Plant and Other Poisoning (new)
(c) Forse 1999
Prevention of plant poisoning
You can help to stop animals getting poisoned by:
- Making sure animals are well fed and healthy. Healthy well fed animals are much less likely to eat poisonous plants or scavenge for food and eat poisons by mistake.
- Do not graze animals where you know there are poisonous plants
- Avoid pastures that have just been fertilised with nitrogen in any form or sprayed with herbicides or pesticides
- Do not let animals graze near rubbish where people have thrown things that may be poisonous like old paint.
Plant poisoning is usually difficult to diagnose. Different plants act in different ways and therefore produce different symptoms. Diagnosis often has to rest on the history as frequently symptoms and lesions are rarely characteristic. The fact that animals had access to a particular plant or been seen to be eating it, the presence of identifiable fragments in the stomach and the fact that the animals were strangers to the district should be taken into consideration when attempting to reach a diagnosis.
It should be noted that most plants with yellow flowering heads are toxic to stock but, unless the grazing is very sparse, they will avoid eating them.
Some plants are poisonous at certain stage of growth and not at others. For example potatoes are particularly poisonous after they have turned green on exposure to light. Certain parts of a plant may be safe to eat while other parts may not be safe.
Numerous plants have been incriminated as the cause of poisoning in livestock and a few of these are detailed below.
General Diagnosis of Plant Poisoning
This is not easy and may require the assistance of a skilled veterinarian to differentiate the symptoms observed from those of infectious diseases. Plant poisoning is not common but when it does occur it may have devastating effects so rapid diagnosis is vital.
If plant poisoning is suspected often there are signs of gastrointestinal involvement. The gut should be inspected to see if any pieces of plant can be identified.
The sudden death of newly introduced animals may arouse suspicion of plant poisoning. Certain plant poisonings may be more common during times of drought when animals may be forced to eat plants they might otherwise avoid.
Inspection of grazing areas may reveal known toxic plants. When several animals are taken ill at the same time plant poisoning may be suspected.
Prevention, Control and Treatment
The most important plank in prevention is by not allowing animals access to plants which may cause poisoning. This may be difficult when the responsible plants are those which may be normally safe to eat at certain stages of growth and not at others. But if there are known poisonous plants in an area these should either be physically removed or animals should not be allowed to graze there. Well fed animals are less likely to sample poisonous plants than animals which are hungry. In times of drought try to supply supplementary feed.
in many cases, in the absence of a specific diagnosis, treatment has to be symptomatic, but if poisoning is suspected any of the following can be tried (adapted from Forse 1999).
- Giving a purgative, such as Epsom's salts, may help to remove the toxin from the gut. Give 100g Epsom salt in half litre of water to small animals and up to 500 g Epsom salt in 1 litre of water for large animals given by mouth. Only use about 50 g Epsom salt for horses. Epsom salt (magnesium sulphate) is useful for treating poisoning. It makes more water go into the intestines from the body and gives the animal diarrhea so most of the poison in the intestines mixes with water and comes out as diarrhea.
- Mix kaolin (fine white clay powder) in water until it is a milky liquid. Give by mouth. For a large animal use about 200g Kaolin for a small animal about 10 g. Give every day for a few days if needed.
- Mixing a handful of charcoal powder in a bottle of clean water and give the solution by mouth may help in some cases. Charcoal can inactivate poisons in the stomach.
- Give milk or coconut milk by mouth
- Mix ground cereals or rice with water and give by mouth
- Mix 6 eggs and half kilo of sugar with about 1 litre of water and give by mouth.
- Animals which are depressed may benefit from the administration of stimulants.
- Animals which are excited may benefit from sedatives.
- In some cases, eg Prussic Acid Poisoning, or Nitrate/Nitrite Poisoning, there is a specific antidote, but in the majority of plant poisoning there is not and so one has to treat the symptoms as they appear.
Numerous plants have been incriminated as the cause of poisoning in livestock and a few of these are detailed below.
These small spreading trees have received much notoriety as being the main provider of many arrow poisons. The leaves are glossy and pointed. Being ever green the tree is attractive to stock when conditions are dry. Although the ripe fruits are edible it may be presumed that all other parts of the tree are poisonous.
In cattle death occurs suddenly, but rapid shallow breathing may be seen together with diarrhoea. Other symptoms include muscular spasms, teeth grinding, grunting respirations, and a profuse, clear, slimy nasal discharge. Post mortem reveals gastroenteritis, pale pink lungs distended with air and haemorrhages within the heart.
(c) Patrick Maundu. Useful Trees and shrubs for Ethiopia
(c) Useful Trees and shrubs for Ethiopia
(c) Blundell 1987
Bracken (Pteridium aquilinum)
In marginal, highland areas of Kenya bracken fern is to be found and is responsible for isolated cases of stock poisoning, mainly in cattle.
- In single-stomached animals such as horses and pigs, poisoning is related to a deficiency of thiamine (vitamin B1) resulting in loss of appetite, weight loss, incoordination, trembling, rapid heart beat and death.
- In cattle bracken poisoning results in bone marrow depletion and anaemia. There is no deficiency of vitamin B1 in cattle as they are able to manufacture this vitamin in the rumen.
- Bracken poisoning is usually cumulative and may require up to three months to develop and sometimes animals have already been moved to a different pasture when symptoms develop. Both the leaves and the roots of the bracken fern are toxic.
- Symptoms are those of an acutehaemorrhagic syndrome, with clots of blood in the faeces, bleeding from body orifices, failure of blood to clot, a high temperature, loss of weight, and death with multiple haemorrhages throughout the carcase.
- Swelling of the larynx and difficulty in breathing has been reported in young cattle. One characteristic clinical picture in bracken poisoning in cattle is Chronic Enzootic Haematuria with tumours and haemorrhages in the urinary bladder which ultimately causes death from anaemia.
Prevention: The most important thing to do is to remove all animals from areas where bracken in growing or uproot all bracken ferns from the pastures continuously as they germinate.
Treatment: to treat horses poisoned by bracken is very effective if started early. Thiamine is given intravenously at the rate of 5mg/kg every 3 hours and then intramuscularly for several days. Treatment of affected cattle is generally much less successful and the recommended treatment with the hard- to- obtain batyl alcohol of doubtful value.
Castor Oil Plant (Ricinus communis)
This is a widespread soft woody shrub or small tree up to 20 feet tall, with large leaves- up to 2 feet long and wide- divided into 5 -11 lobes shaped like the fingers of a hand, with small yellowish flowers and seeds shaped like beans of various colours - red, brown, cream and black. Oil from the seed is used in medicine and industry and the oil is not poisonous, but all other parts of the plant are poisonous. The residue of the seed after extraction of the oil contains ricin.
The main danger to stock is when maize and other crops become contaminated with castor oil seeds due to careless farming or storage.
Symptoms in cattle include bloody diarrhoea. In horses inco-ordination, muscular spasms, and profuse watery diarrhoea have been seen, followed by collapse.
(c) William Ayako, Kari Naivasha
This is an introduced flowering shrub/tree with golden yellow pendant blooms and white berries. Its importance lies in the fact that poisoning produces symptoms similar to those of Rabies.
In the Limuru highland areas very many cases of poisoning have happened due to cows eating wildings of this plant which stay green during the dry season. A few leaves only will kill a grown cow. Affected cows are irritable and hypersensitive to any external stimuli. Sudden sounds or poking with a stick causes affected animals to jump as though they had received an electric shock. On some occasions animals charge with wide open eyes any moving object. Prior to death there may be frequent bellowing followed by paralysis starting at the hindquarters. When opening such a case of poisoning it can be seen that the stomach lining has completely detached from the stomach walls, and it is evident that the death has been very painful.
If this tree is common in the neighborhood it is very important to recognize the leaves and uproot any little seedling in the pasture and removing it from the area. Whereas cattle may stay away from a green plant as it is very bitter, the smell of a cut dry plant left in the boma will not give the same warning but the dry plant is equally poisonous.
Cotton seed contains a toxic substance called Gossypol, which can be poisonous to young ruminants and pigs. This toxin rarely affects adult cattle. It is destroyed by heat. Cotton seed cake which has been produced by heat treatment is therefore safe. But cotton seed is not safe to be given to young ruminants or to pigs. Clinical signs do not appear until after animals have been fed rations containing cotton seed for 1-3 months. These include loss of appetite, weight loss, weakness, rapid breathing and increased susceptibility to stress. Death may occur. There is no effective treatment and in cases of suspected poisoning all cotton seed products should be removed from the diet.
(c) FORMAT, Kenya
These plants are responsible for causing chronic liver damage and laminitis of the hooves. In the former, especially in horses, symptoms include lack of appetite, dullness, wasting, irritability, yawning and aimless walking and a slow staggering gait. In the latter, severe hoof damage results in the affected animal walking on its heels. In some cases the hoof may become deformed and warty.
(c) William Ayako, Kari Naivasha
This is a shrubby herb, 6 inches to 6 feet tall, with almost hairless stems. It has white trumpet like flowers and black, kidney-shaped seeds. It is found between 3000 and 7000 feet. Many cases of poisoning have occurred, mostly human, when seedlings have been mistaken for, or mixed with spinach-like vegetables, or in animals, when the dried plant has become mixed with hay and other foods.
The fresh plant is unpleasantly scented, particularly when bruised, and is therefore avoided by stock.
Signs of poisoning: In cattle paralysis, rapid heart action and death by asphyxia occur.
Datura candida and Datura aborea are the well-known "moon flowers", shrubs with long, white, trumpet-shaped flowers which are fragrant at night. The toxic element in Datura species is an alkaloid.
Hydrocyanic Acid or Prussic Acid Poisoning.
Found in such plants as clover, red oat grass, star grass, and sorghum
Hydrocyanic or prussic acid is a protoplasmic poison which inhibits the oxidative enzyme systems of cellular respiration necessary for the transport of oxygen from the blood to the tissues and causes death by depriving the cells of the body and those of the respiratory centre of oxygen. Oxygen exchange is suspended and oxygen is retained in the blood, giving it a characteristic bright red colour.
A variety of plants under certain conditions contain cyanogenic glycosides which when hydrolysed during digestion yield hydrocyanic acid. Such plants include clover, red oat grass, star grass, and sorghum.
At the early stage of rapid growth such plants contain greater quantities of glycoside than the mature plant and wilted plants are more dangerous than fresh plants because of their high content of preformed hydrocyanic acid. If the normal growth of such plants is checked, for example by drought, trampling or frost, there is a tendency for the amount of free acid in the plant to increase.
Poisoning is always acute, occurring within half an hour to a few hours after ingestion of the responsible plants. There is difficulty in breathing, staggering, tail-twitching, rapid respirations, salivation, muscle twitching, rapid heart rate, collapse and death often within less than half an hour of the onset of symptoms. Death is accompanied by severe asphyxial convulsions. The blood of affected animals is often a bright cherry red as may be the mucous membranes. When the rumen is opened there is often the characteristic smell of "bitter almonds". This is a very dramatic poisoning, caused not by a particular plant which is inherently poisonous, but by certain pasture plants which under most conditions are not poisonous. Treatment must be immediate and involves the antidotes Sodium Nitrite and Sodium Thiosulphate. The former is given as 10ml of a 20% solution i/v followed by 30mls of a 20% solution of sodium thiosulphate also i/v. Alternatively sodium thiosulphate may be given alone at 500mg/kg i/v plus 30g per cow by mouth to detoxify any remaining hydrocyanic acid in the rumen. If large numbers of animals are affected then speed of treatment may preclude i/v treatment and the following has been found to be effective - mix 3g sodium nitrite and 15g sodium thiosulphate together in 30ml sterile water and give by s/c injection.
Prevention involves preventing cattle from grazing potentially dangerous plants such as sorghum when they are immature, frosted, wilted or trampled. Sorghum in particular should be in flower before they are grazed or chopped to be fed green.
There are various species of this shrub, including the introduced Lantana camara. This has coarse, branched stems with small curved prickles and flower heads of various colours, including red, yellow and white. Being unpalatable to stock it is normally avoided, but when occasionally ingested, causes photosensitization and gastro-intestinal disturbances.
(c) William Ayako, Kari Naivasha
(c) William Ayako, Kari Naivasha
This tree is often used as forage for animals, but they get poisoned if they eat too much of it. The tree has a poison called mimosin in it. Horses are poisoned most often but also cattle, goats, sheep and pigs can be poisoned. Some animals are more sensitive to poison than others.
Prevention: Avoid giving animals more than half their food as leucaena. It is best to give only abouth a tenth of the feed as Leucaena.
Treatment: Stop feeding Leucaena immediately. When starting again after some time, feed only small amounts
This plant is also called water parsnip or water celery and is found in swampy places by rivers and streams in highland areas and remains green throughout the year. Thus it is often eaten by stock at watering places during the dry season. When plant poisoning is suspected on a farm immediate examination should be made of all watering points which are accessible to stock. The initial green shoots of the plant, which often come up in ditches before grass appears, are particularly poisonous, as are also the roots.
Symptoms include violent trembling, noisy rapid breathing, profuse diarrhoea, staggering, rotation of the head and neck, dullness, drowsiness, coma and death.
Prevention: This plant should always be eradicated when found.
This ornamental shrub, which grows throughout East Africa from sea level up to and over 6000 feet, is up to 15 feet tall. The flowers are pink or white and the leaves dark green. All parts of the plant are poisonous and horses and cattle have died after eating a single growing branchlet. In cattle lethargy, lack of appetite, cessation of rumination, bloat and foetid diarrhoea have been some of the symptoms seen after eating oleander. Later on colic, dilation of the pupils, rapid breathing, teeth grinding, continuous urination and bloody foetid diarrhoea set in. Finally convulsions and paralysis preceded death.
It has been reported that this straggling bushy plant about 3 - 12 feet tall that can also become a climber is responsible for more plant poisonings in East Africa than any other. The bark and roots are very poisonous, the leaves and green fruits less so, while the ripe fruits appear to be harmless in small quantities. Cattle and sheep eat the soft juicy leaves when grass is scarce in times of drought. The seeds contain saponin and can be used as soap and to control of water snails to reduce billharzia
(c) Blundell 1987
Symptoms: Depression, quivering of the muscles, increased urination and foetid diarrhoea and frothing at the mouth have been reported. On post mortem intense congestion of the stomach and intestines is found together with haemorrhages within the left ventricle of the heart. Eradication of this plant is the only practical method of control
All species of Senecio should be regarded with suspicion. Fifty species have been recorded from East Africa . In Europe ragwort poisoning is well recognized. Poisoning is usually chronic with death usually occurring two to several months after commencement of feeding on the plant. Cirrhosis of the liver leads to loss of condition, lack of appetite, jaundice, and later to various nervous symptoms, including yawning, drowsiness, and a staggering gait. In cattle nervous derangement usually takes the form of mania. Acute poisoning is uncommon.
(c) Blundell 1987
Tribulus terrestris is a small plant, creeping flat on the ground, spreading for a few inches and has yellow flowers, small hairy leaflets and flattened fruit. It is widespread throughout the tropics up to 7000 feet, especially in open or sandy ground.
This plant contains a hepatotoxin, a poison which damages the liver. This causes photosensitization in affected animals, usually sheep. Sometimes there is swelling of the head, fever and jaundice, refusal to eat, and discharge from the eyes and nose. Wilting of the plant appears to increase its toxicity. Goats seem to be unaffected and in cattle the young plant is liable to cause non-fatal bloat.
(c) Blundell 1987
Other Causes of Poisoning in Livestock
Aflatoxin poisoning is unfortunately common in Africa. Any mouldy grain or feed can contain toxic(poisonous) amounts of Aflatoxin. Feeds that are not properly dried at harvesting very often contain Aflatoxin in varying degrees. To avoid this it is wise to make sure all feeds stored at the farm are a) dried properly at harvest time and b) will not be subjected to any water in the store from leaking roofs or similar.
Prolonged periods of wet weather are conducive to outbreaks of aflatoxicosis. The harvesting of grain, especially maize, during periods of prolonged rain, must always raise the possibility of an outbreak of aflatoxicosis occurring in the near future, in all species of animals, but especially in the young and in species such as pigs, rabbits, fish, calves, dogs and growing poultry.
What is Aflatoxin
- Aflatoxins are poisons produced by strains of the fungi Aspergillus flavus and Aspergillus parasiticus. These toxins target the liver and the most important toxin is Aflatoxin B1
- The fungi grow on stored feeds such as groundnuts, maize, sorghum, soya bean meal and cotton seed meal as well as stored hay, when the temperature and humidity are high. This usually means a consistent day and night temperature of more than 21 deg C, allowing the mould to grow.
- The toxin is not destroyed by milling or by cooking.
- Aflatoxin poisoning occurs world-wide, being especially common in warm climates, affecting growing poultry ( especially ducklings and young turkeys), young pigs, pregnant sows, calves, rabbits, fish such as trout, and dogs.
- Adult cattle, sheep and goats are relatively resistant to the acute form of the disease, but are susceptible if toxic diets are fed over long periods.
- Aflatoxins cause cancer
Dietary levels of less than 50 ppb ( parts per billion) are generally tolerated by young animals and 200-300 ppb by adults, but dietary levels as low as 10-20 ppb may result in measurable levels of aflatoxin being excreted in milk.
It takes at least 6 weeks (often longer) between eating the infected food and the onset of symptoms.
In acute outbreaks death occurs after a short period of loss of appetite. In cattle there may be circling, blindness, ear-twitching, teeth-grinding, diarrhoea, straining and anal prolapse. Death usually occurs after 48 hours, calves of 3-6 months being most likely to die.
Sub-acute and chronic outbreaks are more common. There is unthriftiness, weakness, lack of appetite, yellowing of the mucous membranes, diarrhoea, loss of weight and sometimes sudden death. Concurrent infection, which may respond poorly to treatment, may be common.
Post mortem findings in acute cases include widespread haemorrhages and jaundice. The liver is the main target organ, and is usually swollen, firm and there may be haemorrhages, depending on how long the toxins have been ingested. There may be oedema of the gall bladder and the bile ducts may be fibrotic. There may be a haemorrhagic enteritis.
The disease history, the PM findings, examination of the liver and testing of the feed in a laboratory in Nairobi should confirm the diagnosis.
Prevention and Control
There is no treatment other than changing the food. Palliative treatment in the form of administering various vitamins may assist recovery.
- Batches of feed and stores of harvested maize must be checked and examined for the presence of mould. Batches of feed should be periodically checked by a reputable laboratory for aflatoxin levels.
- Feeds, if possible, should not derive from a single source or consist of a single grain.
- Feed stores should be well ventilated, dry and rain proof.
Occuring mostly where pastures are fertilized with nitrogen fertilizers and spraying with phenoxyacid herbicides.
These two may be considered together as the former owe their toxicity to their reduction to the latter by the rumen or intestinal flora. The nitrite is absorbed into the blood stream where it converts the haemoglobin of the blood into methaemoglobin, thereby producing a state of hypoxia. Nitrates occur in numerous plants and their concentration is increased by factors such as climate- damp cloudy conditions, cool temperatures, rapid growth in hot humid weather, concentration of nitrate in the lower part of the plant if stunting occurs due to drought.
All species are susceptible to nitrate/nitrite poisoning but cattle are the animals most commonly affected. Poisoning is not so much due to the actual quantity ingested as the rate at which it is consumed. Symptoms are abdominal pain, depression, inco-ordination, diarrhoea, rapid breathing, convulsions, coma and death. Cyanosis may be observed. The outstanding PM finding is the chocolate coloured blood.
Treatment is by the I/V injection of methylene blue, 10mg/kg of a 4% solution, repeated as necessary.
Urea poisoning can result from its too liberal use as a food supplement or from its having been unevenly spread on pasture when used as a fertilizer. Sheep and cattle rapidly acquire tolerance to it and can consume unharmed, quantities which would kill an animal unused to it. Urea blocks which are unprotected from the effects of rain or which are soft or crumble easily are especially dangerous.
Symptoms may appear within 20 - 60 minutes in cattle after eating(ingesting) urea. After ingestion in an animal not used to eating urea it releases high amounts of ammonia into the gastrointestinal tract where it is absorbed leading to symptoms of poisoning. These include abdominal pain, muscle tremors, especially of the ears and face, frothy salivation, excess urination and teeth grinding. Cattle are often agitated, aggressive, and violent. Bloat may be evident. There may be bellowing and violent struggling, convulsions, tetanic spasms, rapid breathing and death within 2 hours.
Treatment includes drenching cattle with 2 - 8 litres of 5% acetic acid ( table vinegar) and drenching with iced water - up to 40 litres in cattle and proportionately less in sheep and goats.
Urea should be limited to not more than 1% of the total diet and it must always be introduced slowly at a rate which should not be deviated from. While properly adapted cattle can tolerate up to 1G urea/kg (??) bodyweight per day, but it is safer not to exceed half that amount.
Eating excessive quantities of salt causes inflammation of the intestinal tract resulting in gastroenteritis and diarrhoea. When the water intake is also restricted there is swelling of the brain and the production of nervous signs. In Kenya this has been most frequently seen either when there has been a shortage of salt lick or when salt has been introduced to cattle after a lengthy period when the cattle have not had access to salt.
Symptoms in acute salt poisoning involve the gastrointestinal tract and the central nervous system. There is salivation, increased thirst, regurgitation, abdominal pain and profuse watery diarrhoea. This may be followed by staggering, circling, blindness, seizures and partial paralysis. Sometimes there is aggression and violent behaviour.
A sequel to salt poisoning in cattle may be dragging of the hindquarters and knuckling of the fetlock joint.
Treatment: There is no specific treatment. The salt must be removed at once and fresh water offered, initially in small amounts at frequent intervals as the ingestion of large volumes may worsen the nervous signs by increasing the oedema of the brain.
Salt in whatever form must always be introduced gradually to stock. Cattle are able to tolerate large amounts when they are used to it but it must be given gradually.
Most species of snakes avoid livestock and move away when disturbed. The exception is the puff adder whose venom is haemotoxic, necrotizing and anticoagulant. Most bites occur on the muzzle, lower leg and neck. Cattle seldom die from snakebite but may suffer acute local swelling and have considerable difficulty in breathing if bitten on the nose..
The spitting cobra's venom may do serious damage to the surface of the eye which should be immediately washed out with copious volumes of clean water. This should be followed by the instillation of antibiotic/corticosteroid eye ointment applied to the cornea several times daily until healing is evident.
Treatment may include the use of snakebite antiserum, but this is so expensive as to be uneconomical except in the case of very valuable animals. Corticosteroids may be used to minimize swelling but must NEVER be used in pregnant animals as they will cause abortion. Antibiotics should be given to minimize infection. Incising the wound or applying tourniquets are of little value and usually too late anyway. Supportive treatment by improving the diet of the patient is essential
Success with electric shock in snakebite treatment has been reported: Connect starter cables to the car battery while the car is running and put the other ends close together on the snakebite to create an electric shock. This is reported to neutralize the poison.
The most common source of arsenic which may affect stock is old dips in which arsenic was previously used as an acaricide. Arsenic is extremely stable and may remain intact in soil adjacent to an old dip virtually indefinitely. Where cattle have stood following their immersion from the dip to drain is the danger zone. The soil and vegetation may be impregnated with arsenic. Large numbers of animals have died from grazing within the vicinity of these old unfenced dips. Poisoning is generally very acute with major effects on the gastrointestinal tract and the cardiovascular system.
Symptoms: There is profuse watery diarrhoea, sometimes tinged with blood, severe colic, dehydration, acute depression, weak pulse and cardiovascular collapse. Onset is rapid, usually within a few hours, and in peracute cases animals may be found dead. Post mortem reveals very severe inflammation of the gastrointestinal tract which is usually extremely red, the contents are usually very fluid and foul smelling, may be blood tinged and contain shreds of epithelial tissue.
To be effective treatment must be started very early. A delay of more than 12 hours is usually fatal.
Treatment is by using Sodium Thiosulphate. This compound is almost completely non-toxic and can be given in large amounts without accurate measurement. Intravenous injection is best as an initial treatment using 15 - 30g. of the salt in 100 - 200ml of water followed by oral dosing of 30 - 60g at 6 hourly intervals. Treatment should be continued until recovery occurs which may take 3 - 4 days.
Cases of acute copper poisoning may occur when stock accidentally eat soluble copper salts such as those used to control fungi on plants. It can also occur when drinking water is contaminated by copper sulphate during snail eradication programes, or by the too liberal ingestion of mineral mixtures containing copper or when animals are grazed on pastures too soon after they have been dressed with a copper salt to correct a copper deficiency. Of more frequent occurrence, particularly in sheep, is "chronic" poisoning caused by the continual ingestion of small quantities of copper derived from food additives or agricultural or industrial contamination. After a period of weeks or months there is a sudden rise in the level of copper in the blood, due to the release from the liver of massive stored amounts of copper, causing a haemolytic crisis. This results in jaundice, haemoglobanaemia and haemoglobinuria. The haemolytic crisis may bestarted off by many factors, including transportation, pregnancy, lactation, strenuous exercise or a deteriorating plane of nutrition.
Certain plants such as subterranean clover, senecio and heliotropicum europaeum may induce excessive copper retention in the liver. Likewise low dietary intakes of sulphur and molybdenum may reduce the excretion of copper in the urine or faeces, resulting in chronic copper toxicosis. Acute copper poisoning causes severe gastroenteritis, abdominal pain, salivation, lack of appetite, convulsions, dehydration, shock, collapse and death. Often there is evidence in the faeces of copper as they may be a blue-green colour.
"Chronic" copper poisoning is associated with the sudden onset of symptoms associated with the haemolytic crisis. These include depression, lack of appetite, weakness, recumbency, thirst, rapid breathing, pale mucous membranes, blood in the urine and jaundice. Most affected animals die within 1-2 days. Losses may continue for several months after the dietary problem has been rectified.
Post mortem there is severe gastroenteritis in acute copper poisoning, and liver, kidney and splenic damage in "chronic" copper poisoning together with port-wine coloured urine. Often treatment is unsuccessful due to the nature of the damage inflicted by the copper. In addition the recommended drugs for treatment are generally unavailable.
Plants which induce copper retention should be eradicated. The top dressing of pastures with molybdenum or adding molybdenum to the diet of lambs has been shown to greatly reduce the uptake of copper by the liver.
Lead poisoning is, fortunately, not common in Kenya . Cattle and dogs are the species most usually affected. Paint, especially when it is old and flaking, old car batteries, lead shot, lead weights, putty and red lead are the most common sources of lead. Poisoning may be either acute or chronic, but there is no clear demarcation between the two. Acute lead poisoning in cattle is more common in young animals. The most common symptoms are those associated with the gastrointestinal tract and the nervous system. Signs that appear within 24-48 hours of exposure include staggering, blindness, salivation, spastic twitching of the eyelids, jaw champing, muscle tremors, excitement and convulsions. Death may occur within a few hours of the onset of symptoms.
Subacute lead poisoning in cattle is characterized by lack of appetite, stasis of the rumen, colic, dullness, transient constipation, frequently followed by diarrhoea, blindness, head pressing, hyperesthesia and incoordination.
Post mortem may reveal flakes of lead in the gastrointestinal tract. There may be gastroenteritis, degenerative changes in the liver and kidney but often the finding are not dramatic. Diagnosis may be confirmed by chemical analysis of the liver and kidneys of dead animals or the blood and urine of the living. The lack of laboratory facilities may present problems, as may treatment, as the usual antidote, calcium disodium edetate is unlikely to be available. Thiamine has been found to be helpful in alleviating clinical signs and reducing tissue deposition of lead. Epsom salts may help in removing lead from the gastrointestinal tract. Preventing animals from accessing lead, therefore, is all important in avoiding poisoning.
This includes most dips available in the market today. They can get into the animal through mouth or through the skin. Also some of the insecticides used in agriculture are of this nature.
Signs of organophosphate poisoning:
- The animals behave unusually. They often stagger about and have tremors or twitches under the skin
- Much saliva comes from the mouth and a clear discharge comes from the eyes and eyes have very small pupils
- Animals have pain in the stomach. They do not eat much. Some animals may vomit. They may urinate more than usual.
- Breathing becomes distressed
They soon become paralyzed, collapse and die.
Has to start immediately in order to save the animal: Wash the animal with water and soap. If poison may have been swallowed give charcoal powder. If the vet is near ask to have the animal given an injection of Atropine sulphate (0.4 mg/kg under the skin).
- Draft By William Ayako, Aug - Dec 2009
- Review by Hugh Cran March 2010 - Jan 2011
- Review workshop team. Nov 2 - 5, 2010
- Anne Bruntse, Jan 2013
- For Infonet: Anne, Dr Hugh Cran
- For KARI: Dr Mario Younan KARI/KASAL, William Ayako - Animal scientist, KARI Naivasha
- For DVS: Dr Josphat Muema - Dvo Isiolo, Dr Charity Nguyo - Kabete Extension Division, Mr Patrick Muthui - Senior Livestock Health Assistant Isiolo, Ms Emmah Njeri Njoroge - Senior Livestock Health Assistant Machakos
- Pastoralists: Dr Ezra Saitoti Kotonto - Private practitioner, Abdi Gollo H.O.D. Segera Ranch
- Farmers: Benson Chege Kuria and Francis Maina Gilgil and John Mutisya Machakos
- Language and format: Carol Gachiengo
Information Source Links
- Blundell, Michael 1987: Collins Guide to Wild Flowers of East Africa.William Collins Sons & Co. Ltd.
- Common Poisonous Plants of East Africa Verdcourt & Trump Collins St Jame's Place London 1969
- The Merck Veterinary Manual 9th Edition 2005 ISBN 0-911910-50-6
- Clarke: Poisoning in Veterinary Practice The Association of the British Pharmaceutical Industry 162 Regent Street London W1R 6DD 1975
- Forse, Bill 1999: Where There Is No Vet. Macmillan publishers Limited. ISBN 978 0 333 58899 4 ISBN: 0 85598 409 0
- Radostits and Henderson: Veterinary Medicine A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses Blood, 6th Edition ISBN 0-7020-0988-1
- World Agroforestry Centre 2007: Useful Trees and shrubs for Ethiopia. RELMA Publication, ICRAF. ISBN 92 9059 212 5