Plant toxin

Plant toxin

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  Poisonous Plants Prepared by: KiranNiure BVSc & A.H Agriculture and forestry university Rampur, Chitwan, Nepal Plants producing photosensitization, Plant producing oxalate poisoning, Datura and related plants poisoning
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  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
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  Types of photosensitization 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
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  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.
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  Photodynamic substance comesto 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
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  • 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
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  • Diagnosis andtreatment: – 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
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  Plant producing oxalatepoisoning • 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
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  • Toxicity: – Dependslargely 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
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  Toxicokinetics • After ingestionby 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
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  – Metabolized toformate and then to CO2 and excreted from body – Detoxified in the rumen and converted to carbonate and bicarbonate which in excess may produce alkalosis
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  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
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  Clinical signs: – Earlyclinical 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
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  Diagnosis: – History offeeding, 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
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  Datura And RelatedPlants 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)
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  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
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  • Poisoning occursmainly 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
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  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
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  Clinical signs: – Signsusually 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
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  Treatment: – No specificantidote; 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