Jatropha multifida
| 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 multifida
1.2 Family
Euphorbiaceae
1.3 Common name(s)
Adenoropium multifidum
Coral plant
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 multifida is a small tree or shrub, commonly
3-7 feet tall, but may reach 20 feet.
Leaves: dark green; alternate, simple, palmately cut
into 9-11 deep narrow lobes. Large up to 1 foot
across.
Flowers: Small, scarlett centres with small yellow
petals, resemble a piece of coral. Borne in small,
loose clusters in ther axils of the leaves
Fruit: Yellow in colour, usually 3 angled capsule;
slightly over an inch long. The capsule does not open
on its own at maturityas do some of the other
Jatropha species. Each capsule contains 3 seeds. 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).
The latex of J. multifida contains a thioglucoside
which yields irritant mustard oil ( Micromedex, 1974-
1994).
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 99.8°F (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