Mycotoxins and their impact on the poultry industry

 

 

Dr. Abdul Jabbar Kazim Al-Kanani / Basra

 

Mycotoxins are natural products of fungi as a result of growth and there are many types, the most important of which are in poultry (Aspergillus spp, Penicillium, Fusarium,).

 

How do mycotoxins enter the feed?

 

Before harvest: – When the grains ripen and remain for a period (delayed harvest), fungi begin to grow on the grains while they are still in the stems and as a result of this growth, they begin to produce mycotoxins on the grain wall.

 

After harvest: – Poor transportation and storage operations from the field – collection – transportation of all kinds. These factors lead to the growth of fungi and thus the production of mycotoxins.

 

Feed factory: – Using grains infected with fungi or damaged to produce feed (with the aim of reducing the price of the product) causes this problem and the heat generated as a result of manufacturing feed does not help in reducing fungal growth. Fungi can be killed, but mycotoxins are not affected by heat. Not allowing the produced feed to cool to room temperature (20-22) Celsius and direct rapid transport of feed from the factory to the field while it is hot and in the presence of oxygen fungi grow back and produce mycotoxins. Not adding anti-mycotoxins to the manufactured feed in order to reduce the price of the product.

 

Field: Stacking feed in field stores or hall controls and not leaving air gaps between the feed stack and the wall causes fungi to grow and produce mycotoxins. Storing feed inside the halls is a very encouraging factor and accelerates the production of mycotoxins because the existing and dormant fungi in the feed obtain the necessary moisture and appropriate temperature from the atmosphere of the hall. Keeping the feed stored for periods exceeding two weeks in these atmospheres causes mycotoxin infections.

 

Mechanism of action of mycotoxins present in feed provided to poultry

• The effect on the beneficial microorganisms present in the intestines and thus their numbers decrease or these germs turn into pathogenic as in the case of E. coli.
• Impact on the effectiveness of the intestinal wall (intestinal villi) and reduce the efficiency of food absorption.
• Penetration of the intestinal wall and turns into systemic infections and the first affected organs will be the liver, causing bleeding inside the liver cells and the inability to secrete enzymes or perform the physiological action required of the liver.

 

Clinical and anatomical symptoms of poisoning with feed toxins

 

• Sudden increase in mortality, especially from day 16-18 and continues in the event of incorrect diagnosis and immediate treatment.
• Lethargy and sitting of birds and a decrease in the feed consumed and a state of weight rebound in the flock
• Weights decrease from before the infection).
• The beginning of the appearance of cases of dwarfism in the flock and a difference and inhomogeneity in weights.

 

Anatomical characteristic:-

 

• Bleeding in the intestines, especially in the duodenum and ileum regions.
• Bleeding and hemorrhagic lines in the liver.
• Intestinal swelling due to inflammation and diarrhea.
• In advanced cases, bleeding may be caused by the exploitation of the infected area in the intestine by CL.PREFRENGIS bacteria, causing necrotic enteritis and the intestines being like a velvet bed (shell(

Rapid measures in the field

• Lift the feed for 12 hours.
• Give regular vinegar (ASETIC ASID) at a rate of 2 liters per 1000 liters of water for twenty-four hours.
• Reduce the lighting by half to rest the birds.
• On the second day, give highly absorbable and slowly absorbable antibiotics together.
• Give sorbitol (sugar or dextrose with drinking water to rest the liver) in the evening. The feed is re-given in smaller quantities than the ration (half a feed). After replacing the feed with new feed.

 

Diagnosis of mycotoxins

The ELISA test is used to determine the level of mycotoxins present in the tested sample. In most cases, the levels are below the internationally specified dangerous limits. This does not prevent the effect of these toxins, even if they are in quantities less than the dangerous limits, on the flock and the appearance of symptoms of the disease.