Understanding aflatoxin poisoning in livestock

JECINTA MWIRIGI

By JECINTA MWIRIGI
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Each of the two encounters that I have had with aflatoxin left me devastated. The first one was more than 10 years ago when one of my male dogs developed loss of appetite, deep yellow mucous membranes of the eyes, followed by death in three days.

Initially, I thought it was babesiosis, a tick-borne disease that exhibits similar signs, but the dog did not have ticks and a laboratory diagnosis was negative.

A month later, as I was still grappling with the loss, the other dog (a female) developed an enlarged abdomen, loss of appetite and depression.

As a veterinarian, this not only shed light to the first case but also led to a recollection of the history of both cases.

Two weeks before the first case, I had bought a 70kg bag of maize flour for workers at a construction site but after two meals or so, they rejected the ugali (maize meal) from the flour, claiming that it had a bad taste and smell. I then decided to use it for dogs.

The latest case is few months ago and it was a replica of the first one. In this case, both of my dogs, an adult male and a six-month old male puppy, went off feed.

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An examination of the unga proved that it had a bad smell and it was withdrawn but it was too late. In the course of one week, the puppy developed yellowish mucous membranes; pot belly, had convulsions and died.

Two months later, the adult developed a ball shaped belly but medication to remove the water brought the conditions under control.

The dog is still on medication. In all the four cases, there was no exhibition of pain and thus the disease can be called a silent killer.

Although Aflatoxicosis may not be totally avoided, understanding the condition plus identification and elimination of the predisposing factors could reduce the incidence in both humans and animals.

Aflatoxin is produced by toxigenic strains of moulds (fungi) on peanuts, soybeans, maize and other cereals either in the field or during storage when the moisture content is high.

The toxic response and clinical manifestation of the Aflatoxicosis in animals varies in relation to the species, sex, age, nutritional status and duration and level of aflatoxin in the ration.

Young animals as well as the pregnant ones are highly susceptible and in all cases, the liver is mostly affected.

Although testing and confirmation of the presence of aflatoxin in feeds and animals is possible, the results are complicated by the transient nature of the toxin whereby once ingested, it damages the liver and then it changes from B1 to M1 and then M1 is excreted from the body through urine.

Thus by the time the clinical signs are seen, the toxin might already have destroyed the liver and it might also have been excreted.

Further, the batch of feed that was contaminated by the fungi might have been exhausted. Negative results of aflatoxin therefore do not confirm its absence in all cases.

MANIFESTATION OF AFLATOXICOSIS

Effects of aflatoxicosis in animals include predisposing them to gastrointestinal infections such as coccidiosis and clostridium; low feed efficiency and stunted growth.

The clinical manifestations in the acute form of the disease include death of young ones while in sub-acute and chronic forms, there is belly water, deep yellow mucus membranes, reduced appetite, dullness and reduced productivity.

At post-mortem, the liver is congested, jaundiced and enlarged when animals die from acute illness but the liver is shrunken, pale and hardened when they die from the chronic condition.

During post-mortem, nodular (cancerous) lesions can also be seen especially in poultry. Tolerable levels are up to 100 (parts per billion) ppb for adult and 50 ppb for young chicken; 50 ppb for young pigs, 200ppb for adult pigs; 100 ppb for calves and 300ppb in adult cattle. In dogs, it is < 50 ppb. Twice the tolerable rate in the listed species leads to clinical signs.

Management of aflatoxicosis

Once the clinical manifestation of the disease occurs, the only treatment option is management. It is, therefore, desirable that contamination of feeds and food be prevented at all costs.

At the farm and storage levels, once the susceptible produce like maize is contaminated, its disposal is very costly as it contaminates the soils thus propagating the fungi.

Farmers should minimise farm level contamination by removing all visibly affected produce from the farm, harvesting when the environment is less warm and humid, stacking the maize stalks in a standing position to allow dripping and drying, drying and storing the produce at the recommended moisture content levels and applying recommended mould control agents during planting.

Varieties that are resistant to fungal invasion are also recommended. Some micro-organisms in the soil have been known to degrade aflatoxin in 72 hours thus burying of affected materials in a deep pit that makes aflatoxin unavailable to roots of other crops is a disposal option. It is good to note that some green leafy vegetables have been found to have aflatoxin as result of root absorption.

Although challenging and requiring sophisticated tools like the florescent light technique, feed and food processors should test for aflatoxin in raw materials.

However, testing of finished products is affordable and available but might end up being costlier to manage. It is also possible to reduce the contamination in grains by sorting and removal of affected produce.

The processors should also conform to Kenya Burear of Standards minimum aflatoxin levels in feed (10ppb) as higher but tolerable levels to adult animals lead to release of low aflatoxin in products such as milk which when consumed by young ones turns out to be lethal.

Further, toxin binders like natural clay and other chemical compounds might have side effects while studies have demonstrated reversions of the altered aflatoxin molecule to the original toxic chemical structure in some instances.

Processors who use contaminated grains for other permitted products like ethanol should avoid use of the distillation waste.

In addition to formulation of laws, regulatory agents should carry out surveillance not only in leading agents/suppliers of aflatoxin susceptible feeds and foods but also in medium and micro suppliers.

Shop owners and other flour outlets should keep affected product away from moist goods likes fruits and vegetables and ensure that the environment is well-ventilated while consumers too should store the commodity in similar conditions.

Approved waste disposal agents should take up the task of disposing aflatoxin affected materials through burning as the toxin is completely destroyed at temperatures of 269°C and incineration temperatures are often more than 500°C.

The incineration can also be carried out profitably by cement manufacturers or for heat generation by using the spoilt produce as a source of heat energy.

The later has been carried out in Kenya. Open air burning is discouraged due to air pollution from smoke.


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