Plants producing photosensitization, Plant producing oxalate poisoning, Datura and related plants poisoning

1. Poisonous Plants
Prepared by:
Kiran Niure
BVSc & A.H
Agriculture and forestry university
Rampur, Chitwan, Nepal
Plants producing photosensitization, Plant
producing oxalate poisoning, Datura and related
plants poisoning

2. Plants producing
photosensitization
• Photosensitization:
– a syndrome of abnormal sensitization of the
lightly pigmented areas of skin to sunlight
• Medicago sativa (alfa alfa), Trifolium spps.
(Clovers), Brassica spps (Rape), Lolium perenne
(perenial rye grass), etc. are plants involving in
primary photo sensitization
• Lantana camara ( Lantana), Kochia scoparia
(Kochia), Crotoloria spp. (Rattle box) etc. are
plants involving in secondary photosensitization

3. Types of photo sensitization
1. Primary photosensitization:
 Occurs when a photodynamic agent is directly
ingested or the biotransformed photodynamic
metabolite which reaches skin and reacts with
the UV light to cause photosensitization
 Photodynamic pigments are present in highest
concentration in green plant and through GI tract
, circulate in peripheral blood.
 In pigmented skin they react with UV light to
produce dermatitis and photosensitization

4. 2. Secondary photosensitization:
 Occurs due to ingestion of substances that give rise to
liver dysfunction and obstruction of bile duct which
result the elimination of plant in bile to reach
peripheral circulation and give rise to
photosensitization
 Most frequent type of photosensitization in livestock
caused by photosensitizing agent Phylloerythrin, a
bacterial breakdown product of chlorophyll
 In normal, phylloerythrin is removed by liver and is
excreted by bile duct but if the liver is severely
damaged or if the bile duct is ocluded, phylloerythrin
accumulates in the peripheral blood producing
photosensitization.

5. Photodynamic substance comes to
peripheral circulation
Energized by certain wavelength of UV light and attain higher
energy state
Return to less energized state and releases energy which is
transferred to receptor molecules to initiate chemical reaction
Tissue injury due to reactive oxygen intermidiates which cause cell
membrane damage and alter membrane permiability
Histamine released due to tissue distruction initiates
local inflammatory reactions i.e erythema, oedema,
vesicles and bullae, intense pruritis and necrosis
Mechanism Of Action

6. • Clinical Signs:
– Animals feel discomfort and scratches or rubs lightly
pigmented exposed areas of skin.
– Frequently the skin around ears, eyelids, muzzle and
coronary band of hooves are most severly affected due
to heavy vascularized skin and less protection by hair
– Affected skin rapidly becomes reddened, painful and
oedematous
– If exposure is prolonged, there is marked serum
exudation , scab formation and skin necrosis
– If photosensitization is of hepatic origin : depression,
anorexia, weight loss and jaundice
– Similarly, abdominal distention, ascites
– Neurological signs due to accumulation of toxin in brain
– Death in few days due to extensive liver damage

7. • Diagnosis and treatment:
– Dermatitis limited to areas of non pigmented skin
– Liver biopsy to confirm presence of hepatomegaly,
fibrosis and biliary hyperplasia are optimal test for
hepatogenous photosenitization
Treatment :
only supportive
• Remove plants and photodynamic substances and provide
shelter from sun or housed
• Corticosteroid in early stage: helpful
• Secondary skin infection and suppuration should be treated and
flies strike must be prevented
• In hepatogenous photosensitization : supportive therapy such
as fluid and electrolyte therapy

8. Plant producing oxalate poisoning
• Oxalate poisoning in animals from pure substance is rare
but usually occurs through oxalate containing plants
• Panicum spps. (Elephant grass), Quercus spps. (oak),
Rumex crispus (Sorrel), Halogeton glomeratus
(Halogeton), Beta vulgaris (sugar beet)
• Properties:
– Oxalates occur in plants as primarily as calcium, sodium,
ammonium, potassium and magnesium.
– Calcium and magnesium oxalates : insoluble
– Sodium and potassium oxalates (more common in plants) :
soluble , absorbed or react with calcium in GI tract to form
insoluble salt

9. • Toxicity:
– Depends largely on species of animal, type of
plant, form of oxalate present in plant, and
duration of exposure
– Ruminant especially cattle can tolerate
comparatively large amount of oxalate because of
effective production of insoluble oxalate from free
oxalate than the simple stomach animal
– Commonest in sheep and also occurs in cattle and
horse
– Gradual low feeding of halogeton plants usually
show less toxic response than abrupt high feeding

10. Toxicokinetics
• After ingestion by ruminant may undergo
various pathways:
– May be degraded by rumen bacteria to form toxic
metabolites, which on combination with calcium
or magnesium in rumen form insoluble salt and
excreted. OR,
– May be absorbed from GI tract and combine with
blood calcium and magnesium to produce
hypocalcaemia and hypomagnesaemia
respectively
– Insoluble oxalate salts may accumulate in various
tissues, especially the rumen wall and kidneys

11. – Metabolized to formate and then to CO2 and
excreted from body
– Detoxified in the rumen and converted to
carbonate and bicarbonate which in excess may
produce alkalosis

12. Mechanism Of Action
• Produce toxicity by number of ways:
I. Forms a complex with serum calcium to form calcium
oxalate which depletes ionized calcium and causes
hypocalcaemia resulting in impairment of normal
cellular function
II. Interferes with the cellular energy metabolism that
contribute to the acute death of affected animals
III. Insoluble oxalate crystals accumulate to various
organs and produce direct organ damage like oxalate
nephrosis, CNS disorders and paralysis, haemorrhages
in ruminal wall etc.
IV. Ruminal dysfunction in continued low level dosing in
sheep due to change in pH of ruminal content and
interfere with cellulose digestion and also produce
alkalosis
V. Oxalic acid is corrosive and direct contact may cause
gastrointestinal and skin irritation

13. Clinical signs:
– Early clinical signs include: dullness, reluctant to move,
slobbering, lowering of head, loss of appetite, stasis of
ruminal motility and bloat
– In acute poisoning: salivation, progressive weakness,
incoordination, prostration, laboured respiration,
dilation of pupil, twiching of muscles, tetany,
convulsion, coma
– In subacute poisoning: frequent attempt to urinate
and recumbency. Urine may be red-brown in colour.
– In chronic poisoning: renal damage resulting uraemia,
severe depression, stop eating and after few days
become comatose and die

14. Diagnosis:
– History of feeding, clinical signs and lesion
– Demonstration of calcium oxalate in the kidney and
rumen epithelium histologically
– Packed cell volume decreases but BUN and blood
potassium level may increase
Treatment:
– No specific treatment, only supportive therapy
– Calcium salt: for correcting hypocalcaemia
– Excessive and forceful administration of water :
flushing out oxalate
– Administration of lime water (Ca[OH2]): to prevent
further absorption of soluble oxalate

15. Datura And Related Plants
Poisoning
• Certain member of solanaceae (nightshade)
family show poisoning in animals and human :
– Datura stramonium (jimson weed, thornapple)
– Atropa belladona (deadly nightshade)
– Hyoscyamus niger (black henbane)
– Solanum nigrum (black nightshade)
– Physalis virginiana (ground cherry)

16. Properties and toxicity
• Datura exists in more than dozen varieties: D.
stramonium, D. metal, D. tatula, D. alba , D. niger,
etc.
• Datura spp. and related plants contain tropane
alkaloids like hyoscine, atropine, hyoscyamine,
daturine and solanine. Tans, nitrites, fatty acid
glycerides, etc. are also present
• The toxins (alkaloids) are present in the entire
plant but are more concentrated in seeds

17. • Poisoning occurs mainly when hungry animals
ingest the plant or when large amount of toxic
plant is present in hay.
• Oral toxic and lethal doses are not known in
all species. Pig appears to be very sensitive to
datura seeds with 2.2-2.7 mg/kg/day causing
toxic sgns

18. Mechanism of Action
• Tropane alkaloids of datura plants interact with
and inhibit all muscarinic receptors in the body.
• This lead to blockade of the action of
neurotransmitter acetylcholine at muscarinic
receptor site and hence parasympathetic nervous
system
• High dose may also block nicotinic receptors at
the autonomic ganglia and neuromuscular
junction

19. Clinical signs:
– Signs usually occur 30-60 minutes after ingestion
and may continue for 24-68 hours due to delayed
gastric emptying and absorption
– Toxic signs includes: dryness of mouth and throat,
dysphagia and difficulty in swallowing followed by
staggering gait, incoordination, dry-hot skin,
photophobia, dilated pupils, urine retention,
tachypnoea, tachycardia
– Bloat and rumen atony may be observed in cow
and horse
– Very high doses produce coma, skeletal muscle
paralysis and death from respiratory failure

20. Treatment:
– No specific antidote; only symptomatic and supportive
care
• Physostigmine: used to stimulate cholinergic secretions
and activities. It competitively inhibit cholinestrase
enzyme and increase Ach concentration which compete
with atropine for cholinergic receptor sites
• Diazepam for sedation and control of convulsion if
marked excitement is present.
• Cold water or ice pack to reduce fever, artificial
respiration to restore respiration, general GI
detoxification to remove recently ingested poison
Contraindication:
– Phenothiazine tranquilizers should not be given for
sedation and controlling CNS excitation because they
posses anticholinergic action and aggravates the
datura intoxication