Animal Health & Disease Management

Other Causes of Poisoning in Livestock

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 ° 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.


Clinical Findings

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.


Organophosphate insecticides

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).

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