Abstract and Figures

large number of plants can cause signs of toxicity when ingested by animals. Consumption of some plants even at small quantities can result in rapid death. The most common plant species that are responsible for pant toxicity in ruminants includesRicinus communis, Lantana camara, Nerium oleander, Abrus precatorius, Pteridium aquilinumandDatura stramonium. Consumption of cyanogenic plants and nitrate containing plants can also cause toxicity in ruminants.The diagnosis of plant toxicity can be challenging in veterinary medicine since in most cases the history of exposure to a toxic plantsmight be lacking.For most of the plant poisoning cases the treatment is general with symptomatic and supportive therapysince there is no antidote for most of the toxins.Removing the poisonous weeds from the grazing area and providing good quality forages reduces the risk of plant poisoning.
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Volume 6 Issue - 11 November - 2019
ISSN 2394-1227
Pages - 130
Emerging trends and scope
Editorial Board
Dr. V.B. Dongre, Ph.D.
Dr. A.R. Ahlawat, Ph.D.
Dr. Alka Singh, Ph.D.
Dr. K. L. Mathew, Ph.D.
Dr. Mrs. Santosh, Ph.D.
Dr. R. K. Kalaria, Ph.D.
Agriculture
Dr. R. S. Tomar, Ph.D
Veterinary Science
Dr. P. SenthilKumar, Ph.D.
Home Science
Dr. Mrs. Surabhi Singh, Ph.D.
Horticulture
Dr. S. Ramesh Kumar, Ph.D
Indian Farmer
A Monthly Magazine
(Note: ‘Indian Farmer’ may not necessarily subscribe to the views expressed in the articles published herein. The views are expressed by
authors, editorial board does not take any responsibility of the content of the articles)
Editor In Chief
Editor
Members
Subject Editors
Volume: 6, Issue-11 November-2019
Sr.
No. Full length Articles Page
1 Eutrophication- a threat to aquatic ecosystem
V. Kasthuri Thilagam and S. Manivannan
697-701
2 Synthetic seed technology
Sridevi Ramamurthy
702-705
3 Hydrogel absorbents in farming: Advanced way of conserving soil moisture
Rakesh S, Ravinder J and Sinha A K
706-708
4 Urban farming-emerging trends and scope
Maneesha S. R., G. B. Sreekanth, S. Rajkumar and E. B. Chakurkar
709-717
5 Electro-ejaculation: A method of semen collection in Livestock
Jyotimala Sahu, PrasannaPal, Aayush Yadav and Rajneesh
718-723
6 Drudgery of Women in Agriculture
Jaya Sinha and Mohit Sharma
724-726
7 Laboratory Animals Management: An Overview
Jyotimala Sahu, Aayush Yadav, Anupam Soni, Ashutosh Dubey, Prasanna Pal and M.D.
Bobade
727-737
8 Goat kid pneumonia: Causes and risk factors in tropical climate in West Bengal
D. Mondal
738-743
9 Preservation and Shelf Life Enhancement of Fruits and Vegetables
Sheshrao Kautkar and Rehana Raj
744-748
10 Agroforestry as an option for mitigating the impact of climate change
Nikhil Raghuvanshi and Vikash Kumar
749-752
11 Beehive Briquette for maintaining desired microclimate in Goat Shelters
Arvind Kumar, Mohd. Arif, Ravindra Kumar, and N Ramachandran
753-756
12 An Overview on Nutritional Deficiencies in Swine Production
Jyotimala Sahu and Aayush Yadav
757-760
13 Nutritional Practices of Laboratory Animals
Aayush Yadav, Ashutosh Dubey, Rajkumar Gadpayle,AnupamSoni, SudheerBhagat,
UpasanaVerma, SandhyaKashyap and Kiran Kashyap
761-766
14 Biofortified wheat: food security along with nutritional quality
Suresh, Antim and Ashish
767-769
15 Farmer field school on improved animal husbandry practices: a report
Dr. S. Senthilkumar
770-774
16 Seaweed An Alternative Source of Plants Nutrients in Agriculture
Ankita Begam and Dulal Chandra Roy
775-779
17 Nabothian cyst in animals and humans-a review
Thangamani A, B. Chandra Prasad and Manda Srinivas
780-786
18 Toxicity of Common Toxic Plants and Poisoning in Farm Animals
I. Subhedar and S. Umap
787-794
19 Anthocyanin pigments role in plants and its health benefits
S.Sheelamary and Sujayanand G.K
795-801
20 Sustainable disposal of livestock waste for ecofriendly environment for forthcoming gen-
erations
Suresh.C and Sujatha.V
802-806
21 Salt Production-Major Livelihood Security of Farmer’s in Coastal Odisha
R. Srinivasan, Rajendra Hegde and M. Chandrakala
807-811
22 Toxicological aspects of common plant poisoning in ruminants
Haritha C. V., Khan Sharun, Manjusha K. M. and Amitha Banu S.
812-822
23 Lethal genes types and classification
Savalia, K. B., Ahlawat, A.R., Verma, A.D., Odedra,M. D and Dodiya P.G.
823-827
Indian Farmer 6(11):812-822; November-2019 Haritha et al
812 | P a g e
Toxicological aspects of common
plant poisoning in ruminants
Haritha C. V.1, Khan Sharun2*, Manjusha K. M.2 and Amitha Banu S.2
1Division of Pharmacology and Toxicology, ICAR-Indian Veterinary Research Institute, Izatnagar,
Bareilly, Uttar Pradesh
2Division of Surgery, ICAR-Indian Veterinary Research Institute, Izatnagar, Bareilly, Uttar Pradesh
*Corresponding Author: sharunkhansk@gmail.com
ABSTRACT
A large number of plants can cause signs of toxicity when ingested by animals.
Consumption of some plants even at small quantities can result in rapid death. The most
common plant species that are responsible for pant toxicity in ruminants includesRicinus
communis, Lantana camara, Nerium oleander, Abrus precatorius, Pteridium
aquilinumandDatura stramonium. Consumption of cyanogenic plants and nitrate
containing plants can also cause toxicity in ruminants.The diagnosis of plant toxicity can
be challenging in veterinary medicine since in most cases the history of exposure to a
toxic plantsmight be lacking.For most of the plant poisoning cases the treatment is
general with symptomatic and supportive therapysince there is no antidote for most of
the toxins.Removing the poisonous weeds from the grazing area and providing good
quality forages reduces the risk of plant poisoning.
Keywords - Plant poisoning; Ruminants; Ricinus communis; Lantana camara
INTRODUCTION
Toxic plants affecting ruminants are of major concern for both the practicing
veterinarian and farmer. Numerous poisonous plants have known to cause negative
impact on the livestock industry. Although grazing is considered as normal routine in
livestock management,it exposes the animals to a variety of poisonous plants
particularly when there is reduction in fodder availability.Ingestion of poisonous plants
by animals produces toxic effects like physical upset, loss of productivity and even
death. There are several factors that contribute to plant poisoning like season and
weather conditions, feeding of livestock with poor quality roughage, transportation and
handling. Poisoning can occur either by accidental ingestion of plants with usual feed or
by wilful consumption of toxic plants when pastures are dry.
Animals which are already under nutritional stress are more susceptible to plant
poisoning. Good practices of grazing with proper observation of grazing animals along
with intense knowledge about poisonous plants and strategic approaches to therapy
helps to resolve the problem.Plants that are seen in a particular geographical region
may not be found in other regions due to difference in geographical distribution.
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Invasion of poisonous plants into non-native areas affect this distribution. For most of
the plant poisoning cases the treatment is general with symptomatic and supportive
therapysince there is no antidote for mostof the toxins.The ultimate goal of treatment
should be removal of toxins from the body.Treatment includes administration of
activated charcoal and stabilization of the animal with fluid and electrolytes. Removing
the poisonous weeds from the grazing area and providing good quality forages reduces
the risk of plant poisoning.
The present paper aims to discuss in detail about the common plants that are
responsible for plant toxicity in ruminants and their respective therapeutic strategies.
Ricinus communis
Common names:Castor oil plant, Castor bean
Ricinus communis is an extremely toxic plant that is commonly known as castor oil plant
or castor bean.The toxic principle present in this plant is a water-soluble ribosome-
inactivating protein called ricin which is mostly concentrated in its seeds.Ricin is a heat
labile protein which can be destroyed during the extraction process. The leaves and
fruits of the plant contains an alkaloid, ricinine which can stimulate the central nervous
system (Audi et al., 2005).Mechanism of toxicity is mainly due to the inhibition of
protein synthesis. The other devastating effects includes apoptosis, direct damage to
cell membrane by altering membrane structure and function, and release of cytokine
inflammatory mediators (Day et al., 2002). A glycoprotein lectin called agglutininis
also present in castor bean plant which is having more affinity for the red blood cell
thus causing agglutination and thereafter haemolysis. Ricinus communis agglutinin is
poorly absorbed from the gut and hence significant haemolysis is not observed in oral
ingestion cases (Hegde and Podder,1992).
Figure 1 - Ricinus communis plant, Fruits (Left) and Seeds (Right)
Among the farm animals horses seem to be the most susceptible with ruminants
having intermediate susceptibility,whereas the chicken being most resistant
animal(Aslani et al., 2007). The initial toxicity signs include nausea, gastro-intestinal
irritation, abdominal pain, diarrhoea, tenesmus, dehydration, cessation of rumination,
muscle twitching,dullness of vision, convulsions, weakness, profuse watery diarrhoea
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and dehydration within 624 h.Biochemical examination reveals a high packed cell
volume and increased levels of serum creatine kinase, aspartate aminotransferase
(AST),blood urea nitrogen(BUN) and creatininevalue along with leukocytosis and
hyperbilirubinemia. Necropsy lesions include gastroenteritis, necrosis and
haemorrhage in heart and kidney.
Diagnosis can be made from case history and clinical signs exhibited by the
animal. Due to the non-specific nature of the clinical manifestations in plant toxicity, one
cannot confirm the intoxication merely based on the clinical signs unless the suspicious
particles are not found in vomitus, faecesor in the intestine. Hence confirmatory
diagnosis is necessary with the detection of toxins either in clinical or feed
samples.Confirmatory diagnosis can be made by using antibody based immunoassay
which helps to detect and quantify the toxin(Royet al., 2003; Heet al., 2010)Ricinine can
be detected successfully instead of ricin using paper chromatography, UV detection and
liquid chromatography (Knight and Walter, 2001).
Management of Ricinus communis poisoning includes general and symptomatic
therapy as there is no antidote against ricin. Administration of activated charcoal to
adsorb toxins would be helpful. Intravenous hydration and fluid replacement is
necessary to combat dehydration and fluid loss in affected animals.
Nerium oleander
Common names: Oleander, Oleana, Rose bay
Nerium oleander is a flowering shrub commonly grown as an ornamental plant in
gardens and parks.It is originated from Mediterranean countries and widely distributed
in tropical and subtropical regions (Knight and Walter, 2001).Oleander is known to be
poisonous to animals (Frohn and Pfander, 1983).Nerium oleander and Thevetia
peruviana (yellow oleander) are the two common varieties in which all the plant parts
are known to be toxic (Langford and Boor, 1996).The toxic principle present in oleander
are mostly cardiac glycosides which includes oleandrin, folinerin and digitoxigenin that
exhibits cardiotoxicity.The mechanism of action of cardiac glycosides is mediated
through the inhibition of Na+/K+-ATPase pump resulting in electrolyte disturbance and
thus affecting the electrical conductivity of heart by increasing the intracellularcalcium
ion concentration (Joubert, 1989).
Figure 2 -Nerium oleanderplant (Left) and
Thevetia peruviana (yellow oleander) plant (Right)
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The major toxic signs exhibited by animals are associated with disturbances in
cardiac and gastrointestinal system. The toxic effects exhibited by oleander includes
ventricular arrhythmia which leads to ventricular fibrillation and finally death of the
animal. Initial stages of intoxication in ruminants include ruminal atony with moderate
tympany (Aslani et al., 2004). Other clinical signs includes abdominal pain, frequent
urination, bradycardia, tachycardia, depression, and weakness.
Since there is no specific remedy, the general treatment includes symptomatic
and supportive care. Activated charcoal can be administrated to eliminate or reduce
toxins from the gastrointestinal tract. Providing adrenergic blockers along with atropine
helps the animal to relieve from tachycardia and atrioventricular block.Rehydrating the
animal is of utmost importance while dealing with affected animals.Calcium containing
fluids are contraindicated as it potentiates the action of cardiac glycosides (Knight and
Walter, 2001). Administration of anti-digoxin antibodies found to be highly effective in
managing digoxin toxicity hence considered as the first line of treatment(Joubert, 1989).
But administration of anti-digoxin antibodieshavelimitations in livestock management
owing to its high cost and scarce availability.
Abrus precatorius
Common names: Rosary Pea, Bead Vine, Coral Bead Plant, Crab’s Eyes, Jumbi Beeds,
Love Bead
It is commonly grown as an ornamental plant where the seeds are used in
jewellery and handicrafts.The toxic principle of the plant is a lectin called abrinwhich is
present in its seeds.Mechanism of action is by inhibition of protein synthesis which is
mediated through ribosomal subunit inactivation.Cattle are more prone to abrin
poisoning compared to other animal species.Toxicity of abrin is similar to ricin
poisoning. Clinical signs associated with oral ingestion includes gastroenteritis with
vomiting and diarrhoea which then leads to circulatory collapse.Animal may exhibit
local signs such as conjunctivitis and dermatitis(Rajeev, 2012).
Figure 3 -Abrus precatorius plant and seed (Right)
Further exposure can be prevented by keeping the animal away from the source.
Management of abrin poisoning can be done by administering activated charcoal at the
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total dose of 250-500g in large ruminants. Anti-abrin serum can also be given as a
specific antidote. Administration of saline purgatives at the rate of 100-200g and
alkalinisation of urine will help to excrete the absorbed toxins.Symptomatic treatment
along with fluid therapy will facilitate faster recovery.
Lantana camara
Common names: Lantana weed, Wild sage,Red sage
Lantana camara is the most popular ornamental garden plant. Some varieties of
L. camara complex are known to cause toxicity in ruminants especially to sheep.The
toxic effect is due to the presence of some triterpene ester metabolites, lantadene A and
B .The leaves and immature berries are more toxic to livestock. Metabolism of
lantadeneA occurs extensively in the liver to yield more polar compounds which are
then excreted into the bile. The drastic effect of lantana poisoning includes cholestasis
and hepatotoxicity due to the continuous absorption of toxins from the rumen.As a
result, ruminal stasis and anorexia develops. Other related consequences of cholestasis
are jaundice and photosensitisation. Accumulation of bilirubin due to failure of biliary
secretion causes jaundice. Photosensitisation develops due to the accumulation of
phylloerythrin. Experimental studies shows that lantana poisoned sheep becomes
dehydrated and hypokalaemic.
General line of treatment includes administration of laxatives to remove toxins
from the body (Blood et a1., 1983). Manual removal of the toxic rumen contents
enhance the recovery. Administration of activated charcoal can be done to adsorb the
toxins in the rumen and helps to prevent further absorption. Antihistaminic and
antibiotics should also be administered. Moving the animal into the shade helps to
prevent the development photosensitive dermatitis (Blood et al 1983).
Figure 4 -Lantana camaraplant and flower (Right)
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Cyanogenic plants
The common cyanogenic plants include Sorghum, Sudan grass, Corn, Lima beans,
Cherry, Apple,Peach and Apricot. The toxic principle in cyanogenic plants are
cyanogenic glycosides like amygdalin, prunacin, linamarin, lotaustralin, dhurrin, and
taxiphyllin.These glycosides as such are not toxic but they become toxic when they get
hydrolysed in the body.Processing of the plants like freezing, chopping or chewing
render them more toxic due to release of enzymes(Gracia and Shepherd, 2004).It is
reported that the level of toxicity increases depending on the factors such as ruminal pH
and microflora, rapid ingestion,consuming large amount of immature cyanogenic plant,
amount of cyanogenic glycoside or free HCN in the ingested plants. Excess application of
nitrogen fertilisers and herbicides like2,4-Dichlorophenoxyacetic acid increases the
toxicity. Increase in pH of rumen and abomasum potentiates the toxicity. It has shown
that at a pH less than 5.0, the enzymes that separate the glycosides gets inactivated and
the risk of toxicity decreases.
Figure 5 Sorghum or Sorghum bicolor(Left) and Lima beansor Phaseolus
lunatus(Right)
Hydrogen cyanide is released in the rumen which combines with
methaemoglobin to form cyanmethemoglobin.This complex inactivates cytochrome
oxidase enzyme and inhibits the last step of oxidative phosphorylation. Utilisation of
oxygen does not occur resulting in cessation of cellular respiration. Death of the animal
in cyanide poisoning is due to histotoxic anoxia.The lethal dose of HCN for ruminants is
about 2mg/kg of body weight. Plants containing over 200ppm of these glycosides are
categorised as toxic.
Clinical signs are exhibited within minutes to a few hours.Death in animals
usually occurs within 2 hours after consuming the lethal dose of cyanogenic
plants.Laboured breathing, dyspnoea, restlessness, tremors,terminal clonic convulsions
and opisthotonus are the clinical signs shown by the intoxicated animal. Initially the
mucous membranes are bright and cherry-red color due to oxygen abundance in blood.
Later it turns cyanotic due to hypoxia.Then the animal enters into coma and die if not
treated promptly.Diagnosis can be made by qualitative analysis of cyanogenic material
in rumen content or plant sample by using the picric paper test.For this rumen contents
and forages should be preserved in the frozen condition until analysis.
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Treatment involves intravenous administration of a mixture containing 1 ml of
20% sodium nitrate and 3 ml of 20% sodium thiosulfate, given at a dose rate of 4 ml
mixture per 45 kilogram body weight.In sheep, the recommended doses of sodium
thiosulfate @ 660 mg/ kg can be given in combination with conventional doses of
sodium nitrite @ 6.6 mg/ kg.
Nitrate containing plants
Nitrate poisoning is a condition which may affect ruminants consuming certain
forages like Oats, Cape weed, Sorghum,Maize, Lucerne,Turnip tops, Sudan
grass,Wheat,Barley which contains nitrate in excess amounts. In normal conditions
nitrate ingested by ruminants is converted to ammonia and then to bacterial protein in
the rumen where the conversion of nitrate to nitrite is much faster than conversion of
nitrite to ammonia. Excess intake of nitrate containing plants results in accumulation of
nitrite in the rumen.This nitrite enter into bloodstream and will convert haemoglobin to
methaemoglobin which leads to prevention of oxygen transport.Hence the animal dies
due to anoxia in nitrate poisoning. The conditions like drought, cold weather, herbicide
application, wilting causes the plants to accumulate more nitrate. The nitrate content in
the plant tissues depends on factors like type of plant species, stage of maturity and part
of the plant. Immature plants contain higher concentrations of nitrate than mature
plants. The leaves and flowers contain less nitrate because most of the nitrate is located
in the bottom third of the plant.
Clinicalsigns of nitrate poisoning include salivation,abdominal pain,vomiting, and
diarrhoea. Whereas the nitrite poisoning results in clinical signs such as salivation,
tremors, staggering, bloat, dyspnoea,rapid and noisy breathing, chocolate coloured
mucous membranes.Pathological lesions include reddening and stripping of the
gastrointestinal epithelium,pinpoint haemorrhages in internal organs,pooling of blood
in the stomach wall and poorly clotting blood with coffee brown colour. Diagnosis of
nitrite poisoning can be made from history of exposure to plants, clinical signs and
pathological lesions.Antidote for nitrate poisoning includes intravenous administration
of methylene blue which converts the methaemoglobin to haemoglobin.
Points to be considered for the prevention of nitrate poisoning are:
• Feed the animals with mature forages
• Do not allow the animals to graze highly fertilised crops
• Feed only dried cereal hays
• Avoid the animal from grazing the plants one week after rainfall and cloudy weathers
• Silaging of high nitrate content plants
• Avoid feeding green chop that has heated after cutting
• Mouldy hay should not be fed to animals
Pteridium aquilinum
Common names: Bracken fern, Brake, Hog Pasture Break
Bracken fern (Pteridium aquiline var. pubescens) is a poisonous weed that are not
preferred by ruminants due to high silicon content that reduces its palatability. It is
widely distributed in many places around the world where it grows in woodlands and
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other shaded places, on hillsides and open pastures (Stegelmeier et al., 1999).All parts
of the fern are poisonous. Thiaminase inhibitors present in the plant causes thiamine
deficiency. Consumption of milk from poisoned cows is harmful to humans. Poisoning
usually occurs during late summer when scarcity of the fodder happens.In cows the
diseases usually takes acute form after the consumption of large amount of plant. Nor-
sesquiterpene glycoside called ptaquiloside present in plant causes aplastic anaemia in
cattle, which has delayed onset of action.Overtime consumption causes bovine enzootic
haematuria which gives urine the characteristic red color.
Figure 6 - Bracken fern plant (Pteridium aquiline var. pubescens)
Clinical signs in cattle and sheep include high fever, with loss of appetite,
depression, dyspnoea, excessive salivation, nasal and rectal bleeding,haematuria,
haemorrhages on mucous membranes, thrombocytopenia, anaemia, leukopenia, plastic
bone marrow and bladder tumors in cattle (Davis et al., 2011). Poisoning can be treated
with administration of thiamine hydrochloride,batyl alcohol, activated charcoal and
saline cathartics
Datura poisoning
Common names:Devil’s trumpet, Mad apple, Jimsonweed, Thornapple
Figure 7 - Datura stramoniumplant and seed pods (Right)
Datura stramonium is an annual plant with white funnel shaped flowers. It is
cultivated as an ornamental plant. Generally animals do not prefer to consume this plant
due to strong smell and unpleasant taste.The whole plant is considered as toxic
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including the nectar.Seeds are the most toxic part(Glen, 2008). Toxic principle present
in the plant includes alkaloids like atropine, hyoscyamine, scopolamine, and other
anticholinergic alkaloids.Initial symptoms exhibited includes rapid pulse with increased
heart rhythm, pupil dilatation, dry mouth, and vision impairment (Everest et al., 2005).
Later there will be decreased body temperature, nausea, loss of muscle coordination,
violent tremors,aggressive behaviour, slow breathing, rapid and weak
pulse.Management includes provision of supportive and symptomatic care.
Administration of an antidote, physostigmine should be done in severe intoxication.
Table 1 Brief information on the major plants responsible for toxicity in ruminants
CONCLUSION
Numerous poisonous plants have known to cause negative impact on the
livestock industry.Grazing is considered as normal routine in livestock management, but
it exposes the animals to a variety of poisonous plants particularly when there is a
reduction in fodder availability. For most of the plant poisoning cases the treatment is
Plant
Active
compounds
System affected
Treatment
Lantana
camara
Lantedene A and
B
Hepatotoxic
Liver supplements
Fluids and electrolytes
Abrus
precatorius
Abrin
Cytotoxic
Symptomatic and
Supportive care
Nerium
oleander
Oleandrin,
Thevetin
Cardiotoxic
Anti-digoxin fab
fragments, Atropine,
Beta blockers
Castor bean
(Ricinus
communis)
Ricin, Rcinin,
Gastrointestinal
toxicity
Symptomatic and
supportive care,
Activated charcoal
Bracken fern
Thiaminase
inhibitors and
ptaquiloside
Aplastic anaemia.,
Bovine enzootic
haematuria, Bladder
carcinoma
Thiamine
Batyl alcohol
Corn,
Sorghum,
Tapioca,
Apple
Cyanogenic
glycosides
Hematotoxic
Sodium nitrate and
Sodium thiosulfate
Oats, Wheat,
Lucerne
Nitrates and
Nitrites
Hematotoxic
Methylene blue
Datura
stramonium
Tropane alkaloids
Anticholinergic
Physostigmine
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general with symptomatic and supportive therapy since there is no antidote for most
poisons.Delay in treatment and unattained cases may lead to loss of animal, partially or
completely.Toxin specific antibodies are available for treating several plant toxicity.
Unfortunately, due to the high costs and scarce availability of these antidotes
veterinarians may not have ready access to all of those that are clinically useful in
managing plant toxicity.
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... Due to attractiveness of the plant, many house owners and municipalities plant it; thus, the potential for exposure amongst humans is high. All parts of the plant are toxic upon ingestion, especially the seeds (1). The cases of accidental poisoning have been reported worldwide, especially in children (2,3). ...
... The Cardiac Glycosides contained in White oleander are Oleandrin, Folinerin, and Digitoxigenin. Thevetin A, Thevetin B, Thevetoxin, Nerifolin, Peruviside and Ruvoside are the cardiac glycosides in Yellow oleander (1). Seeds have the highest concentration of cardiotoxic glycosides. ...
... The cardiac glycosides contained in both yellow and common oleanders bind to the sodium-potassium ATPase pump on the extracellular phase, thus, inhibiting its action and causing a rise in intracellular sodium and calcium. This excess intracellular calcium causes increased ionotropic effect and makes the heart prone to arrythmias and hypotension (1). Patients present to the Emergency medicine department with complaints of nausea, vomiting, altered sensorium, sweating, abdominal pain and diarrhea (5,6). ...
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Objective: Through the reporting of this case series, we aim to establish whether a conservative approach, through managing arrhythmias and vital signs, can be reliably used as a treatment modality for oleander poisoning in developing countries. Methods: This study is a case series of 11 patients who presented with oleander poisoning and were conservatively managed in the absence of standard antidote. Results: All 11 patients treated with conservative approach survived. Conservative approach included use of atropine for management of symptomatic bradycardia followed by Dopamine infusion, correction of serum potassium and magnesium levels, standby defibrillation, and transvenous pacing. Conclusion: The absence of reliable dosage of poison ingested, the lack of facilities for serum digoxin estimation, and the unavailability of digoxin fab antibodies pose challenges for the management of patients with oleander poisoning. Patients can, however, be managed conservatively following the Advanced Cardiac Life Support (ACLS) algorithm in a setting that lacks the standard treatment of this poison.
... Poisonous plants most often affect grazing livestock, which is a major concern for both farmers and veterinarians. Grazing is considered a common routine in livestock management, but it exposes animals to a variety of poisonous plants, especially when there is a lack of fodder availability [30]. Animals that are already experiencing nutritional stress are more vulnerable to plant toxicity. ...
Research
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Indian Himalayan region (IHR) supports a wide diversity of plants and most of them are known for their medicinal value. Humankind has been using medicinal plants since the inception of civilization. Various types of bioactive compounds are found in plants, which are directly and indirectly beneficial for plants as well as humans. These bioactive compounds are highly useful and being used as a strong source of medicines, pharmaceuticals, agrochemicals, food additives, fragrances, and flavoring agents. Apart from this, several plant species contain some toxic compounds that affect the health of many forms of life as well as cause their death. These plants are known as poisonous plants, because of their toxicity to both humans and animals. Therefore, it is necessary to know in what quantity they should be taken so that it does not have a negative impact on health. Recent studies on poisonous plants have raised awareness among people who are at risk of plant toxicity in different parts of the world. The main aim of this review article is to explore the current knowledge about the poisonous plants of the Indian Himalayas along with the importance of these poisonous plants to treat different ailments. The findings of the present review will be helpful to different pharmaceutical industries, the scientific community and researchers around the world.
... Poisonous plants most often affect grazing livestock, which is a major concern for both farmers and veterinarians. Grazing is considered a common routine in livestock management, but it exposes animals to a variety of poisonous plants, especially when there is a lack of fodder availability [30]. Animals that are already experiencing nutritional stress are more vulnerable to plant toxicity. ...
Article
Full-text available
Indian Himalayan region (IHR) supports a wide diversity of plants and most of them are known for their medicinal value. Humankind has been using medicinal plants since the inception of civilization. Various types of bioactive compounds are found in plants, which are directly and indirectly beneficial for plants as well as humans. These bioactive compounds are highly useful and being used as a strong source of medicines, pharmaceuticals, agrochemicals, food additives, fragrances, and flavoring agents. Apart from this, several plant species contain some toxic compounds that affect the health of many forms of life as well as cause their death. These plants are known as poisonous plants, because of their toxicity to both humans and animals. Therefore, it is necessary to know in what quantity they should be taken so that it does not have a negative impact on health. Recent studies on poisonous plants have raised awareness among people who are at risk of plant toxicity in different parts of the world. The main aim of this review article is to explore the current knowledge about the poisonous plants of the Indian Himalayas along with the importance of these poisonous plants to treat different ailments. The findings of the present review will be helpful to different pharmaceutical industries, the scientific community and researchers around the world.
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Ricin (also called RCA-II or RCA(60)), one of the most potent toxins and documented bioweapons, is derived from castor beans of Ricinus communis. Several in vitro methods have been designed for ricin detection in complex food matrices in the event of intentional contamination. Recently, a novel Immuno-PCR (IPCR) assay was developed with a limit of detection of 10 fg/ml in a buffer matrix and about 10-1000-fold greater sensitivity than other methods in various food matrices. In order to devise a better diagnostic test for ricin, the IPCR assay was adapted for the detection of ricin in biological samples collected from mice after intoxication. The limit of detection in both mouse sera and feces was as low as 1 pg/ml. Using the mouse intravenous (iv) model for ricin intoxication, a biphasic half-life of ricin, with a rapid t(1/2)α of 4 min and a slower t(1/2)β of 86 min were observed. The molecular biodistribution time for ricin following oral ingestion was estimated using an antibody neutralization assay. Ricin was detected in the blood stream starting at approximately 6-7 h post- oral intoxication. Whole animal histopathological analysis was performed on mice treated orally or systemically with ricin. Severe lesions were observed in the pancreas, spleen and intestinal mesenteric lymph nodes, but no severe pathology in other major organs was observed. The determination of in vivo toxicokinetics and pathological effects of ricin following systemic and oral intoxication provide a better understanding of the etiology of intoxication and will help in the future design of more effective diagnostic and therapeutic methods.
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More than 350 PAs have been identified in over 6,000 plants in the Boraginaceae, Compositae, and Leguminosae families (Table 1). About half of the identified PAs are toxic and several have been shown to be carcinogenic in rodents. PA-containing plants have worldwide distribution, and they probably are the most common poisonous plants affecting livestock, wildlife, and humans. In many locations, PA-containing plants are introduced species that are considered invasive, noxious weeds. Both native and introduced PA-containing plants often infest open ranges and fields, replacing nutritious plants. Many are not palatable and livestock avoid eating them if other forages are available. However, as they invade fields or crops, plant parts or seeds can contaminate prepared feeds and grains which are then readily eaten by many animals. Human poisonings most often are a result of food contamination or when PA-containing plants areused for medicinal purposes. This is a review of current information on the diagnosis, pathogenesis, and molecular mechanisms of PA toxicity. Additional discussion includes current and future research objectives with an emphasis on the development of better diagnostics, pyrrole kinetics, and the effects of low dose PA exposure.
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This book contains 124 chapters focusing on the various poisonous plants and mycotoxins and their effects on livestock. The effects of the chemical constituents of these poisonous plants and mycotoxins on the liver, reproductive, nervous and other organ systems of laboratory and farm animals are discussed and the different methods used in assessing the chemical compounds associated with poisoning, their control measures and their medicinal properties are highlighted. The chapters published in this book were presented at the 8th International Symposium on Poisonous Plants (ISOPP8) held in Joâo Pessoa, Brazil, May 2009.
Article
The oleander is an attractive and hardy shrub that thrives in tropical and subtropical regions. The common pink oleander, Nerium oleander, and the yellow oleander, Thevetia peruviana, are the principle oleander representatives of the family Apocynaceae. Oleanders contain within their tissues cardenolides that are capable of exerting positive inotropic effects on the hearts of animals and humans. The cardiotonic properties of oleanders have been exploited therapeutically and as an instrument of suicide since antiquity. The basis for the physiological action of the oleander cardenolides is similar to that of the classic digitalis glycosides, i.e. inhibition of plasmalemma Na+,K+ATPase. Differences in toxicity and extracardiac effects exist between the oleander and digitalis cardenolides, however. Toxic exposures of humans and wildlife to oleander cardenolides occur with regularity throughout geographic regions where these plants grow. The human mortality associated with oleander ingestion is generally very low, even in cases of intentional consumption (suicide attempts). Experimental animal models have been successfully utilized to evaluate various treatment protocols designed to manage toxic oleander exposures. The data reviewed here indicate that small children and domestic livestock are at increased risk of oleander poisoning. Both experimental and established therapeutic measures involved in detoxification are discussed.
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This study elucidates some structural and biological features of galactose-binding variants of the cytotoxic proteins ricin and abrin. An isolation procedure is reported for ricin variants from Ricinus communis seeds by using lactamyl-Sepharose affinity matrix, similar to that reported previously for variants of abrin from Abrus precatorius seeds [Hegde, R., Maiti, T. K. & Podder, S. K. (1991) Anal. Biochem. 194, 101-109]. Ricin variants, subfractionated on carboxymethyl-Sepharose CL-6B ion-exchange chromatography, were characterized further by SDS/PAGE, IEF and a binding assay. Based on the immunological cross-reactivity of antibody raised against a single variant of each of ricin and abrin, it was established that all the variants of the corresponding type are immunologically indistinguishable. Analysis of protein titration curves on an immobilized pH gradient indicated that variants of abrin I differ from other abrin variants, mainly in their acidic groups and that variance in ricin is a cause of charge substitution. Detection of subunit variants of proteins by two-dimensional gel electrophoresis showed that there are twice as many subunit variants as there are variants of holoproteins, suggesting that each variant has a set of subunit variants, which, although homologous, are not identical to the subunits of any other variant with respect to pI. Seeds obtained from polymorphic species of R. communis showed no difference in the profile of toxin variants, as analyzed by isoelectric focussing. Toxin variants obtained from red and white varieties of A. precatorius, however, showed some difference in the number of variants as well as in their relative intensities. Furthermore, variants analyzed from several single seeds of A. precatorius red type revealed a controlled distribution of lectin variants in three specific groups, indicating an involvement of at least three genes in the production of Abrus lectins. The complete absence or presence of variants in each group suggested a post-translational differential proteolytic processing, a secondary event in the production of abrin variants.
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Ricin is a heterodimeric protein toxin in which a catalytic polypeptide (the A-chain or RTA) is linked by a disulfide bond to a cell-binding polypeptide (the B-chain or RTB). During cell entry, ricin undergoes retrograde vesicular transport to reach the endoplasmic reticulum (ER) lumen, from where RTA translocates into the cytosol, probably by masquerading as a substrate for the ER-associated protein degradation (ERAD) pathway. In partitioning studies in Triton X-114 solution, RTA is predominantly found in the detergent phase, whereas ricin holotoxin, native RTB, and several single-chain ribosome-inactivating proteins (RIPs) are in the aqueous phase. Fluorescence spectroscopy and far-UV circular dichroism (CD) demonstrated significant structural changes in RTA as a result of its interaction with liposomes containing negatively charged phospholipid (POPG). These lipid-induced structural changes markedly increased the trypsin sensitivity of RTA and, on the basis of the protein fluorescence determinations, abolished its ability to bind to adenine, the product resulting from RTA-catalyzed depurination of 28S ribosomal RNA. RTA also released trapped calcein from POPG vesicles, indicating that it destabilized the lipid bilayer. We speculate that membrane-induced partial unfolding of RTA during cell entry may facilitate its recognition as an ERAD substrate.
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Ricin is a toxic lectin derived from the seed of Ricinus communis (castor plant). It is lethal in small quantities when disseminated as an aerosol. We determined the impact of using two types of exposure chambers and different particle sizes on the deposition of ricin aerosols in mice. Initially, two types of inhalation exposure chambers (whole-body [WB] or nose-only [NO]) were compared using the same size aerosol (1 micro m) to determine the potential impact upon respiratory deposition and presented dose. We then assessed the role of particle size on deposition by using aerosols with two distinctly sized particle distributions. Selected organs were collected at four time points after exposure and were analyzed by quantitative enyzme-linked immunosorbent assay (ELISA) and epifluorescence microscopy. Results of the exposure chamber comparison, using 1- micro m particles only, indicated approximately 50% of the total ricin in the 4 organs was detected in the lung tissue 1 h after exposure. The trachea and nasopharyngeal region of the animals exposed using the WB chamber contained significantly more ricin than those of animals exposed in the NO chamber. Histopathology indicated an accumulation of ricin in both the tracheobronchial and pulmonary regions with pronounced bronchiolar degradation 48 h postexposure. When particles larger than 3 micro m were used, results indicated a considerable amount of ricin initially detected in the trachea, although this finding was discounted due to the heterodispersity of the particles generated. Interestingly, no animals died as a result of exposure to the equivalent of 4 LD50s (as determined using a 1- micro m particle) when exposed to the larger size distribution of particles. This result indicates a differential lethality that is contingent upon aerosol size.
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Cyanide is both widely available and easily accessible throughout the world. Although the compound is not frequently encountered, it has been used as a poison and contaminant in the past and is a potential terrorist agent. Cyanide has the ability to cause significant social disruption and demands special attention to public health preparedness. It can be obtained from a variety of sources, including industrial, medical, and even common household products. Another frequently encountered source of cyanide exposure is residential fires. Exposure to high concentrations of the chemical can result in death within seconds to minutes. Long-term effects from cyanide exposure can cause significant morbidity. The only treatment for cyanide toxicity approved for use in the United States is a kit consisting of amyl nitrite, sodium nitrite, and sodium thiosulfate. Future research aims to find a faster-acting, more effective, and better tolerated treatment for cyanide toxicity.