Here is a list of twelve toxic plants having deleterious effect on animal health. They are: 1. Lantana Camara 2. Ipomea Carnea 3. Ipomea Batata 4. Nerium Indicum; Thevetia Nereifolia 5. Datura Stramonium; Datura Metel 6. Abrus Precatorius 7. Ricinus Communis 8. Strychnos Mux-Vomica 9. Sorghum Spp 10. Seleniferous Plants 11. Cyanogenic Plants 12. Oxalate Producing Plants.
1. Lantana Camara:
(Synonyms: Bara phulanoo, Panch phool booti, Curi, Chadurang gheneri, Puli kumpa, Unichedi, Arripuv, Konkanichipu, Raimumiya)
The plant grows up to an elevation of 2000 meters above MSL. The growth is abundant in the temperate climate. The plant is spread widely over the large tract of Himachal Pradesh, Jammu and Kashmir, hilly regions of Uttar Pradesh and North Eastern Himalayan region. It was introduced in India as ornamental plant during early nineteenth century. As many as 15 taxa of the species are toxic. The plant (Lantana camara var aculeata) possessing red flowers is perhaps the most toxic.
The toxins responsible for hepatotoxic action are mainly triterpenes. Only leaves elicit hepato toxicity and photo sensitization in experimental animals. The two important triterpinoids whose toxicity have been established are lantadene A and lantadene C. There is still ambiguity regarding the biological activity of the lantadenes B and D.
Mechanism of Toxic Action:
The exact information regarding the primary site of action on hepatocytes with which lantana toxins bind is not known. It is, however, observed that a decrease in activity of Na+K+– ATPase in the canalicular plasma membrane is perhaps associated with decrease in the bile flow and chlolestasis which leads to hepatotoxic action of lantana toxins.
Lantana poisoning in animals is observed round the year and ruminants are the prime victims. Incidence is maximum during the summer months owing to the scarcity of the fodder. Lantana toxins are absorbed from all parts of the digestive tract. Within couple of hours of intake (24 to 48 hours), the animals go off feed. There is severe constipation, ataxia and incoordination of movements. The urination becomes scanty and animals become icteric.
The intrahepatic cholestasis leads to jaundice, photosenstization and ruminostasis. Absorption of toxins from rumen further aggravates the situation by maintaining the hepatic injury. In sheep head gets swollen, eyelids are swollen, ears become pendulous and swollen. In later stages, there is accumulation of bilirubin.
Phylloerythrin, metabolite chlorophyll, triggers photo chemical reactions leading to appearance of fissures on muzzle, ear tips and non-hairy parts of the body. The low doses of lantana toxins are also known to cause immuno-suppression.
The most consistent biochemical alternation in the body includes a significant rise in serum levels of conjugated bilirubin.
On postmortem liver of the affected animals is found to be yellow and mottled. There is hepatomegaly. Kidney and rest of the viscera are yellow. Urinary bladder is full of urine.
The treatment of sick animals by use of laxatives i.e. mineral oil or saline purgatives is only partially successful. The rational approach for checking absorption of lantana toxins is, therefore, to use adsorbents (activated charcoal and bentonite) in large volumes of multiple electrolyte solution by intraluminal route through a stomach tube.
The hepatic injury caused by lantana toxins can be treated by using liver tonics, glucose saline or electrolyte solutions. Secondary toxicosis (hyperbilirubinemia and hyperphylloery threnemia) can be treated by giving antihistaminic and skin ointments.
Bovine serum albumin and haemocyanin conjugated lantadenes A and B have been used with partial success for protection of the poisoning. There is need of developing teller immunogens for an effective protection. Aversion therapy based on conditioning of animals before they are left for grazing in pastures infested with poisonous plants is underway in Kimron Veterinary Research Institute, Bet Dagon, Israel.
No rational therapy based on structure of lantana toxins and molecular mechanism of action is available so far. The best way, therefore, is to protect the animals from having access to lantana foliage and in case animals are poisoned they should be protected from the sunlight so that they do not develop secondary complications like photosensitization. The animals should also not be given green fodder during the course of sickness.
2. Ipomea Carnea:
Jangaliakh; Besharmi booti
The plant is found in tropical regions of the country. The plant is grown as hedges. It was brought to India as an ornamental plant.
The plant is extremely toxic to livestock and leaves contain a polysaccharide, ipomose, an anthracene glucoside, a gum resin, jalap and saponins. Administration of water soluble toxin causes haemolysis of red cells and fall in blood pressure. Ether soluble toxin affects respiratory and cardiac system.
The leaves of plant produce weakness, tremors, ataxia and death in goats. A staggering gait, reluctance to move, weakness of hind limbs and an increase in body temperature has been observed in sheep and calves. A long term intake causes anaemia. The aqueous extract of root of the plant produces non specific hypotensive effect.
The toxins cause hepatic necrosis and congestion of brain in goats.
Treatment is symptomatic
3. Ipomea Batata:
Sweet potato; shakarkund.
Found throughout India especially in tropical parts.
Unknown toxic principle produced in tubers.
The tubers of the plant cause respiratory distress in animals. It is believed that toxicity is caused by the metabolites of the mould, Fursarium solnni. It has also been suggested that condition is not caused by mycotoxins but by the metabolites produced by tubers in response to injury caused by moulds and trauma.
There is pulmonary oedema and lesions in liver, spleen and kidneys in cattle.
4. Nerium Indicum; Thevetia Nereifolia:
Kaner, Karber, Kuruvira, Sweet scented oleander, Indian oleander, Kanhera, Karaviram.
It is a large evergreen shrub found in upper Gangetic plains, Madhya Pradesh and in Flimalaya upto an altitude of 2000 meter above MSL. It is also grown in gardens for its fragrant and showy flowers.
All parts of the plant i.e. the roots, bark and seed contain toxic digitalis like glycoside namely oleandroside, karbin and neriodorein.
Mechanism of Action:
The glycosides are reported to possess paralyzing action on heart and stimulant action on spinal cord.
The Indian Oleander appears to be very toxic. Cattle consuming a few leaves of the plant are reported to have died within 24 hours. The clinical signs include dullness, depression, anorexia, respiratory distress, nervous irritability, tremors, tetanic convulsions, salivation and vomition.
Drowsiness in animals passes into loss of consciousness. In horses leaves are extremely toxic and toxicity is characterized by vomiting (a rare symptom), convulsions, diarrhoea and colic. The dogs show continuous vomition and respiratory distress.
The gross postmortem findings include gastro-enteritis with petecheal haemorrhages. The haemorrhages are also observed on heart, serous and mucus membranes.
Atropine in conjunction with corticosteroids and antihistaminic has been found to be an effective therapy.
5. Datura Stramonium; Datura Metel:
Jimson weed; Sada Dhatura, Dhatura, Tittu Dattura, Umatai.
The plant is found in all parts of India and occasionally grown in garden. Found in Himalayas up to an altitude of 9000 ft. above MSL.
The alkaloids-atropine, hyoscyamine and hyoscine are responsible for toxic action. The alkaloids are present in all parts of the plant.
Mechanism of Action:
The clinical symptoms occur mainly due to the blockade of muscarinic receptors of smooth muscles, cardiac muscles and glands by atropine and its competitive antagonism with acetyl choline.
The symptoms in cattle include dilation of pupil and staggering gait. The symptoms in sheep and goats are characterized by impaired movements, dyspnoea, tremor, recumbency, hyperaesthesia, rapid respiration and reduced water intake. The horses develop chemical symptoms of poisoning within 6-24 hours of ingestion of seeds.
The clinical symptoms in horse include restlessness, colic, dyspnoea, tachycardia, peripheral circulatory insufficiency, constipation, tympany and cessation of peristalsis, dilated pupils, drying of oral and nasal mucosa. The death of animals occurs 24-72 hours post ingestion of seeds.
In pigs a condition known as congenital arthrogryposis has been reported in piglest born to sows intoxicated by Datura stramonium during pregnancy.
The postmortem changes observed in cattle include submepicardial haemorrhages, hyperaemia of liver and catarrhal inflammation of intestine. The postmortem findings in horses include pulmonary emphysema, cardiac dilatation. In sheep and goats congestion of lungs, haemorrhagic and fatty liver, hydro peritoneum and hydro pericardium have been observed.
The treatment is mainly symptomatic and comprises fluid therapy and use of purgatives etc. Pilocarpine has also been used in alleviating cholinergic blocking action of atropine and atropine like toxic principles.
6. Abrus Precatorius:
Jaquirity pea, Ratti, Gunja, Ghungehi, Kunch, Gundumani, Gurigija Kakani, Gunji.
Found throughout India ascending the outer Himalayas up to an altitude o/ 35C6 k above MSL. The seeds of the plant are widely used for making necklaces and other articles of jewellery for tourists.
The seeds contain phytotoxin, abrin whose action is similar to that of ricin
Mechanism of Toxic Action:
The toxicity depends upon the manner in which seeds are administered. Orally seeds are not much poisonous as outer coat is too hard to disintegrate. The phytotoxin (toxalbumin), abrin, has the property of agglutinating the red cells.
Subcutaneous implantation of spikes containing crushed seeds have been used for malicious killing of animals. The affected animals die within two to four days of clinical symptoms. The clinical symptoms include salivation, stiffness, incoordination, muscular spasm, convulsions. There is extensive painful swelling around the site of implant.
Abrus seeds given orally in goats produce in-appetence, bloody diarrhoea, dyspnoea, dehydration, loss of condition and recumbency. The whole seeds given orally may not have any deleterious effect in cattle but may produce lethal effect in poultry. Abrus seeds are widely used to induce abortion. Abrus seeds are also known to decrease sperm motility.
The pathological changes following oral intake include fatty changes and necrosis of hepatocytes and renal convoluted tubules, pulmonary haemorrhages, oedema, emphysema and erosions of abomasal and intestinal epithelium. The post-mortem changes recorded following subcutaneous administration include congestion of visceral organs and petechial haemorrhages throughout the body.
Animals can be immunized against abrin and protection can be provided by subcutaneous injection of anti-abrin serum. Saline purgatives and arecoline are of limited value in the poisoning.
7. Ricinus Communis:
Castor oil plant, Eranda, Bherenda, Erendi, Eri, Manda, Erandam, Amankku, Erandamu
It is cultivated throughout India and naturalized near habitations especially in tropical parts.
The seeds or beans contain toxic protein or phytotoxin, ricin. The pericarps of the fruits and leaves contain the alkaloid, ricinin.
Mechanism of Action:
Ricin unlike majority of similar toxins, is absorbed from the gut. Poisonings occur due to accidental or intentional mixing of seeds or castor cake with other feed stuffs. Ricin also has property of agglutinating the red cells.
The main clinical symptom in cattle is bloody diarrhoea. The administration of the pericarp of the ripe fruit causes neuromuscular signs including swaying gait, muscular tremors, salivation and chewing movements. The gastrointestinal symptoms are caused by ricin whereas nervous symptoms are caused by alkaloid ricinin.
In horses initially there is dullness followed by signs of incoordination and in severe cases there is profuse sweating, tetanic spasms of muscles and tumultuous heart. There is profuse watery diarrhoea but without blood.
In pigs vomiting and diarrhoea are noted. The animals become very weak and show symptoms of incoordination and abdominal pain. The skin of ears, flanks and ham becomes cyanotic.
The toxicity in chickens is characterized by locomotor disturbances, abnormal posture, enterohepato-nephropathies and anemia. Adult birds are less severely affected.
In dogs clinical symptoms include haemorrhagic gastro-enteritis and cyanosis with fever in first three days followed by circulatory collapse.
On post-mortem examination, contents of gut are found fluid or semifluid. There is patchy inflammation of gastric and intestinal mucus membranes which at times is accompanied by punctiform haemorrhages. The lungs are oedematous. The trachea and bronchi are filled with frothy oedematous fluid. Lymph nodes are swollen. The animals poisoned by leaves or percicarp show only limited pathological manifestations.
The poisoned animal can be treated with ricin antiserum. Symptomatic treatment can be instituted with instravenous fluid, broad spectrum antibiotics, vitamin B complex and atropine etc.
8. Strychnos Mux-Vomica:
Kuchla, Visha-mushti, Kuchila, Kajra, Kanjira, Kanniram, Etti, Mushti.
It is found in forests of Eastern U.P., Bihar, Orissa, Konkan, Karnataka, Tamilnadu and found up to 4000 ft. above MSL in hilly regions of Tamilnadu.
The main toxic alkaloid, strychnine, is predominantly present in seeds. The alkaloid is also found in root, wood, bark, leaves and pulp etc. The other alkaloid, brucine, is present in bark. Seeds contain about 1.5 to 3.4% of total toxic alkaloids, half of which is strychnine.
Mechanism of Action:
The alkaloid, strychnine, competitively blocks glycine receptors in the spinal cord. This causes inhibition of post synaptic inhibitory neurotransmission in the spinal cord. Strychnine, thus, impairs the modulation of efferent motor impulses to skeletal muscles leading to over stimulation of skeletal muscles. Strychnine also has GABA inhibitory action and direct depolarizing and firing threshold lowering effect on neuronal membranes.
The dogs are most susceptible followed by horses, ruminants and poultry. In ruminants strychnine is partially destroyed in rumen. The oral lethal dose of strychnine varies from 0.2 to 5.0 mg/kg in most species. The lethal doses by parenteral route are less as compared to oral route.
The initial chemical symptoms of poisoning are nervousness, restlessness, twitching of muscles followed by stiffness. As the condition progresses, the muscular twitchings become more severe. At this stage convulsions also start appearing.
The skeletal muscles of the body contract in opposite direction and body assumes arched back or opisthotonus condition. As the poisoning progresses further, the periods of relaxation of muscles become shortened.
During these periods of relaxation, the muscles show exaggerated response to even slightest external stimuli. At the terminal stage the frequency and severity convulsion gets increased. Death occurs due to respiratory failure and may occur within few hours of ingestion of the poison. In certain cases death may be delayed up to 48 hours. In dogs vomition is also observed.
The venous blood is found dark. The lungs and cerebral meninges are engorged. Internal organs are congested.
The treatment in the initial phase (before starting of convulsions) comprises gastric lavage with potassium per-magnate or tannic acid solution followed by lavaglng with activated charcoal slurry (The lavage is contraindicated once the Convulsions have started). Alternatively, emetics (Apomorphine or locally acting) can be given prior to start of convulsions.
The success in therapy can be achieved by controlling convulsions. Pentobarbital sodium, mephenesin, glycereyl guaicolate, xylazine and methocarbamol have been used by various clinicians with varying degree of success. Godfrain and colleagues have used diazepam (2 mg/kg) intravenously followed by apomorphine (2 mg/kg, S/C) in dogs. In severe cases, the therapy can be followed by pentobarbital administration and forced acid diuresis. The poisoned animals should not be unnecessarily disturbed and should be housed in a dark room.
9. Sorghum Spp:
Four species of sorghum responsible for toxicity are Sorghum halepense (Bare grass, Kala mucha, Bikhonda Gaddijfanu), Sorghum sudanese (Sudan grass) Sorghum vulgare (Millet, Joar, Jowar, Cholam, Jonalu, Jolah) and Sorghum vulgare var saccharatum (Deodhan, Tella-jonuoh).
The various varieties of the plant are grown world-over as fodder for livestock. Some species are wild and found throughout India in open places.
Various species of sorghum may contain dangerous concentrations of cyanogenetic glycoside, dhurin and nitrates in leaves and perhaps in other parts due to adverse climatic conditions.
Mechanism of Action:
Symptoms of cyanide or nitrite toxicity may develop in domestic animals especially ruminants following metabolism of cyanogentetic glycosides or nitrates in the digestive tract. These conditions are dealt separately under cyanide or nitrite toxicity. A typical condition, sorghum cystitis ataxia syndrome caused possibly by lathyrogenic nitriles present in growing fodder is discussed here.
Ataxia and incontinence caused due to grazing of Sorghum spp. have been widely reported in cattle and horses. The condition appears to be associated with the growing grass only. Death usually occurs due to pyelo-nephritis.
There is generally accumulation of yellow material in the bladder. Both the ataxia and paresis of bladder are, perhaps, due to focal axonal degeneration of the spinal cord. Wallerian degeneration of white matter of spinal cord, cerebellar peduncle and cerebellum also occurs in poisoned animals. Pregnant mares grazing on Sudan grass have been reported to develop dystocia and give birth to foals with ankylosis of joints.
There is no known treatment except antibiotic therapy. The recovery is usually rare. Prevention is the only cure.
10. Seleniferous Plants:
Selenium is the essential trace element. The major source of poisoning in livestock is forage or feed that comes from soil rich in this element. Seleniferous areas are in general characterized by low rainfall areas. In high rain fall areas, selenium is leached out of the top soil.
Iron oxide present in soil converts selenuim into insoluble form. Only soluble forms, both inorganic and organic forms are made available to plants through soil. The plants can be divided into three groups namely obligate accumulators, facultative accumulators and passive accumulators.
(a) Obligate accumulators:
Indicator plants are those plants which require selenium for their development and growth.
(b) Facultative accumulators:
Are those plants which can survive in the absence of selenium but if it is available in soil they will accumulate it in sufficient amount.
Following plants (obligate and faculative) accumulate selenium from soil.
Acacia spp. Guterrezia spp.
Aster spp. Machaerathera spp.
Astragalus spp Morinda reticulata
Atriplex spp. Oonopsis spp*
Castilleja spp. Fentstemon spp.
Comandra pallida Sideranthus spp.
Greyia spp. Stanleya spp.
Grindelia spp. Xylorrhiza spp*
* obligate accumulators or indicator plants
(c) Passive Accumulators:
They comprise majority of vegetation. Some of the plants may contain harmful amounts of selenium while others can not tolerate and are killed by it. At many occasions accumulators convert selenium in such a form that is taken up by passive accumulators. Corn, wheat, barley, grasses and hay belong to this category.
The minor sources (non vegetable sources) of selenium toxicitty include selenuim based shampoos.
2. Mechanism of toxic action:
Selenium is considered essential micronutrient required for prevention of cellular degeneration and cell membrane damage in man and animals.
From toxicological point of view, all the three oxidation states namely selenate (+6), selenite (+4) and selenide (-2) are important. The exact mechanism of toxic action is not known but following biochemical effects are observed in the intoxicated animals.
(a) Replacement of sulphur in amino acids such as cysteine and methionine with possible synthesis of abnormal proteins.
(b) In chronic cases, there may be decrease in ATP synthesis due to inhibition of sulph-hydryl containing enzymes leading to decreased energy utilization in liver, kidney and brain.
(c) There is interference in haeme containing selenoproteins and selenoproteins found in selenium treated animals.
(d) There is dramatic reduction in tissue GSH concentration. This results in loss of cell membrane integrity.
(e) There is decrease in cellular NADPH which has multiferous role in metabolic processes.
(f) There may be interference in synthesis of vitamin A and C.
The minimum lethal dose of selenium in form of sodium selenite is about 3.3 mg/kg in horse, 10 mg/kg in cow and 17mg/kg in pig. Organic form of selenium present in plants is almost two times more toxic when ingested as selenide or selenite.
4. Clinical Symptoms:
Selenium poisoning (Selenosis) occurs in acute, sub-acute and chronic forms. Sub-acute to chronic from is known as blind staggers and chronic form is known as “alkali disease.”
Acute Selenium Poisoning:
The poisoning mainly occurs in ruminants and results from ingestion of selenium rich plants. The symptoms appear, within few hours to few days. The clinical symptoms include a rapid and weak pulse, colic, bloat, dark and watery diarrhoea, polyuria, fever (39-40°C), mydriasis and uncertain gait.
The animals show peculiar rooted to one spot stance with head and ears lowered, mucus membrane becomes cyanotic .There is dyspnoea with fluid sounds in lungs. The blood tinged fluid is seen coming out of nares. Death occurs in few hours or within a day.
The post-mortem lesions include degenerative changes in all organs. The prominent changes are seen in liver and spleen. The liver is found atrophied, necrotic and cirrhotic. Ascitis is a common finding. Congestion, oedema and softening of brain have also been recorded. In pigs there is anorexia, emesis, diarrhoea, lethargy, unsteady gait, weakness, paresis, dyspnoea, prostration, coma and death within 1-2 days. Horses, generally do not suffer from acute selenium poisoning.
Pulmonary congestion and oedema as well as degenerative changes in the liver, kidney are the important post mortem findings.
Sub-acute to chronic form (Blind staggers):
The poisoning results due to ingestion of highly seleniferous plants (containing > 30 ppm.) over a short period (about eight weeks). During the course of disease, animals initially show poor appetite, walk aimlessly in circles without avoiding obstacles and stumbling over them.
In second stage the animals show depression, incoordination and foreleg weakness causing animal to go down on its knees. In third and final stage the animals manifest salivation, lacrimation, severe abdominal pain, subnormal temperature, emaciation, swollen or inflammed eyelids clouded corneas, near blindness. As the disease progresses there is complete paralysis, dyspnoea, tachypnea, coma and death within few days of onset of symptoms.
Chronic Selenium poisoning (Alkali disease):
The poisoning is caused by the daily ingestion of cereals, grasses and fodder plants containing small amount of selenium. The disease has nothing to do with the drinking of alkali water as it was earlier thought. The selenium in the feed stuffs producing the alkali disease is believed to be found in plant proteins and is relatively in insoluble form.
Alkali disease is characterized by loss of long hair from mane and tail of horses and from the switch of cattle, a rough coat, dullness and anorexia. There is partial blindness in animals, paresis, in coordination and peripheral circulatory insufficiency and lameness.
The lameness is due to erosion of articular surfaces of long bones. There is painful separation of hoof just below coronary band. However, there is incomplete separation and old hoof fuses with new hoof to form abnormally long rocker shaped hoof. The fetuses may also develop abnormal joints and hooves.
Poultry is not directly affected in chronic selenosis but hatchability of eggs is depressed and chicks which hatch may be weak and may lack vitality. The death in acute/sub acute poisoning is attributable to respiratory insufficiency resulting from pulmonary oedema and haemorrhages. In chronic selenosis, death occurs directly from metabolic lesions.
The most prominent lesion in chronic selenium toxicity includes atrophy of heart and atrophy and cirrhosis of liver. Gastroenteritis and nephritis may also be present in alkali disease.
The diagnosis is primarily based on history. If animal has an access to known seleniferous plants, the poisoning can be suspected. The odour of rotten garlic or rotten horse radish in fresh carcass is suggestive of acute or sub-acute selenosis.
But absence of the odour also does not rule out the possibility of selenium in the blood. 1-4 ppm concentration in blood in chronic toxicity, 25 ppm in blood in acute toxicity; 4-25 ppm in liver and kidney; 0.1 to 8 ppm in urine and 3 ppm in milk are considered toxicologically important.
Prophylaxis and Treatment:
The first and foremost thing is to stop feeding of the source of selenium. Saline purgatives can be used for removal of selenium from the gut. High protein diet protects animals from selenium poisoning. Feeding of salt containing arsanillic acid (50-100 ppm) in ration can benefit animals in facilitating the excretion of selenium. Selenosis in chicks can be partially prevented by feeding of 1% ascorbic acid. Treatment of acute selenosis with thiosulfate given orally has only been found to be partially successful.
11. Cyanogenic Plants:
The most important sources of cyanide (hydrocyanic acid) poisoning in animals are plants containing cyanogenetic glycosides, organic compounds, yielding cyanide on hydrolysis. The natural cases of hydrocyanic acid poisoning have been widely reported from various parts of India.
The following plants may contain dangerous levels of cyanides in form of cyanogenetic glycosides.
Sorghum hcilepense (Johson grass)
Sorghum sudanese (Sudan grass)
Sorghum vulgare (Common sorghum)
Prunus spp. (wild cherry)
Linum usitatissimum (Flax)
Prunus spp contains glycoside, amygdalin and Sorghum spp contains glycoside dhurin. The glycosides themselves are nonpoisonous but when they come in contact with specific enzyme during digestion they are converted into hydrocyanic acid.
In stunted or wilted plants or those which have been damaged by frost or trampling, there is liberation of hydrocyanic acid. Treatment of crops or plants with nitrogenous fertilizers or with herbicides such as 2, 4-D also increases the cyanide contents. However, treatment of crops with superphosphate decreases HCN contents of fodder. The cyanide contents of grasses and fodder decrease with the age of the plants.
Rumnimants are more susceptible than monogastric animals for cyanogenic plant toxicity and cattle are more susceptible than sheep.
Inorganic salts of cyanide present in plants do not necessarily cause sings of cyanide poisoning. Thiocyanates or thiocyanate glycosides found in rape-seeds, turnip, broccoli, soya bean or flax may have goitrogenic potential. Cyanates or thiocyanates can also cause CNS and endocrine effects but these are of little veterinary significance. The intake of cyanogenetic glycosides through white clover silage affects selenium status of sheep and increases the susceptibility of lambs to nutritional myopathy.
Mechanism of Toxic Action:
The CN” radical complexes with the ferric ion of cytochrome oxidase in mitochondria. Cyanide blocks electron transport in cytochrome α – α3 complex. As a consequence, oxygen utilization is decreased and oxidative metabolism may slow to the point that it can not meet metabolic demand.
The severity of the symptoms depends upon the rate of ingestion of toxic plant, cyanide contents of plant and rate of liberation of cyanide upon hydrolysis. In acute cases the animals show muscle tremors and die within few minutes. In sub-acute toxicity the course of toxicity is distinctly observed and onset is characterized by salivation and dyspnoea.
Muscular spasm generally develop gradually and just prior to death. Animals stagger and struggle before collapse. Other symptoms include behavioral abbertations, lacrimation, mydriasis, urination, defecation, severe colic, prostration and bloat.
The mucus membrane becomes bright red due to hyper-oxygenation. Death is due to cessation of respiration and heart continues to beat for several minutes thereafter. During cyanide toxicity the animal remains responsive and conscious even 4-5 minutes prior to death. Occasionally in per-acute cases the animals die without manifesting clinical signs
The minimum lethal dose of hydrocyanic acid in most species by oral route is 2.0-2.3 mg/kg.
In acute toxicity the blood may be bright red which turns to dark red on exposure to air. The blood remains un-clotted. There may be congestion and haemorrhages of lungs and reddening and congestion of mucus membranes of stomach. When abdomen/rumen is opened, it is filled up with gas and odour of “bitter almonds” can be detected.
The diagnosis of cyanide toxicity can be made on the basis of history, typical clinical signs, post mortem findings and demonstration of hydrocyanic acid in the stomach contents. For confirmatory diagnosis 150-250 g of stomach contents should be collected soon after death and immersed in 1-3% solution of mercuric chloride.
Muscle, liver can be collected within 4 hours of death. Plant materials possessing 200 ppm or more are considered potentially toxic. The cyanide contents of 1.4 ppm in liver and 10 ppm in rumen contents are regarded as indicators of cyanide intoxication.
Prophylaxis and Treatment:
As a prophylactic measure, the animals should not be grazed on pastures during adverse climatic conditions or during conditions which increase the potential of toxicity (low rainfall and use of nitrogenous fertilizers etc.). The danger of cyanide intoxication can be reduced by providing well cured hay to animals (but potential for nitrite intoxication should be assessed in such cases.
The objective of treatment is to free the CN- from ferric ions of cytochrome oxidase. To achieve this, sodium nitrite. (15-25 mg/kg) is injected intravenously followed by 25% sodium thiosulfate injected intravenously at the dose rate of 1.25 g/kg. Sodium thiosulfate can be repeated with half the dose if needed. However, sodium nitrite should not be repeated because of the danger of producing nitrite toxicosis.
The rationale behind treatment is that the nitrite converts haemoglobin into methaemoglobin and methaemoglobin possesses greater affinity for CN” ions. CN” ions are thus dissociated from ferric ions of cytochrome oxidase.
Sodium thiosulfate reacts with cyanide in blood or CN” liberated from cyanomethaemoglobin and forms thiocyanate which is excreted. In cattle a solution of 3g of sodium nitrite and 15g of sodium thiosulfate in 20 ml water given subcutaneously has been found useful. Sodium thiosulphate can also be given orally (30g/cow) which can be repeated at hourly interval to prevent further absorption of cyanide.
In sheep, sodium nitrite and sodium thiosulfate can be given at half the recommended dose for cattle i.e. 1g of sodium nitrite and 2g of sodium thiosulfate given in 15 ml of water. Alternative therapeutic measures include administration of p-amino propriophenone (1.5 mg/kg) along with sodium nitrite (22 g/kg).
According to Burrows, sodium thiosulfate administered alone in high dose (660 mg/kg) seems to be an antidote of choice as it satisfies the requirements of high efficacy and low toxicity. Vick and Foroechlich have successfully used phenoxy benzamine and amyl nitrite intravenously in the prevention and treatment of cyanide poisoning, respectively, in dogs.
Vitamin B12a and vitamin B12b can also be given in the treatment to speed up the recovery. Possibly, cobalt in these preparations complexes with additional cyanide. Burrows and Way have shown that 10.6 mg/kg of cobalt sulfate can be used to enhance the therapeutic effectiveness of thiosulfate nitrite mixture. Chlorpromazine hydrochloride can antagonize cyanide intoxication due to hypothermia but its therapeutic efficacy needs to be established.
Other therapeutic measures include cooling, diluting and acidifying of ruman contents by giving vinegar or 5% acetic acid in cold water to slow down the microbial hydrolysis of cyanagenetic glycosides. Mineral oil can be given to soothe the irritated gastrointestinal membranes.
12. Oxalate Producing Plants:
Oxalate poisoning in animals occurs due to absorption of soluble oxalates such as sodium and potassium oxalates. Calcium oxalate is insoluble and therefore, not toxic.
The cases of oxalate poisoning mainly occur due to ingestion of following plants having sufficient quantity of soluble oxalates.
Besides the above mentioned plants minor sources of oxalates include moist straw infected with mould Aspergillus niger. A. falvus and with certain species of Penicillium. The oxalate contents of plants are highest at the leafy stage of growth.
Mechanism of Toxic Action:
The toxicity of oxalates in ruminants mainly depends on the plane of nutrition and functioning of the rumen. Normally soluble oxalates are converted into carbonates and bicarboriates. However, if same are produced in sufficient quantity, there may be alkalosis. Oxalates once absorbed may produce toxic effects in following manner.
(a) They may produce hypocalcaemia and hypomagnesemia leading to rapid death. Calcium metabolism is upset to the extent that milk production is decreased.
(b) In kidney, oxalate crystals interfere in the tubular function. Kidney damage is usually due to chronic ingestion of oxalates.
(c) Oxalates may cause haemolysis of the blood.
(d) Accumulation of oxalate crystals in ruman may be associated with oedema and extensive haemorrhages.
(e) Oxalates may inhibit various respiratory enzymes activated by calcium or magnesium.
(f) In certain, rare circumstances, oxalates may crystallize in brain tissue and may cause paralysis. The exact mechanism of action is however, obscure.
The oral toxic dose of oxalic acid in a dog is about 1g whereas in a cat it is about 0.2g. The dose as low as 30g orally may prove fatal to an unaccustomed sheep.
The animals initially show dullness and anorexia. In acute poisoning, there is salivation with progressive weakness, rapid shallow breathing and collapse.
The pathological findings include accumulation of calcium oxalate crystals in kidney and urinary tract. The lungs may be dark red and filled with blood. There may be petechial or widespread haemorrhages.
The diagnosis is based on history, clinical symptoms and presence of oxalates in rumen fluid and urine. Plants containing 10% oxalates on dry basis are considered unsafe.
Prophylaxis and Treatment:
Animals maintained on oxalate rich diet can be protected from oxalate poisoning by giving calcium supplementation in form of 25% di-calcium phosphate of salt ration. Sheep being introduced on oxalate rich pastures should be provided a supplementary feed such as hay for a few weeks or can be rotated on non oxalate pastures.
Treatment of oxalate poisoned animals is usually of little avail as much damage seems to have occurred prior to presentation of animals for the treatment, Games and Johnson have shown that calcium chloride is of some value in increasing the survival rate if given within few hours of poisoning.
Dicalcium phosphate can be given to poisoned animals at following dose rates by oral route:
Dogs- 0.3 -0.6g
Cats -.06-0.3 g
Calcium borogluconate 25% can also be administered intravenously at following dose rates.
Cattle -300-500 ml
Sheep- 50- ml
Ancillary treatment should include the provision of ample fluids to decrease precipitation of oxalate crystals in urinary tract.