PLANT TOXICOLOGY

1. NATURAL
TOXICANTS

2. DEFINITION
Toxic plant may be defined as
“One which detrimentally affects the health of
man or animal when eaten in such amount as
would be taken normally or under special
circumstances like restriction of choice of diet or
extreme hunger, due to the presence of known or
unknown toxic chemical substance in it” .

3. CLASSIFICATION OF PLANT
TOXINS
1. ALKALOIDS
2. GLYCOSIDES
3. ORGANIC ACIDS
4. ESSENTIAL OILS
5. FIXED OILS
6. TOXIC PROTEINS
7. BITTER PRINCIPLES
8. SAPONINS

4. 1. ALKALOIDS
 Complex nitrogen containing organic compounds having
one/more heterocyclic rings.
 Alkaline in nature.
 Bitter in taste and sufficient protection from being eaten by
cattle.
Some of the poisonous alkaloids are
1. Morphine from Poppy capsules
2. Emetine from Ipecacuanha
3. Strychnine from Nux-vomica seeds

5. 2. GLYCOSIDES
A glycoside is a molecule consisting of a sugar and a non-sugar
group, called an aglycone. The sugar group is known as the
glycone and can consist of a single sugar group or several sugar
groups..
Glycosides which produce harmful components on hydrolysis are
1. Sinigrin in Black mustard seeds
2. Sinalbin in White mustard seeds
3. Digitoxin in Digitalis

6. 3. ORGANIC ACIDS
Significant in poisonous point of view is oxalic acid.
Protoplasmic poison occurring in large amounts of
plants in form of oxalates.
Formic acid is an irritant is also found in some plants
specially in family “Urticaceae”

7. 4. ESSENTIAL OILS
 Volatile oils or essential oils are the odorous
principles found in various parts of plants. As they
evaporate when exposed to air at ordinary
temperature, that is why they are called Volatile
oils/essential oils.
 They sometimes possess sharp burning taste.
 At large doses can cause irritation to GIT with
diarrhoea ,vomiting , pain etc.

8. Some plants containing oils with toxic constituents are
Artemsia, Ruta, Ferula etc.

9. 5. FIXED OILS
These are compounds of glycerol with different kind
of fatty acids containing sterols and other substances
dissolved in them.
 Generally have laxative properties.
 Croton oil from Croton tiglium produces irritation to
skin.

10. 6. TOXIC PROTEINS
These are known as “TOXALBUMIN”.
 Observed in Leguminosae and Euphorbiaceae.
 Abrin from Abrus precatorious.
Croton from Croton tiglium.

11. 7. BITTER PRINCIPLES
Possess characteristic nauseous and bitter taste.
Purgative action.
Example
 Picrotoxin from Anamirta cocculus

12. 8. SAPONINS
Occurs in 400 species belonging to 50 families.
Toxic to cold blooded animals.
Poisonous saponins are known as SAPOTOXINS.

13. PLANT TOXICITIES IN
HUMANS & ANIMALS
Plant toxicities are produced due to the plant toxins.
Plant toxins effect the human body adversely & there
are some examples of some human toxicity of some
better known plants.

14. Plant examples Symptoms Toxin/comment
Philodendron, poison
ivy
Toxicodendron
radicans
Anacardiaceae
Allergic dermatitis. Rashes. Allergens located on the outer cells of the plant.
Dumb cane
(Dieffenbachia exotica
)
Araceae
Contact dermatitis.
Inflammation of mouth,
pain & stinging sensation.
Calcium oxalate crystals coated with
inflammatory proteins. Fine tubes contain
histamine & serotonin.
Rhamnus californica
Rhamnaceae
(California buckthorn)
Direct stomach irritation,
nausea, vomiting & diarrhea.
Emodin, Esculine.,Oil from seeds & nuts.

15. Apple
Malus domestica
Rosaceae
Seeds are mildly poisonous, containing a small amount
of amygdalin, a cyanogenic glycoside. The quantity
contained is usually not enough to be dangerous to
humans, but it is possible to ingest enough seeds to
provide a fatal dose.

16. Lemon
Citrus limon
Rutaceae
As well as lime, orange and other citrus fruits are
known to contain aromatic oils and compounds
of Psoralen which is toxic to dogs, cats and some
animals. The acid is found all over the entire plant.
Symptoms include vomiting, diarrhea, depression
and photosensitivity.

17. Genus Aconitum
Aconitum napellus
Ranunculaceae
Commonly called aconite, Wolfsbane and Monkshood.
All parts are poisonous. The poison is an alkaloid
called Aconitine which disables nerves, lowers blood
pressure and can stop the heart. Even casual skin
contact should be avoided; symptoms include
numbness, tingling and cardiac irregularity.

18. Strychnos nux-vomica
Loganiaceae
Commonly known as the strychnine tree.
The seeds usually contain about 1.5% strychnine, an
extremely bitter and deadly alkaloid. This substance
throws a human into intense muscle convulsions and
usually kills within three hours. The bark of the tree
may also contain brucine, another dangerous chemical.
It is used to kill the dogs.

19. Mango tree
Mangifera indica
Anacardiaceae
Mango peel and sap contain urushiol, the allergen in
poison ivy and poison sumac that can cause urushiol-
induced contact dermatitis in susceptible people.

20. HIGHER PLANT
TOXINS

21. 1. ESSENTIAL OILS
Cineol
Terpenes
Pine oil
CINEOL/EUCALYPTOL
B.O. Eucalyptus globulus
Family: Myrtaceae
Eucalyptol is also known by a variety of synonyms: 1,8-cineol, 1,8-cineole,
eucalyptol, cineol, cineole

22. Properties
Eucalyptol has a fresh camphor like smell and a spicy,
cooling taste. It is insoluble in water but miscible with
ether, ethanol and chloroform. The boiling point is 176
°C. Eucalyptol comprises up to 90 percent of the
essential oil of some species of the generic product
Eucalyptus oil, hence the common name of the
compound. It is also found in Camphor.

23. Uses
1. Flavoring and fragrance:
Because of its pleasant spicy aroma and taste, eucalyptol is
used in flavorings, fragrances and cosmetics. Cineole-based
eucalyptus oil is used as a flavoring at low levels (0.002%) in
various products, including baked goods, confectionery, meat
products and beverages. In a 1994 report released by five top
cigarette companies, eucalyptol was listed as one of the 599
additives to cigarettes. It was claimed that it was added to
improved the flavor.

24. 2. Medicinal:
Eucalyptol is an ingredient in many brands
of mouthwash and cough suppressant as well as an
inactive ingredient in body powder.
3. Insecticide and repellant:
Eucalyptol is used as an insecticide and insect repellent.

25. • The probable lethal dose of pure eucalyptus oil for
an adult is in the range of 0.05 ml to 0.5 ml/per kg
body weight.
• Severe poisoning has occurred in children after
ingestion of 4 ml to 5 ml of eucalyptus oil.

26. Toxicology
In higher-than-normal recommended doses,
eucalyptol is hazardous via ingestion, skin contact
or inhalation. It can have acute health effects
on behavior, respiratory tract and nervous system.
The acute oral LD50 is 2480 mg/kg (rat).
 It is classified as a reproductive toxin for females
and a suspect reproductive toxin for males.

27. Pine oil / Pineol
B.O. Pinus longifolia
Family: Pineacea
Pine oil is an essential oil obtained by the steam
distillation of twigs and cones from a variety of species
of pine.
USES:
It is used in aromatherapy, as a scent in bath oils, as a
cleaning product, it is naturally deodorizing and
antibacterial. It may also be used as a massage oil and
an antiseptic.

28. Chemical Composition
Chemically pine oil consists mainly of cyclic terpene
alcohols. It may also contain terpene hydrocarbon, ethers
and esters. The exact composition depends on various
factors such as the variety of pine from which it is
produced and the parts of the tree used.

29. Toxicology
Pine oil has a relatively low human toxicity level, a low
corrosion level however, it irritates the skin and
mucous membranes and has been known to cause
breathing problems. Large doses may cause central
nervous system depression.

30. 2. PHENYL PROPENES
1. Apiol
2. Safrole
3. Myristicin

31. APIOL
• Liquid Apiol
• Green oil of parsley
• Parsley apiol
 Apiol is an organic compound, phenyl propanoid derivative,
extracted from the leaves of parsley Petroselinum crispum
belonging to family Apiaceae.

32. Toxicity
In the middle age, plant containing apiol were used
by women to avoid pregnancy.
But many death cases, due to its abortion have been
reported.
Now more safer methods of abortion are available
so, apiol is almost forgotten.
At large doses, it cause nausea, damage liver and
kidney.

33. Safrole
Safrole is a phenyl propane it is a colorless or slightly
yellow oily liquid typically extracted from the root, bark
or the fruit of sassafras plants in the form of sassafras
oil.
B.O: Sassafras albidum
Family: Lauraceae

34. Uses
• Safrole is a simple organic compound found in
sassafras oil: It has a pleasant odor and used to flavor
root beer, but sassafras oil has fallen out of favor in
the past few years for a few reasons: first, safrol has
been deemed carcinogenic and banned as a flavoring
agent by the US FDA in June 8, 2007.

35. Toxicity
1. Besides being a cancer-causing agent, sassafras
can induce vomiting, stupor and hallucinations.
It can also cause abortion, diaphoresis and
dermatitis. Sassafras oil and safrole have been
banned for use as flavors and food additives by the
FDA because of their carcinogenic potential.

36. Myristicin
Source: It present in small amount in the essential oil of nutmeg,
the dried ripe seed of Myristica fragrans (Myristicaceae) and to lesser
extent in other species such as parsley and dill.
Toxicity: When myristicin is consumed in large portion, it become
toxic and causes fatty degeneration in the liver. Several intoxication
have been reported after the ingestion of approximately 5g of
nutmeg correspond to approximately 1-2mg myristicin/kg body
weight.
Sign and symptoms: In human consumption of nutmeg seeds in
large quantity has been reported to lead to facial flushing,
tachycardia, hypertension, dry mouth, blurred vision, psychoactive
hallucination and delirium.

37. 3. MONOTERPENES
THUJONE
Botanical source: Artemisia absinthium (Wormwood)
Family: Asteraceae
Part used: Oil from flowers and leaves
TOXICITY AND ACTIONS.
Thujone is reported to be toxic to brain, kidney and liver cells and could
cause convulsions if used in too high dose. Other thujone-containing plants
such as (Thuja occidentalis) are used in herbal medicine, mainly for their
immune-system stimulating effects. Side effects from the essential oil of this
plant include anxiety and sleeplessness, which confirms the central nervous
system effects of thujone.

38. MENTHOFURAN
Botanical source: Mentha piperita
Family : Labiatae
Part used : Leaves
Chemical nature : Menthofuran is an organic
compound which is highly toxic and produce fatal effects. It is
monoterpene which is 1.7% in peppermint oil.
Toxicity: After ingestion of menthofuran, it is metabolically
activated to chemically reactive intermediates that cause
hepatotoxicity.

39. 4. PLANT ACIDS
Oxalic acid
Source: Rhubarb, Spinach, Tea, Nuts, chocolate and some
grains are other good sources of oxalic acid.
Family: Polygonaceae, Amaranthaceae, Theaceae.

40. Toxicity: Oxalic acid is toxic because of its acidic and
chelating properties. It is especially toxic when ingested. As
little as 5 grams (71 mg/kg) may be fatal. Ulcerations of the
mouth, vomiting of blood and rapid appearance of shock,
convulsions, twitching and cardiovascular collapse may occur
following ingestion of oxalic acid or its soluble salts.
Oxalic acid can bind calcium to form calcium oxalate which is
insoluble at physiological pH. Calcium oxalate thus formed
might precipitate in the kidney tubules and the brain.
Hypocalcemia secondary to calcium oxalate formation might
disturb the function of the heart and nerves.

41. Resin Acid
Source: Pinus elliottii
Pinus taeda
Family: Pinaceae
Toxicity: It causes polymorphonuclear leukocytes and
human gingival fibroblasts in vitro.

42. Amino acids
Source: Pisum sativum( Peas)
Family: Leguminosae
Source: Sesamum indicum (Til)
Family: Pedaliaceae
Toxicity:
Cause growth depression.
Pulmonary Disease
Renal and hepatic disfunctioning.

43. GLYCOSIDES
CARDIOTONIC GLYCOSIDES
DIGITALIS
Synonyms: Foxglove, purple foxglove, folia digitalis,
digitalis folium
Biological source: Digitalis purpurea
Digitalis lanata
Part used: Dried leaves
Family: Scrophulariaceae

44. Habitat: Its habitat is southern and central European countries,
England, Germany, Holland , France, Northern USA and Kashmir.
Chemical constituents: Digitalis contains about 35 glycosides. The most
important compounds of medicinal importance are digitoxin, gitoxin and
gitaloxin which are secondary glycosides.
Digitoxin and gitoxin are the main active components of dried drug.
Uses: Digitalis is used as a cardiac stimulant and tonic. The drug
stimulates cardiac muscles, increase the systole of heart ventricle. The
drug is also useful in congestive heart failure and atrial fibrillation.
Toxicity: Digitalis toxicity produces CNS, visual, GI and cardiac
manifestations. Nausea, vomiting, and drowsiness are among the most
common extracardiac manifestations.

45. CNS symptoms of digitalis toxicity include Drowsiness, Lethargy, Fatigue, Neuralgia,
Headache, Dizziness, Confusion, Hallucinations, Seizures (rare) and neuropathic pain.
Visual aberration often is an early indication of digitalis toxicity. Yellow-green
distortion is most common but red, brown, blue and white distortions also occur.
Drug intoxication also may cause Snowy vision, Photophobia, Decreased visual acuity
,Yellow halos around lights (xanthopsia).
GI symptoms in acute or chronic toxicity include Anorexia ,Weight loss, Failure to
thrive (in pediatric patients), Nausea, Vomiting, Abdominal pain and Diarrhea.
Cardiac symptoms include Palpitations, Shortness of breath, Swelling of lower
extremities, Bradycardia and Dyspnea.
•

46. STROPHANTHUS
Synonyms: Strophanthus seeds, Semina strophanthi.
Biological source: Strophanthus kombe
Strophanthus hispidus
Part used: Ripe seeds
Family: Apocyanaceae
Habitat: East and central Africa

47. Chemical constituents:
Strophanthus contains a cardioactive glycoside
strophanthin-K (2-5%), kombic acid, choline, trigonelline, fixed oil
(30%), resin and mucilage. Strophanthin–K is a mixture of K-
strophanthoside, K-strophanthin-β and cymarin. Genin part of all
these glycosides is strophanthidin.
Uses:
It is used as cardiac tonic.
It also possess diuretic property.

48. Toxicity
In toxic doses the systolic contractions become very frequent and very
brief, followed, consequently, by enormous increase of blood pressure,
to which is added sudden cessation of the heart in systole. Respiration
ceases last.
It causes violent contraction of the heart muscle in extreme cases
being the only one of the heart poisons to leave the heart in systole
after death from its use.
It may induce gastric irritation if given too long or too frequently but
this effect rarely occurs.
Its action on unstriped muscular fiber is similar to that of ergot. In
some cases it affects the respiratory muscles so profoundly as to
produce respiratory paralysis and death.

49. SQUILL
Synonyms: Sea onion , bulbus scillae , scilla bulb, white
squill.
Biological source: Urginea maritime
Part used: Dried sliced scales of fleshy inner bulb.
Family: Liliaceae
Habitat: It grows in Mediterranean sea coasts of
Spain, France, Italy, Greece, Algeria , Morocco, Cyprus.

50. Chemical constituents:
The drug contains about dozen of cardioactive
glycosides Scillaren A , Scillaren B, Glucoscillaren A,
Proscillaridin A, Scillaridin A, Scilliglaucoside,
Uses:
Squill is used as expectorant .
It is also used as diuretic.
It also possess cardiotonic activity.

51. Toxicity
Subsequent effects seen with intoxication included
nausea, vomiting, seizures, hyperkalemia,
atrioventricular block and ventricular arrhythmias
resembling digitalis toxicity.

52. CYANOGENIC GLYCOSIDES
BITTER ALMOND
Synonyms: Badam, Amygdala amara
Biological source: Prunus amygdalus
Part used: Dried ripe seeds
Family: Rosaceae
Habitat: Its habitat is Italy, Spain, Southern France,
North America and Kashmir.

53. Chemical constituents:
Bitter and sweet almonds contain fixed oils (40-55%), proteins
(20 %), mucilage and emulsin. The bitter almond contains a colourless
crystalline cyanogenic glycoside (about 3%).
It also contains prunasin and β sitosterol.
Uses:
Bitter almond seeds have demulcent property.
It also possess mild laxative property.
It is also used as flavoring agent.
It is also used as a vehicle for oily injections.

54. WILD CHERRY BARK
Synonyms: Wild black cherry, cherry bark, prune bark.
Biological source: Prunus serotina
Part used: Dried stem bark
Family: Rosaceae
Habitat: United state and Canada.

55. Chemical constituents:
Wild cherry bark contains a cyanogenic glycoside,
prunasin, the enzyme prunase, benzoic acid, trimethyl gallic
acid, starch, tannin and volatile oil.
The enzyme emulsin hydrolyzes prunasin to benzaldehyde,
glucose and hydrocyanic acid.
Uses:
It is used in cough preparations as sedative, expectorant and
as a flavoring agent.

56. Toxicity of Cyanogenic
Glycosides
Potential toxicity of cyanoglycosides arises from enzymatic degradation to produce
hydrogen cyanide, resulting in acute cyanide poisoning. The enzyme responsible (β-
glucosidase) may arise from the plant material or from gut microflora. Clinical
symptoms of acute cyanide poisoning include rapid respiration, drop in blood pressure,
rapid pulse, headache, dizziness, vomiting, diarrhoea, mental confusion, stupor, blue
discoloration of the skin due to lack of oxygen (cyanosis), twitching and convulsions.
Cyanide is one of the most potent rapidly acting poisons known. Cyanides inhibit the
oxidative processes of cells causing them to die very quickly.
Because the body rapidly detoxifies cyanide, an adult human can withstand 50-60 ppm
for an hour without serious consequences. However, exposure to concentrations of
200-500 ppm for 30 minutes is usually fatal.
Aside from death, acute cyanide toxicity at small doses can cause headache, tightness in
throat and chest and muscle weakness. The effects of chronic (long-term) exposure to
cyanide are less well know.

57. Alkaloid Toxicity
Imidazole alkaloids
Botanical origin: Pilocarpus jaborandi
Family: Rutaceae
Part use: Dried leaflets
Toxicity and its treatment: Pilocarpine can enter the brain and
cause CNS disturbances. Poisoning with this is characterized by
exaggeration of various parasympathetic effects, including
diaphoresis and salivation.
Parenteral atropine, at doses that can cross the Blood-Brain barrier,
is administered to counteract its toxicity.

58. Tropane Alkaloid
Botanical origin: Atropa belladonna
Family: Solanaceae
Part used: Dried leaves & flowering tops.
Toxicity and its treatment: Depending on dose it may cause dry mouth, blurred vision,
sandy eyes, tachycardia, urinary retention and constipation. Effects on CNS include
restlessness, confusion, hallucinations and dillurium which may progress to depression,
collapse of circulatory and respiratory systems and cause death. In older individuals, the
use of atropine to induce mydriasis and cycloplegia is considered to be too risky, because
it may exacerbate an attack of glaucoma due to an increase in intraocular pressure in
someone with a latent condition. It may be dangerous in children, because they are
sensitive to its effects, particularly to the rapid increase in body temperature that it may
elicit. Low doses of cholinesterase inhibitors such as physostigma may be used to
overcome its toxicity.

59. Pyrrolizidine Alkaloids
There are more than 500 different pyrrolizidine alkaloids which are found in
over 6,000 plant species. The pyrrolizidine alkaloid-containing plants are
mostly members of the composite plants (asteraceae), borage families
(boraginaceae) as well as the legume family (fabaceae).
Toxicity: The typical toxic effects of PA affect the liver and in some case
the lungs. Animal experiments have demonstrated that certain pyrrolizidine
alkaloids are genotoxic carcinogens. Even though there are no findings
confirming that such an effect exists in humans, the data from animal
experiments are deemed to be relevant to human risk assessment as well.
The embryo toxic effect of certain PA is also known from animal
experiments. However, the data are incomplete and nothing is known about
the possible toxicity of PA to human development.

60. Lower Plant Toxins
Introduction:-
The term "biotoxin" is sometimes used to clearly confirm the
biological origin. Biotoxins are further classified into fungal
biotoxins or short mycotoxins, microbial biotoxins, plant
biotoxins, short phytotoxins and animal biotoxins. Toxins
produced by microorganisms are important virulence determinants
responsible for microbial pathogenicity and/or evasion of the
host immune response. Biotoxins vary greatly in purpose and
mechanism, and can be highly complex (the venom of the cone
snail contains dozens of small proteins, each targeting a specific
nerve channel or receptor), or relatively small protein.

61. Biotoxins in nature have two primary functions:
Predation in the spider, snake, scorpion, jellyfish, wasp
Defense in the bee, ant, termite, honeybee, wasp

62. Bacterial toxins
Clostridium botulinum
It is a Gram-positive, rod-shaped. It is an obligate anaerobe, meaning
that oxygen is poisonous to the cells. However, C. botulinum tolerates
traces of oxygen due to the enzyme superoxide dismutase, which is an
important antioxidant defense in nearly all cells exposed to oxygen. C.
botulinum is only able to produce the neurotoxin during sporulation,
which can only happen in an anaerobic environment, spore-forming,
motile bacterium with the ability to produce the
neurotoxin botulinum. The botulinum toxin can cause a severe flaccid
paralytic disease in humans and other animals. And is the most potent
toxin known to humankind, natural or synthetic, with a lethal dose of
1.3–2.1 mg/kg in humans.

63. Botulinum toxin:
Neurotoxin production is the unifying feature of the species.
Seven types of toxins have been identified that are allocated a
letter (A-G). All toxins are rapidly destroyed at 100 °C, but they are
resistant to degradation by enzymes found in the gastrointestinal
tract. This allows for ingested toxin to be absorbed from the
intestines into the bloodstream.
Most strains produce one type of neurotoxin, but strains
producing multiple toxins have been described. C. botulinum
producing B and F toxin types have been isolated from human
botulism cases in New Mexico and California.

64. Botulinum toxin types:
Only botulinum toxin types A, B, E, and F cause
disease in humans. Types A, B, and E are associated
with foodborne illness, with type E specifically
associated with fish products. Type C produces limber
neck in birds and type D causes botulism in other
mammals. No disease is associated with type G.

65. Foodborne botulism:
"Signs and symptoms of foodborne botulism typically begin between 18 and 36 hours
after the toxin gets into your body, but can range from a few hours to several days,
depending on the amount of toxin ingested.
Double vision
Blurred vision
Drooping eyelid
Nausea, vomiting, and abdominal cramps
Slurred speech
Trouble breathing
Difficulty in swallowing
Dry mouth
Muscle weakness
Constipation
Reduced or absent deep tendon reactions, such as in the knee.

66. Wound botulism:
Most people who develop wound botulism inject drugs several
times a day, so it's difficult to determine how long it takes for signs and
symptoms to develop after the toxin enters the body. Most common in people
who inject black tar heroin, wound botulism signs and symptoms include.
Difficulty swallowing or speaking
Facial weakness on both sides of the face
Blurred or double vision
Drooping eyelids
Trouble breathing
Paralysis

67. Infant botulism:
Infant botulism is related to food, such as honey, problems generally begin
within 18 to 36 hours after the toxin enters the baby's body. Signs and symptoms include:
Constipation (often the first sign)
Floppy movements due to muscle weakness and trouble controlling the head
Weak cry
Irritability
Drooping eyelids
Tiredness
Difficulty sucking or feeding
Paralysis

68. Beneficial effects of botulinum toxin:
Purified botulinum toxin is diluted by a physician for treatment:
Spasmodic dysphasia (the inability of the muscles of the larynx
Strabismus (crossed eyes)
Paralysis of the facial muscles
Failure of the cervix
Blinking frequently
Vaccine:
There is a vaccines but its usefulness is unclear as it is associated with significant adverse
effect. From 2013 there are efforts ongoing to develop a better vaccine.

69. Treatment:
Botulism is generally treated with botulism antitoxin and supportive
care.
Supportive care for botulism includes monitoring of respiratory
function. Respiratory failure due to paralysis may require mechanical
ventilation for 2 to 8 weeks, plus intensive medical and nursing care.
After this time, paralysis generally improves as new neuromuscular
connections are formed.
In some cases, physicians may try to remove contaminated food still in
the digestive tract by inducing vomiting and/or using enemas. Wounds
should be treated, usually surgically, to remove the source of the toxin-
producing bacteria.

70. Staphylococcus aureus
S. aureus is a spherical bacterium (coccus) which on microscopic
examination appears in pairs, short chains, or bunched, grape-like
clusters. These organisms are Gram-positive. Some strains are
capable of producing a highly heat-stable protein toxin that causes
illness in humans.
Toxins:
Depending on the strain, S. aureus is capable of secreting
several exotoxins. Many of these toxins are associated with specific
diseases. Staphylococcal toxins that act on cell membranes
include alpha toxin, beta toxin, delta toxin and several bio component
toxins.

71. Diagnosis of Human Illness
In the diagnosis of staphylococcal foodborne illness, proper interviews with the
victims and gathering and analyzing epidemiologic data are essential.
Incriminated foods should be collected and examined for staphylococci. The
presence of relatively large numbers of enterotoxigenic staphylococci is good
circumstantial evidence that the food contains toxin. In cases where the food
may have been treated to kill the staphylococci, as in pasteurization or heating,
direct microscopic observation of the food may be an aid in the diagnosis. A
number of serological methods for determining the enterotoxigenicity of S.
aureus isolated from foods as well as methods for the separation and detection of
toxins in foods have been developed and used successfully to aid in the diagnosis
of the illness.

72. Treatment of staphylococcal
enterotoxin B
In the event of dehydration, vigorous administration of intravenous fluids is
indicated.
For patients exposed via inhalation, supportive treatment with humidified
oxygen may be all that is necessary, assisted ventilation with high oxygen
concentrations. For most patients, staphylococcal food poisoning will cause a
brief illness. The best treatments for these patients are rest, plenty of fluids,
and medicines to calm their stomachs. Highly susceptible patients, such as the
young and the elderly, are more likely to have severe illness requiring
intravenous therapy and care in a hospital. Antibiotics are not useful in treating
this illness. The toxin is not affected by antibiotics.

73. Mycotoxins
Mycotoxin is derived from two Greek words. “Mykes or Mukos”
which means fungus and “Toxikon” which means poison.
Mycotoxin is a toxic secondary metabolite produced by organisms of
the fungi kingdom, commonly known as molds. The term mycotoxin
is usually reserved for the toxic chemical products produced by fungi
that readily colonize crops.
There are over 400 known types of mycotoxins. According to the
FAO (Food and agriculture organization) 25% of the world’s crop
harvests are contaminated with mycotoxins.

74. Characteristics of Mycotoxins
Mycotoxins are often invisible (as small as 0.1 microns), tasteless,
chemically stable and resistant to temperature and storage.

75. Toxicity of Mycotoxins
There are following three types of toxicities caused by mycotoxins;
Acute Toxicity; It interfere with protein synthesis. It causes neuronal
damage, deterioration of liver and kidney, skin sensitivity and
immunodeficiency.
Chronic Toxicity; It causes induction of tumors and cancer (liver,
esophagus etc.)
Mutagenic Toxicity and Teratogenic Toxicity; It causes the
replication of DNA and producing mutagenic and teratogenic effects.

76. Aspergillus
Aspergillus is a group of molds, of which about 200 species have been
identified. Aspergillus molds are found throughout the world and are
the most common type of fungi in the environment. About 16 species
of Aspergillus molds are known to be dangerous to humans, causing
disease and infection.
Aflatoxin is a type of mycotoxin produced by Aspergillus molds.
Aflatoxin is probably the most well-known mycotoxin.

77. Toxic Constituents
Aflatoxin B1 and B2 produced by Aspergillus flavus and A.
parasiticus (Aflatoxin B1 is the most common aflatoxin, as
well as the most toxic and carcinogenic).
Aflatoxin G1 and G2 produced by Aspergillus parasiticus
Aflatoxins M: This group includes aflatoxins M1 and M2.
These aflatoxins are metabolic products which are found in
the urine and milk produced by animals which have been
given feed with aflatoxins in it.
Aflatoxicol

78. Signs & Symptoms of Toxicity
Liver damage
Liver cancer due to DNA mutation caused by aflatoxins.
Mental impairment
Abdominal Pain
Vomiting
Convulsions
Pulmonary Edema
Hemorrhaging
Growth and development impairment
Disruption of food digestion, absorption or metabolism
Coma
Death

79. Treatment
For both primary skins infection and that associated with invasive
aspergillosis, antifungal like amphotericin, voriconazole, itraconazole
and caspofungin are used. Voriconazole is becoming the treatment of
choice for invasive aspergillosis.

80. Calviceps
Ergot or ergot fungi refers to a group of fungi of the
genus Claviceps. The most prominent member of this group
is Claviceps purpurea ("rye ergot fungus"). This fungus grows
on rye and related plants and produces alkaloids that can
cause ergotism in humans and other mammals who consume grains
contaminated with its fruiting structure (called ergot sclerotium).

81. Claviceps Species
Claviceps includes about 50 known species, mostly in the tropical regions.
The species include;
Claviceps purpurea
Claviceps fusiformis
Claviceps paspali
Claviceps africana
Claviceps lutea
C. purpurea most commonly affects out crossing species such as rye (its most
common host), wheat and barley. It affects oats only rarely.

82. Toxic Constituents
The ergot sclerotium contains high concentrations (up to 2% of dry
mass) of the alkaloid ergotamine and other alkaloids of the ergoline
and also contains ergocristine, ergonovine.

83. Signs & Symptoms of Toxicity
Vasoconstriction of blood vessels.
Sometimes leading to gangrene and loss of limbs due to severely
restricted blood circulation.
The neurotropic activities of the ergot alkaloids may also
cause hallucinations, convulsions and even death.
Nausea, Vomiting, Colic, Seizures and unconsciousness.
May induce abortions and strong uterine contractions.

84. Treatment
Preliminary care consists of gastric decontamination with either
activated charcoal or gastric lavage.
Inducing vomiting with syrup of ipecac is no longer recommended in
any poisoning situations.

85. Mushrooms
A mushroom (or toadstool) is the fleshy, spore-bearing fruiting
body of a fungus, typically produced above ground on soil or on
its food source.
Mushroom poisoning (also known as mycetism or mycetismus)
refers to harmful effects from ingestion of toxic substances present in
a mushroom.

86. Biological Sources
Amanita muscaria Amanita phalloides
Amanita magnivelaris Amanita elliptosperma
Amanita ocreata Amanita pantherina
Amanita porphyria Amanita regalis
Amanita virosiformis Amanita smithiana
Amanita verna Amanita virosa

87. Toxic Constituents
Amanita phalloides contains amatoxins, α-amanitin is the chief
component and along with β-amanitin is likely responsible for the
toxic effects. Their major toxic mechanism is the inhibition of RNA
polymerase II, a vital enzyme in the synthesis of messenger
RNA (mRNA), microRNA, and small nuclear RNA (snRNA).
Without mRNA, essential protein synthesis and hence cell metabolism
grind to a halt and the cell dies.
Amanita muscaria contains muscimol.

88. Signs & Symptoms of Toxicity
Gastrointestinal disturbance i.e. watery diarrhea, nausea and vomiting which
may lead to dehydration if left untreated and in severe cases.
Hypotension, Tachycardia, Hypoglycemia, Acid–base disturbances.
Liver involvement may then occur — jaundice, diarrhea, delirium, seizures
and coma.
Kidney failure (either secondary to severe hepatitis or caused by direct toxic
kidney damage).
Life-threatening complications include increased intracranial pressure,
intracranial bleeding, pancreatic inflammation, acute kidney failure and Death
generally occurs six to sixteen days after the poisoning.

89. Treatment
Preliminary care consists of gastric decontamination with either
activated charcoal or gastric lavage.
Inducing vomiting with syrup of ipecac is no longer recommended in
any poisoning situations.
Benzodiazepine such as diazepam or lorazepam can be used to control
combativeness, agitation, muscular over activity and seizures.
Rifampicin, Penicillin, Paclitaxel, Cyclosporine and Prednisolone are
used.

90. Study of Toxins,
their Prevention
and Control
Methods

91. Definition
Toxicology is the branch of medicines that deals with properties,
actions, lethal dose, toxicity, detection or estimation of poison and
signs & symptoms, diagnosis, treatment & autopsy findings of
poisoning cases.

92. Plants having nicotine like action
Botanical origin:
Nicotiana tobacum
Family:-
Solanaceae
Common name:
Tobacco plant
Toxic part:
Dried leave

93. Toxic principle:
Nicotine
Mechanism of action :
Stimulation & depression followed by paralysis of cells of peripheral
autonomic ganglia, midbrain, spinal cord & muscles etc.

94. Signs and symptoms
Mild poisoning:
Dizziness
Nausea
Vomiting
Headache
Perspiration
Weakness
Cardiac irregularities

95. Acute poisoning:
Burning in mouth, throat & stomach.
Cardiac irregularites, Cardiac arrest & death.
Chronic poisoning:
Chronic cough, Bronchitis
Laryngitis, Pharyngitis
Dermatitis
Tremors
Fatal dose:
2 gm of tobacco or 60 mg of nicotine & 5 ml of any of nicotine
insecticide.

96. OPIUM
B.O:
Papaver somniferum
Family:
Papaveraceae
Common name:
Poppy plant, opium(afeem)

97. Toxic Part:
Unripe fruit capsule latex juice
Active Principle:
Opium has about 25 alkaloids divided in to 2 groups.
1)Phenanthrine Derivatives
Morphine(10%)
Codeine(0.5%)
Thebain(0.3%)
2)Benzyl Isoquinidine derivatives
Papaverine(1%)
Narcotine(6%)

98. Mechanism Of Action
It acts initially by stimulation of central nervous system producing a
“stage of excitement”, followed by stage of depression or stupor, to
merge into a third and final stage of narcosis.
Therapeutic and Fatal doses:
Compound Therapeutic
dose (mg)
Fatal dose
(mg)
Morphine 10-15 200
Codeine 10-60(oral) 800(oral)

99. Signs & Symptoms
Stage of Excitement:
This stage is due to initial stimulation of CNS and includes following;
Euphoria, Hallucination, Convulsions.
Stage of stupor(depression):
In this stage victim presents with fatigue, weakness, headache,
heaviness in limbs, urge to sleep and pin point pupil.
Stage of narcosis:
Here the victim passes into deep coma from which he cannot awaked,
muscles are relaxed and reflex are abolished. B.P falls, temperature is
subnormal, comma deepens and death usually results.

100. Cannabis
B.O:
Cannabis sativa
Family:
Cannabinaceae
Common name:
Dagga, Hashish, Marijuana
Toxic Parts:
Whole plant

101. Active principle
Cannabinol

102. Mechanism of action
THC (Tetrahydrocannbinol) demonstrates weak barbiturates like
actions such as anti-convulsant activity and opioid like effects,
including analgesia, increased catecholamines synthesis, hypothermia
and antidiarrheal activity, Increased limbic system activity has also
been described with cannabis use.

103. Signs & Symptoms
Euphoria
Hallucination
Confusion
Drowziness
Dilated pupil
Paralysis of muscles
Loss of reflexes
Coma
Death

104. Fatal dose
Charas(2g)/body wt
Bhang(10g)/body wt
Fatal period:
12 hours.

105. Abrus precatorius
Botanical origin:
Abrus precatorius
Family:
Fabaceae
Common name:
Jequirity , Indian liquorice.
Toxic part:
Whole plant specially seeds are toxic
Toxic principle:-
Abrin( toxalbumin)

106. Mechanism of action
Abrin exerts it's action by attaching itself to the cell membrane.
Abrin's toxic effect is due to it's direct action on paranchymal cells(
liver, kidneys & RBC's). Abrin inactivates the ribosomes & arrest
protein synthesis & cause cell death.

107. Signs and Symptoms
Locally:
Dermatitis, Conjunctivitis, Rhinitis, Asthma
Oral ingestion:
Severe pain, Vomiting, Bloody purging, Circulatory collapse.
Fatal dose:
60-120 mg of Abrin.
Fatal period:
3-5 days.