s)
                      MAIN TOXINS:
                      
                      Curcin - a phytotoxin (toxalbumin), found mainly in 
                      the seeds and   also in the fruit and sap. 
                      
                      Purgative oil - the seed yields 40% oil, known as 
                      hell oil,   pinheon oil, oleum infernale or oleum 
                      ricini majoris, which   contains small amounts of an 
                      irritant curcanoleic acid, which is   related to 
                      ricinoleic acid and crotonoleic acid, the principle   
                      active ingredients of castor oil and croton oil 
                      respectively   (Joubert et al., 1984). 
                      
                      OTHER TOXINS:
                      
                      This genera also may contain hydrocyanic acid (CRC 
                      Critical   Reviews in Toxicology 1977). 
                      There may be a dermatitis producing resin (Lampe & 
                      Fagerstrom,   1968). 
                      There may be an alkaloid, and a glycoside which 
                      produce   cardiovascular and respiratory depression. 
                      Tetramethylpyrazine   (TMPZ), an amide alkaloid has 
                      been obtained from the stem of J.  podagrica (Ojewole 
                      & Odebiyi, 1981). 

                      Atropine-like effects have also been reported 
                      following ingestion   of Jatropha multifida (Aplin 
                      1976). 

             3.3.2    Description, chemical structure, stability
                      Curcin: 
                      Phytotoxins or toxalbumins are large, complex protein 
                      molecules of  high toxicity.  They resemble bacterial 
                      toxins in structure and   physiological effects.  
                      Phytotoxins are heat labile, and can be   positively 
                      identified by precipitin reactions with sera 
                      containing  known antibodies (Kingsbury 1964). Curcin 
                      is said to be highly   irritant and remains in the 
                      seed after the oil has been expressed. 
                      
                      Tetramethylpyrazine (TMPZ):
                      CAS:  1124-11-4
                      MW:  136.22
                      Molecular formula:  C8-H12-N2

             3.3.3    Other physico-chemical characteristics
                      Curcin is unable to penetrate cell walls, this has 
                      been  indicated by the fact that these proteins do 
                      not affect protein  synthesis by Ehrlich ascites 
                      cells.  This is thought to be because  they lack a 
                      carrier moiety or at least the galactose-binding 
                      groups by which ricin binds to cell membranes.  This 
                      was discovered when it was found that the activity of 
                      curcin in cell-free systems is  not increased by 
                      treatment with 2-mercaptoethanol, which greatly  
                      enhances the inhibitory effect of ricin and abrin by 
                      splitting   their molecules into an effector and a 
                      carrier moiety (Stirpe et   al.,1976). 
    3.4      Other chemical contents of the plant
             No further information was available at the time of 
              preparation of the  monograph. 
    4.  USES/CIRCUMSTANCES OF POISONING
    4.1      Uses
             Jatropha is an ornamental plant naturalised in many tropical 
             areas.    The roots, stems, leaves seeds and fruits of the 
             plant have been widely used in traditional folk medicine in 
             many parts of West Africa.  The seeds of J.   curcas have been 
             used as a purgative, antihelminthic and abortifacient as   
             well as for treating ascites, gout, paralysis and skin 
             diseases.  The seed   oil of the plant has been used as an 
             ingredient in the treatment of   rheumatic conditions, itch 
             and parasitic skin diseases, and in the treatment of fever, 
             jaundice and gonorrhoea, as a diuretic agent, and a mouth-
             wash.   
             The leaf has been used  as a haemostatic agent and the bark as 
             a fish  poison.  In certain African  countries people are 
             accustomed to chewing  these seeds when in need of a  
             laxative. 

             J. curcas seeds have been found to be highly effective against 
             Strongyloides papillosus infection in goats (Adam & Magzoub, 

             in press).  It has also been   suggested that J. curcas seeds 
             could be a useful chemotherapeutic agent   provided that it is 
             active at a non-lethal dose (Adam, 1974).  This may be   
             because of it's reported antihelminthic activity. 

    4.2      High risk circumstances
             As these plants are grown as an ornamental they will often be 
             found in  gardens and public areas and therefore will be 
             easily accessible.  As  Jatropha are fruit bearing and the 
             seeds have a pleasant taste, the plants  are particularly 
             attractive to children. 
             This species of plant is not usually eaten by animals but 
             drought leading to an acute shortage of grass creates a 
             situation in which animals are forced to consume the plants 
             and their constituents in varying amounts. 

    4.3      High risk geographical areas
             Found in tropical countries throughout the world; including 
             tropical  America,  warmer parts of Australia (Queensland and 
             the Northern Territory), Florida  (chiefly south of Orlando), 
             Hawaiian Islands and Africa (Mozambique,  Zambia,  Transvaal, 
             Natal), Asia. 
    5.  ROUTES OF ENTRY
    5.1      Oral
             All cases of systemic poisoning have resulted from ingestion 
             of plant  material (in most cases the seeds). 
    5.2      Inhalation
             No relevant information at the time of preparation of the 
             monograph. 
    5.3      Dermal
             No relevant information at the time of preparation of the 
             monograph. 
    5.4      Eye
             No relevant information at the time of preparation of the 
             monograph. 
    5.5      Parenteral
             No relevant information at the time of preparation of the 
             monograph. 
    5.6      Others
             No relevant information at the time of preparation of the 
             monograph. 
    6.  KINETICS
    6.1      Absorption by route of exposure
             INGESTION:  Phytotoxins are well absorbed from the 
             gastrointestinal  tract. The onset of symptoms may be 
             developed one or more hours. 
    6.2      Distribution by route of exposure
             No relevant information at the time of preparation of the 
             monograph. 
    6.3      Biological half-life by route of exposure
             No relevant information at the time of preparation of the 
             monograph. 

    6.4      Metabolism
             Curcin - phytotoxins are partly metabolised in the digestive 
             tract. 

    6.5      Elimination by route of exposure
             No relevant information at the time of preparation of the 
             monograph. 
    7.  TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY
    7.1      Mode of action
             Phytotoxins (toxalbumins):  It has been suggested that in vivo   
             phytotoxins act as proteolytic enzymes, owing their toxicity 
             to the   breakdown of critical proteins and the accumulation 
             of ammonia (Kingsbury,   1964). 
             
             Tetramethylpyrazine (TMPZ):  Has been found to possess a non-
             specific   spasmolytic and vasodilator activity (Ojewole & 
             Odebiyi, 1981).  These   actions may account,  at least in 
             part,  for the reported hypotensive   (depressor) effects of 
             the amide alkaloid in experimental animals.  TMPZ has also 
             been found to possess neuromuscular-blocking effects similar 
             to   d-tubocurarine (Ojewole & Odebiyi, 1980). 

    7.2      Toxicity
             7.2.1    Human data
                      7.2.1.1  Adults
                               In some instances as few as three seeds have   
                               produced toxic symptoms. In others, 
                               consumption of as   many as 50 seeds has 
                               resulted in relatively mild symptoms. There 
                               is one report where the ingestion of only 
                               one seed   in an adult has produced toxic 
                               symptoms.  It has been   suggested that 
                               there may be two strains one with toxic   
                               seeds and one without (Kingsbury, 1964).  
                               Curcin, the   phytotoxin or toxalbumin found 
                               in  Jatropha curcas is   similar to ricin 
                               the phytotoxin found in the castor bean   
                               (Ricinis).  The minimum lethal dose of 
                               ricin, when  administered by injection, may 
                               be as small as 0.00000001% of body weight, 
                               although oral toxicity is probably several   
                               hundred times less (Kingsbury, 1964). 
                      7.2.1.2  Children
                               Toxicity is thought to be the same as for 
                               adults, thus, as few as 1-3 seeds may 
                               produce toxic symptoms. 
             7.2.2    Animal data
                      Poisoning from ingestion of the seeds of the Jatropha 
                      plant  is well known in veterinary practice and 
                      autopsy findings include,  severe gastro-enteritis, 
                      nephritis, myocardial degeneration,   
                      haemagglutination, and subepicardial and 
                      subendocardial   haemorrhages as well as renal 
                      subcortical and subpleural bleeding. 
                      
                      One study found a high mortality rate in mice fed 50% 
                      and 40% J.  curcas.  The important symptoms of 
                      poisoning included diarrhoea,   inability to keep 
                      normal posture, depression and lateral   recumbency.  
                      The degree of the pathological changes observed in 

                      the small intestines, liver, heart, kidneys, and 
                      lungs was related to the level of Jatropha in the 
                      diet.  The most marked pathological  changes were 
                      catarrhal enteritis, erosions of the intestinal 
                      mucosa, congestion and haemorrhages in small 
                      intestines, heart and lungs  and fatty changes in the 
                      liver and kidneys (Adam, 1974). 
                      
                      Another oral dosing study undertaken using mice found 
                      that curcin,  as compared with crotin found in the 
                      seeds of croton tiglium, had a   slightly more rapid 
                      action with symptoms beginning at 12 hours and   most 
                      deaths occurring within 48 hours of poisoning.  An 
                      acute LD50   of 9.11mg/mouse was calculated at 48 
                      hours and a delayed LD50 of   5.83mg/mouse was 
                      calculated at 7 days.  The behaviour of the   animals 
                      was similar to that of mice treated with crotins, 
                      except   for some neurological symptoms (waddling, 
                      fine tremors, rocking,   occasionally convulsions), 
                      which were present especially among   animals 
                      poisoned with the highest doses of curcin.  Post-
                      mortem   examinations showed lesions in the liver, 
                      pancreas and spleen,   hyperaemia of the intestine, 
                      sometimes ascites; the whole picture  resembled that 
                      of rats poisoned with ricin. (Stirpe et al.,1976) 
                      
                      In young ruminants oral doses of 0.5 to 10g/kg/day 
                      caused death  after dosing for periods ranging from 1 
                      day to 2 weeks.  The   clinical, haematological, and 
                      pathological changes indicated that   J. aceroides 
                      reduced the ability of the liver to synthesize 
                      protein, although there was no evidence of 
                      interference with the excretion   of bilirubin.  
                      Kidney dysfunction and haemoconcentration also   
                      occurred.  Postmortem and histological findings were 
                      similar to   those found above in studies with mice. 
                      (Barri et al., 1983) 
                      
                      A study assessing the acute oral toxicity of J. 
                      curcas showed that  different ruminants had different 
                      susceptibilities to the effect of   J. curcas.  
                      Calves which received 0.25 or 1g/kg died within 19 
                      hours of administration, whilst goats given similar 
                      daily doses   were either killed or died within 7 to 
                      21 days.  It was not   established whether this 
                      species difference lies in direct   cytotoxic action 
                      or in the capacity with which the active   substances 
                      contained in J. curcas seed are converted in vivo to   
                      metabolites more or less toxic than the parent 
                      compounds. (Ahmed &  Adam, 1979) 
                      
                      Feeding chicks seeds produced growth depression,  
                      hepatonephropathies, and haemorrhages. (Micromedex 
                      1974-1994) 

             7.2.3    Relevant in vitro data

                      In vitro phytotoxins cause agglutination of 
                      erythrocytes   (Joubert et al., 1984).  It has been 
                      observed that the seeds of J.  curcas contain 
                      proteins that are toxic to animals and inhibit   
                      protein synthesis in a cell-free system (lysate of 
                      rabbit   reticulocytes), but not in whole cells 
                      (Stirpe et al., 1976). 
    7.3      Carcinogenicity
             The seed oil of J. curcas was found to contain skin tumour 
             promoters in a two-stage mouse carcinogenesis experiment.  The 
             "irritant fraction"   contained in the methanol extract of the 
             seed oil when partially purified   induced ornithine 
             decarboxylase in mouse skin and inhibited the specific   
             binding of 3H-12-O-tetradecanoylphorbol-13-acetate to a 
             particulate fraction  of mouse skin.  After initiation with 7, 
             12-dimethylbenz[a]anthracene (DMBA),  this "irritant fraction" 
             induced  tumours in the skin of 36% of the mice  tested in 30 
             weeks (Horiuchi et al., 1987). 
    7.4      Teratogenicity
             No relevant information at the time of preparation of the 
             monograph. 
    7.5      Mutagenicity
             No relevant information at the time of preparation of the 
             monograph. 
    7.6      Interactions
             No relevant information at the time of preparation of the 
             monograph. 
    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
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.1.2  Biomedical analyses
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.1.3  Arterial blood gas analysis
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.1.4  Haematological analyses
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.1.5  Other (unspecified) analyses
                               No relevant information at the time of   
                               preparation of the monograph.
             8.1.2    Storage of laboratory samples and specimens
                      8.1.2.1  Toxicological analyses                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.2.2  Biomedical analyses
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.2.3  Arterial blood gas analysis
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.2.4  Haematological analyses
                               No relevant information at the time of   

                               preparation of the monograph.
                      8.1.2.5  Other (unspecified) analyses
                               No relevant information at the time of   
                               preparation of the monograph.
             8.1.3    Transport of laboratory samples and specimens
                      8.1.3.1  Toxicological analyses
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.3.2  Biomedical analyses
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.3.3  Arterial blood gas analysis
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.3.4  Haematological analyses
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.1.3.5  Other (unspecified) analyses
                               No relevant information at the time of   
                               preparation of the monograph.
    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)
                               No relevant information at the time of   
                               preparation of the monograph.  

                      8.2.1.2  Advanced Qualitative Confirmation Test(s)
                               Extraction of J. curcas seeds for the 
                               preparation of crude curcin has used 8 x 
                               250ml of ethyl ether.  The  ether has been 
                               removed by filtering.  The resulting powder 
                               is then dried and then extrated with 1L of 
                               cold   0.005M-sodium phosphate buffer, pH 
                               7.2, containing   0.2M-NaCl/100g of seeds.  
                               The mixture is stirred and left  overnight.  
                               After centrifugation the supernatant is   
                               brought to 100% saturation with solid 
                               (NH4)2SO4.  The   protein precipitate is 
                               then collected by centrifugation   and 
                               dissolved in a minimum amount of 
                               phosphate/NaCl buffer and then dialysed for 
                               24-48 hour against a continuous  flow  of 
                               the same buffer.  At the end of dialysis a 
                               brown  precipitate remains and is removed by 
                               centrifugation.  (Stirpe et al., 1976) 
                               
                               Analysis of this crude preparation using a 
                               column of   Sephadex G-100 has eluted three 
                               peaks referred to as   curcin I, II and III. 
                               These proteins were found to have  different 
                               properties, curcin I is more toxic and 
                               brings  about different symptoms  and 
                               lesions in vivo, whereas  curcin II was much 
                               more  active on protein synthesis  (Stirpe 
                               et al., 1976). 
                      8.2.1.3  Simple Quantitative Method(s)

                               No relevant information at the time of   
                               preparation of the monograph.
                      8.2.1.4  Advanced Quantitative Method(s)
                               No relevant information at the time of   
                               preparation of the monograph.
             8.2.2    Tests for biological specimens
                      8.2.2.1  Simple Qualitative Test(s)
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.2.2.2  Advanced Qualitative Confirmation Test(s)
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.2.2.3  Simple Quantitative Method(s)
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.2.2.4  Advanced Quantitative Method(s)
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.2.2.5  Other Dedicated Method(s)
                               No relevant information at the time of   
                               preparation of the monograph.
             8.2.3    Interpretation of toxicological analyses
                      No relevant information at the time of preparation of 
                      the   monograph. 
    8.3      Biomedical investigations and their interpretation
             8.3.1    Biochemcial analysis
                      8.3.1.1  Blood, plasma or serum
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.3.1.2  Urine
                               No relevant information at the time of   
                               preparation of the monograph.
                      8.3.1.3  Other fluids
                               No relevant information at the time of   
                               preparation of the monograph.
             8.3.2    Arterial blood gas analyses
                      No relevant information at the time of preparation of 
                      the   monograph. 
             8.3.3    Haematological analyses
                      No relevant information at the time of preparation of 
                      the   monograph. 
             8.3.4    Interpretation of biomedical investigations
                      No relevant information at the time of preparation of 
                      the   monograph. 
    8.4      Other biomedical (diagnostic) investigations and their 
             interpretation 
             No relevant information at the time of preparation of the 
             monograph. 
    8.5      Overall Interpretation of all toxicological analyses and 
             toxicological investigations 
             No relevant information at the time of preparation of the 
             monograph. 
    8.6      References
             No relevant information at the time of preparation of the 
             monograph. 
    9.  CLINICAL EFFECTS

    9.1      Acute poisoning
             9.1.1    Ingestion
                      Symptoms of poisoning are likely to be similar for 
                      species  of Jatropha. There is usually a delay of an 
                      hour or more between  consumption of  the plant and 
                      the occurrence of symptoms.  Symptoms are largely  
                      those associated with gastro-intestinal irritation.  
                      There is acute abdominal pain and a burning sensation 
                      in the throat about half an hour after  ingestion of 
                      the seeds followed by nausea,  vomiting and profuse  
                      watery diarrhoea.  In severe poisoning,  these 
                      symptoms progress to haemorrhagic gastroenteritis and  
                      dehydration.  Polydipsia can be  extreme.  Salivation 
                      and sweating  may occur.  There may be skeletal  
                      muscle spasm.  Intense hyperpnoea or a quick panting 
                      respiration is  seen together with  hypotension and 
                      electrocardiographic  abnormalities.  There may be  
                      CNS and cardiovascular depression,  children are more 
                      susceptible;  this may be either a direct effect  of 
                      toxins or secondary to  dehydration.  
                       
                      In one report, as well as gastrointestinal symptoms, 
                      atropine-like  effects developed eight hours after 
                      ingestion of Jatropha multifida   (Aplin, 1976).  
                      Symptoms included sweating, dry skin and mouth,   
                      slight mydriasis, mild tachycardia and flushing of 
                      facial skin and   persisted for four hours. 

             9.1.2    Inhalation
                      No relevant information at the time of preparation of 
                      the   monograph. 

             9.1.3    Skin exposure
                      Primary chemical irritation from  mechanical and/or 
                      chemical injury (Lampe & Fagerstrom, 1968). 

             9.1.4    Eye contact
                      Primary chemical irritation from mechanical and/or 
                      chemical  injury. 
             9.1.5    Parenteral exposure
                      No relevant information at the time of preparation of 
                      the   monograph. 
             9.1.6    Other
                      No relevant information at the time of preparation of 
                      the   monograph. 
    9.2      Chronic poisoning
             9.2.1    Ingestion
                      No relevant information at the time of preparation of 
                      the   monograph. 
             9.2.2    Inhalation
                      No relevant information at the time of preparation of 
                      the   monograph. 
             9.2.3    Skin exposure
                      No relevant information at the time of preparation of 
                      the   monograph. 
             9.2.4    Eye contact

                      No relevant information at the time of preparation of 
                      the   monograph. 
             9.2.5    Parenteral exposure
                      No relevant information at the time of preparation of 
                      the   monograph. 
             9.2.6    Other
                      No relevant information at the time of preparation of 
                      the   monograph. 
    9.3      Course, prognosis, cause of death
             In non-fatal cases the course of intoxication is short; the 
             patient may become asymptomatic within 24 hours.  Recovery 
             seems to be the rule. 
    9.4      Systematic description of clinical effects
             9.4.1    Cardiovascular
                      Hypotension with a fast weak pulse. Shock due to 
                      fluid and  electrolyte loss may occur. 
                      Electrocardiographic abnormalities. 
             9.4.2    Respiratory
                      Hyperpnoea.
             9.4.3    Neurological
                      9.4.3.1  CNS
                               There may be CNS depression either as a 
                               direct   result of toxins or secondary to 
                               hypotension. Seizures have been mentioned in 
                               association with  toxalbumin poisoning, but 
                               generally in animal cases or in  symptom 
                               summaries rather than actual case reports  
                               (Micromedex, 1974-1994). 
                      9.4.3.2  Peripheral nervous system
                               No relevant information at the time of   
                               preparation of the monograph.

                      9.4.3.3  Autonomic nervous system
                               There have been reports of salivation, 
                               sweating   and abdominal cramping occurring 
                               in human intoxications of Jatropha 
                               macrorhiza root (Consroe and Glow, 1975).  
                               This suggests some cholinergic activity. 
                               
                               Contrary to this, atropine-like effects have 
                               been reported (Aplin, 1976); thus diminished 
                               cholinergic stimulation  may  be evident.  
                               Mydriasis, dry mouth, flushed hot dry  skin,  
                               tachycardia, etc.. 

                      9.4.3.4  Skeletal and smooth muscle
                               The muscles and extremities may be 
                               contracted by  spasms.  Intestinal spasm can 
                               be severe. 
             9.4.4    Gastrointestinal
                      Acute abdominal pain and a burning sensation in the  
                      throat  about half an hour after ingestion of the 
                      seeds.  This is  followed by nausea, vomiting and 
                      profuse watery diarrhoea.  The  vomitus and  faeces 
                      may contain blood.   Lesions  are those of 
                      haemorrhagic gastro-intestinal inflammation.  

             9.4.5    Hepatic
                      Liver damage may occur in serious cases of toxalbumin  
                      poisoning. There may be increases ALT, total 
                      bilirubin, and AST.  (Micromedex, 1974-1994) 
             9.4.6    Urinary
                      9.4.6.1  Renal
                               Oliguria, probably secondary to hypotension   
                               rather than direct renal toxicity.  
                               Urinalysis may reveal  haemoglobinuria and 
                               albuminuria. 
                      9.4.6.2  Others
                               No relevant information at the time of   
                               preparation of the monograph.
             9.4.7    Endocrine and reproductive systems
                      No relevant information at the time of preparation of 
                      the   monograph. 
             9.4.8    Dermatological
                      Dermatitis as a result of primary chemical irritation   
                      possibly in conjunction with mechanical injury can 
                      occur in most,  if not all, individuals.  Reactions 
                      occur soon after exposure.  The severity of the 
                      reaction is dependent on the extent and duration  of 
                      contact.  Hypersensitisation may also develop. 
             9.4.9    Eye, ears, nose, throat:  local effects
                      Retinal haemorrhages, optic nerve injury have been 
                      reported  in toxalbumin poisoning (Micromedex, 1974-
                      1994). 
             9.4.10   Hematological
                      Haemoconcentration secondary to fluid loss.
                      Toxalbumins are haemagluttinating. Effects in 
                      poisoning are minimal even though the effect is 
                      prominent in vitro.  (Micromedex,  1974-1994) 
             9.4.11   Immunological
                      No relevant information at the time of preparation of 
                      the   monograph. 
             9.4.12   Metabolic
                      9.4.12.1 Acid base disturbances
                               Acid base disturbances are not typical in  
                               toxalbumin poisoning (Micromedex, 1974-1994)
                      9.4.12.2 Fluid and electrolyte disturbances
                               Dehydration which is often severe. 
                               Electrolyte  disturbances. 
                      9.4.12.3 Others
                               No relevant in formation at the time of  
                               prparation of the monograph.
             9.4.13   Allergic reactions
                      Stated as being a primary chemical irritant (Lampe &   
                      Fagerstrom, 1968), but hypersensitivity reactions may 
                      occur in   susceptible individuals.  The inflammation 
                      resulting from primary  chemical irritant effects of 
                      Jatropha is a predisposing factor to   the 
                      development of contact allergy. 
             9.4.14   Other clinical effects
                      Toxoalbumin poisoning may produce fever (Micromedex,  
                      1974-1994).

             9.4.15   Special risks
                      No relevant information at the time of preparation of 
                      the   monograph. 
    9.5      Others
             Oedematous swelling of several organs.
    10. MANAGEMENT
    10.1     General principles
             The management of Jatropha poisoning is similar to that for 
             the castor bean (Ricinis).  Decontamination is indicated for 
             all known or suspected  poisonings.  There is no antidote.  
             Rehydration, either voluntary water  ingestion or i.v. fluid 
             administration, to counteract fluid lost due to  vomiting and 
             diarrhoea is critical.  Treatment is essentially  symptomatic  
             and supportive.  The more critical analyses and investigations  
             are fluid  and electrolytes, acid-base status, full blood 
             count, and renal  and hepatic function.  Monitor level of 
             consciousness.  Specific therapy may  be  indicated for 
             haemorrhagic gastrointestinal damage, skeletal muscle and   
             gastrointesinal spasm, excessive salivary secretions and 
             haemoglobinuria.  After substantial exposures to toxalbumin 
             containing plants, an observation  period of up to 8 hours is 
             advised. 

    10.2     Relevant laboratory analyses and other investigations
             10.2.1   Sample collection
                      Blood and urine sample collection.
             10.2.2   Biomedical analysis
                      Complete blood count, electrolytes, blood urea 
                      nitrogen,   creatinine, acid-base status, glucose, 
                      prothrombin time, liver   enzymes, amylase, and 
                      urinalysis. 
             10.2.3   Toxicological/toxinological analysis
                      No relevant information at the time of preparation of 
                      the   monograph. 
             10.2.4   Other investigations
                      Monitor hepatic, renal, pancreatic, and red blood 
                      cell   function. 
    10.3     Life supportive procedures and symptomatic treatment
             Fluid and electrolyte status may deteriorate suddenly and 
             severely.  Give IV fluids and electrolyte as necessary to 
             restore and maintain fluid  and electrolyte balance.   Monitor 
             renal function and alkalinize urine to  minimize effects of 
             haemoglobinuria.  Treat haemorrhagic gastro-intestinal  damage 
             as for peptic ulceration.  Observe for signs of CNS depression 
             and  initiate assisted  ventilation if necessary. 

    10.4     Decontamination
             In all cases of ingestion or suspected ingestion, if the 
             patient is  seen sufficiently soon (within 1-2 hours of 
             ingestion), induce emesis with  Ipecac Syrup or perform 
             gastric lavage unless vomiting has been extensive. 
    10.5     Elimination
             Administer activated charcoal and a cathartic to enhance and 
             hasten  elimination, although severe diarrhoea may make this 
             unnecessary. Cathartic  administration must be cautious due to 
             the risk of exacerbating purgation  and fluid loss. 

             Phytotoxins are non dialysable.  However, methods for 
             eliminating the toxins from the blood (haemodialysis, 
             peritoneal dialysis, charcoal haemoperfusion   etc.) have been 
             suggested as useful, whether this removes plant toxins  other 
             than phytotoxins from the blood and therefore improves the 
             prognosis  and  hastens the recovery, is yet to be 
             demonstrated.  A possible indication  for  this would be life-
             threatening CNS or respiratory depression (not  secondary  to 
             hypovolaemia) which is unresponsive to other supportive  
             measures. 

    10.6     Antidote/antitoxin treatment
             10.6.1   Adults
                      No antidote. Many antidotes have been investigated 
                      for  toxalbumin poisoning, but no specific treatments 
                      are available.  (Micromedex, 1974-1994) 
             10.6.2   Children
                      No antidote. Many antidotes have been investigated 
                      for  toxalbumin poisoning, but no specific treatments 
                      are available.  (Micromedex, 1974-1994) 
    10.7     Management discussion
             In cases of poisoning where dehydration has been severe close 
             follow  up of renal function is imperative. 
    11. ILLUSTRATIVE CASES
    11.1     Case reports from literature
             Case History:  A 3-year-old Hawaiian-Caucasian boy was 
             admitted to   Kauikeoani Children's Hospital on September 20, 
             1958, because of persistent  vomiting and diarrhoea.  The 
             episodes were of sudden onset following the   ingestion of 
             several large black seeds gathered from an over-hanging branch  
             of a neighbour's tree (later identified as Jatropha curcas).  
             He was unable to retain any ingested food or water.  Each 
             intake was vomited almost   immediately after ingestion.  The 
             vomitus was said to contain the white   granulated material 
             and the particles of the black shells.  After several   bouts 
             of vomiting, the child started to have watery bowel movements.  
             The   stools contained seed particles also.  Three and a half 
             hours following the  ingestion of the seeds, the child 
             appeared lethargic.  His skin felt cold   and clammy.  The 
             child was admitted to the hospital in severe dehydration.  The 
             family and past history were non-contributory. 
             Blood pressure was 100/70; pulse 130; respiration 40; 
             temperature 99.8F   (rectal).  The patient appeared 
             lethargic, cyanotic, and acutely ill.  The   peripheral 
             vessels were constricted.  Severe dehydration was indicated by   
             the poor skin turgor, sunken eyeballs, and deepening 
             periorbital shadows.    The bowel sounds were hyperactive.  
             The remainder of the physical   examination was within normal 
             limits.  The haemoglobin was 14.2gm/100mL, the red blood cell 
             count , 5.4 million, and the platelets were normal.  The
             white blood cell count was 27,000 per cu mm, and the 
             differential was   normal.  The urine showed a trace of 
             albumin, and elements consisting of 2-4 white blood cells per 
             high power field and many granular and some hyaline  casts.  
             The carbon oxide level was 17mEq/L; chlorides, 101mEq/L; and   

             potassium, 4.4mEq/L.  The stool cultures were negative for 
             pathogens. 
             
             The child was given 1000mL of isotonic electrolyte solution.  
             Blood was   drawn for type and cross matching.  The patient 
             was oliguric for the first   24 hours.  He responded to 
             treatment, and twenty hours after admission he   was able to 
             tolerate oral feedings without any vomiting or diarrhoea, and   
             was voiding well.  He was discharged from the hospital after 3 
             days without  complication.  (Ho 1960). 
             
             Case History:  Two sisters aged 5 and 3 years respectively 
             were rushed to   Ahmadu Bello University Teaching Hospital, 
             Zaria, Nigeria, with a history of vomiting and drowsiness 
             about 5 hours after ingesting unspecified  quantities  of ripe 
             seeds of J. curcas.  They had each vomited between 6 and 10 
             times  within the hour preceding their arrival.  There had 
             been no  diarrhoea and  the vomitus consisted of a whitish 
             material mixed with the  food they had  taken 2 hour 
             previously.  On examination they were well-fed  children,  
             afebrile, not pale, jaundiced or cyanosed but moderately  
             dehydrated.  There  was neither abdominal tenderness nor any 
             abnormal  finding on rectal  examination.  They were both 
             restless, drowsy but  rousable and their pupils  were normal 
             and reactive.  Laboratory  investigations revealed normal  
             haemoglobin, normal liver-function tests and mild alkalosis. 
             Treatment  consisted of rehydration with intravenous fluids 
             and sedation with small  doses of promethazine hydrochloride.  
             They  recovered rapidly and were both  discharged some 48 
             hours after admission.   (Abdu-Aguye et al.,1986). 
             
             Case History:  An 18 year old, well developed Caucasian male 
             was admitted to hospital at 11:45 p.m. because of persistent 
             vomiting, diarrhoea and   drowsiness.  The patient had 
             ingested 3 pieces (about 2 inches in diameter)  of a plant 
             root (identified as Jatropha macrorhiza) about 4 hours 
             earlier;  symptoms emerged about 1 hour after ingestion.  
             Except for drowsiness and   tenderness of all quadrants of the 
             abdomen, physical examination and   haematologic and urinary 
             laboratory values of the patient showed no striking 
             abnormalities.  Bed rest was prescribed and tap water was 
             given ad libitum to quench the paitients extreme polydipsia.  
             After an uneventful nights   sleep, the patient was discharged 
             at 10:30 the next morning without   complications.  (Consroe 
             and Glow, 1975). 
             
             Case History:  A 48 year old, well developed Caucasian male 
             was admitted to  hospital at 3 p.m. because of persistent 
             diarrhoea after ingesting an   unknown quantity of a sweet 
             tasting potato-like plant root (identified as   Jatropha 
             macrorhiza) at 8 a.m.  Bouts of severe vomiting and diarrhoea 
             about every 3 minutes appeared 45 to 60 minutes after 
             ingestion and persisted   throughout most of the afternoon.  
             The patient also complained of drowsiness, perspiration, 
             salivation, polydipsia, cramps in the legs and abdomen and  of  
             feeling cold and clammy.  Physical examination revealed a poor 

             skin  turgor,  sunken eyeballs excessive salivary secretions 
             and no lesions of  mouth or  throat.  there was tenderness in 
             all quadrants of the abdomen and  deep  tendon reflexes were 
             hyperactive and intermittent muscle spasms in  toes and  calfs 
             were apparent.  Vital signs and urinary and haematological  
             values were  normal except for elevations in haematocrit (60%) 
             and  haemoglobin  (20.2gm/100ml).  Initially, 1 litre of 5% 
             dextrose in water,  atropine (0.5mg  im.) and diazepam (5mg, 
             im.) every 6-8 hours as needed were prescribed.   After a 
             restful night, the patient was discharged at 9 a.m.,  the 
             following  morning without complications.  (Consroe and Glow, 
             1975). 

    11.2     Internally extracted data on cases
             No relevant information at the time of preparation of the 
             monograph. 
    11.3     Internal cases
             No relevant information at the time of preparation of the 
             monograph. 
    12. ADDITIONAL INFORMATION
    12.1     Availability of antidotes/antitoxins
    12.2     Specific preventive measures
    12.3     Other
    13. REFERENCES
    13.1     Clinical and toxicological
             Abdu-Aguye I, A Sannusi, R A Alafiya-Tayo, S R Bhusnurmath. 
             (Jul 1986) Acute Toxcity Studies with Jatropha curcas L.  
             Human Toxicology,   5(4):269-274. 
             
             Adam S E I.  (Mar 1974)  Toxic effects of Jatropha Curcas in 
             mice.    Toxicology, 2(1):67-76. 
             
             Adam S E I, M Magzoub.  Preliminary observations on the 
             anthelmintic   activity of Jatropha curcas against 
             strongyloides and Haemonchus infections  in goats and sheep.  
             Topical Animal Health Production 25: (in press).  Cited   in 
             Ahmed & Adam, 1979. 
             
             Ahmed O M M, S E I Adam. (Jul 1979)  Effects of Jatropha 
             curcas on Calves.   Veterinary Pathology 16(4):476-482. 
             
             Aplin T E H. (May 1976)  Poisonous Garden Plants and Other 
             Plants Harmful to Man in Australia.  Western Australia 
             Department of Agriculture, Bulletin   3964. 
             
             Barri M E S, T O Onsa, A A Elawad, N Y Elsayed, I A Wasfi, E M 
             Abdul Bari, S E I Adam.  (1983)  Toxicity of Five Sudanese 
             Plants to Young Ruminants.    Journal of Comparative 
             Pathology, 93:559-575. 
             
             Consroe P F, Glow D E.  (1975).  Clinical Toxicology of the 
             Desert Potato :  Two Case Reports of Acute Jatropha Macrorhiza 
             Root Ingestion.  Arizona   Medicine, 23(6):475-477. 
             
             CRC Critical Review in Toxicology.  (Nov 1977).  Higher Plant 
             Genera and   their toxins,  pp 213-237 

             Ho Richard K B.  (March-April 1960).  Acute Poisoning From the 
             Ingestion of  Seeds of Jatropha Curcas.  Medical Journal of 
             Hawaii, 19(4):421-423.  
             
             Horiuchi T, H Fujiki, M Hirota, M Suttajit, M Suganuma, A 
             Yoshioka, V   Wongchai, E Hecker, T Sugimura.  (Mar 1987)  
             Presence of tumor promoters in  the seed oil of Jatropha 
             curcas L. from Thailand.  Japanese Journal of   Cancer 
             Research, 78(3):223-236. 
             
             Joubert P H, J M M Brown, I T Hay, P D B Sebata.  (May 1984).  
             Acute   poisoning with Jatropha curcas (purging nut tree) in 
             children.  South   African Medical Journal, 65:729-730. 
             
             Kingsbury J M.  Poisonous Plants of the United States and 
             Canada, 1964. 
             
             Lampe and Fagerstrom.  (1968).  Plant Toxicity and Dermatitis 
             - A Manual for Physicians.  The Williams and Wilkins Company, 
             Baltimore. 
             
             Ojewole J A O, O O Odebiyi. (1980)  Neuromuscular and 
             Cardiovascular Actions of Tetramethylpyrazine from the Stem of 
             Jatroha Podagrica.  Planta Medica, 38:332-338. 
             
             Ojewole J A O, O O Odebiyi. (1981)  Mechanism of the 
             Hypotensive Effect of   Tetramethylpyrazine, an Amide Alkaloid 
             from the Stem of Jatropha podagrica. 
             
             Stirpe F, A Pession-Brizzi, E Lorenzoni, P Strocchi, L 
             Montanaro, S Sperti.  (Apr 1976)  Studies on the Proteins from 
             the Seeds of Croton tiglium and of Jatropha curcas.  Toxic 
             properties and inhibition of protein synthesis in  vitro.  
             Biochemistry Journal, 156(1):1-6. 

    13.2     Botanical
    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
    ADDRESS(ES)
    June 1994
    Juliette Begg and Tania Gaskin
    National Toxicology Group
    P.O. Box 913
    Dunedin
    NEW ZEALAND





    See Also:
       Toxicological Abbreviations