04/11/2020
CAUSES OF POISONING IN CATTLE
Aflatoxin
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.
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 a**l 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.
Diagnosis
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.
Nitrates/Nitrites
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
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 in bodyweight per day, but it is safer not to exceed half that amount.
Salt
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.
