Mycotoxicosis is a major problem in poultry industry. There are about 50 fungi species harmful to poultry known to produce toxins, which are collectively called as mycotoxins. These mycotoxins are metabolites produced by fungi during metabolism of nutrients present in feeds and feed ingredients. High moisture content in fresh maize and grain highly favour mould growth. Many mycotoxins are stable during grinding and crushing in mill and also during feed storage.
The type of fungus, temperature, moisture and grain determine which toxin will be produced and in what amount. According to the United Nation’s Food and Agriculture Organization (FAO), approximately 25% of world’s grain supply is contaminated with mycotoxins. The economic loss due to this has been estimated to run into millions of rupees annually.
Mycotoxins act in synergism?
Individual fungus usually produces more than one toxin. It is uncommon to find a single mycotoxin occurring under field condition. Usually they occur in combination of two or more. These toxins therefore often act in synergism. This means that their combined effect is much more damaging than that of the individual mycotoxins. In feed, even if aflatoxin content is very low, its harmful effect is greatly increased by the presence of ochratoxin, even though its presence may be at a low level.
Aflatoxicosis and Orchatoxicosis mycotoxicosis are the most commonly seen mycotoxicosis in poultry. Other mycotoxicosis is less common. Mycotoxicosis is wide spread under hot and humid Indian conditions as well with poor storage facilities.
Aflatoxins are a group of closely related, highly toxic, mutagenic and carcinogenic compounds. Aflatoxin is the most common and the most important mycotoxin. It is a highly toxic mycotoxin produced by various species of fungi Aspergillus. The fungus Aspergillus flavus produces most of the Aflatoxin and also gives this toxin its name (“A” from Aspergillus and “fla” from flavus). However, aflatoxin is also produced by Aspergillus Parasiticus and Penicillium puberulum. Both the fungi are widespread in the environment and produce aflatoxin in warm (30-35°C) temperature and high humidity conditions (Refer table 1). Mould growth occurs more rapidly when moisture content is more than 10% and temperature at 28-30°C. Aflatoxin can withstand extreme environmental conditions and are highly heat stable. Aflatoxin contamination is more common in grains or handled in a tropical country like India. Handling and storage of grains in these conditions anywhere will also stimulate production of aflatoxin. Poultry feed and ingredients are easily prone to fungal growth and aflatoxin formation.
Aflatoxin is found in maize, groundnut cake, rice, cottonseed, millet, sorghum and other feed grains. Its concentration at field levels is 20-100 ppb and may even up to 500 ppb.
Mycotoxin may get 30-50 times more concentrated in the broken grain as compared to whole grain. Naturally occurring aflatoxin contains B1, B2, G1 and G2. Designations B and G are given after their Blue (B) or Green (G) colour reaction to fluorescent light. Of all, aflatoxin B1 is usually found in the highest concentration and is also the most toxic. It damages mainly liver. Aflatoxin is stable once formed in grains, and is not destroyed during normal grinding and crushing in the mill and storage. Young birds are more sensitive to aflatoxin than adult. There are also large species differences as duck being 10 times more sensitive than chickens.
Post mortem findings
In the affected birds metabolic changes lead to enlargement of liver, kidney and spleen as well as decrease in the size of bursa of fabricus, thymus and testes. With high dose exposure, fat accumulates inside the cell of liver as clear vacuoles. As a result, liver is greatly enlarged, yellow and friable (easily broken). Small haemorrhages may occur following injury due to decreased clotting factor synthesis and increased fragility of minute blood vessels. This leads to a condition known as “bloody thigh syndrome”. Aflatoxin is rapidly excreted in the bile and urine and does not accumulate or persist in the body tissues. This explains the rapid recovery of egg production and hatchability after ingestion of toxin has stopped.
Harmful effects of aflatoxin
Aflatoxicosis causes loss of egg production (layer), anaemia, haemorrhages, liver damage, paralysis and lameless, poor performance, feed efficiency (in broiler), increased mortality from heat stress (in broiler) and increased susceptibility to infectious disease both in broiler and layers. Aflatoxin affects egg production by reducing synthesis and transport of yolk precursors in the liver. Egg size, yolk weight and yolk as percent of total egg size are decreased. Aflatoxicosis affects weight gain, feed intake, feed conversion efficiency, pigmentation, eggs production and reproductive performance of male and female. Even less than 100 ppb in broiler can result in poor feed conversion and reduced weight gain which may be due to liver damage and reduced nutrient absorption. Once the damage has been done, birds may not fully recover even if they return to toxic free ration.
Aflatoxicosis suppresses the immune response. As result, aflatoxicosis is associated with increases susceptibility to infectious disease. In chicken, aflatoxicosis increases susceptibility to or severity of Caecal Coccidiosis, Marek’s disease, E. coli infection, Salmonellosis, Inclusion Body Hepatitis and Gumboro disease. Vaccination failure is emerging as result of aflatoxicosis in chicken. Aflatoxicosis induced immune suppression is due to reduction in the size of bursa of fabricus, thymus and spleen. Immune suppression in breeders can be serious as it reduces the passive maternal immunity.
Ochratoxicosis is caused by the mycotoxin “Ochratoxin”. Its name is derived from the fungus “Aspergillus ochraceous”. Ochratoxicosis is less common in poutry than aflatoxicosis, but is much more harmful. Although, aflatoxin B1 is the most potent of all aflatoxins, ochratoxin is three times more harmful. Thus, Ochratoxin are among the most toxic mycotoxins for poultry. They damage mainly kidney.
Apart from Aspergillus ochraceous, five other species of Aspergillus also produce it. Ochratoxin are formed on numerous grains and feed stuffs and are of four types A, B, C and D. Of these, orchatoxin A is the most toxic, most common, also produced in greater quantities and is relatively stable. Ochratoxin occurs in maize, rice, most small grain and in animal feeds. It readily forms in poultry feeds under conditions of high temperature and high moisture. Field levels are between 20-200 ppb, but may be even up to 2.0 ppm. In the naturally occurring disease, ochratoxin A is the main toxin involved. Ochratoxin B and C occur only with high concentration of ochratoxin. Young birds are most sensitive to ochratoxin ingestion. Severe (acute) ochratoxicosis causes death due to kidney failure.
Harmful effect of Ochratoxin
Ochratoxins is broilers causes mortality and failure to gain weight. Growth rate, feed conversion and pigmentation are also affected. Ochratoxicosis in growers delays sexual maturity. Ochratoxin can reduce egg size and interior quality. Immuno-suppression by ochratoxin-A is mainly due to reduce size of thymus, although all lymphoid organs are affected. Cell mediated immunity is significantly damaged in broilers. Antibody mediated immunity is affected after depletion of antibody containing cells in lymphoid tissues. As a result, vaccination response is severely damaged and the severity of concurrent Coccidiosis and Salmonellosis is increased.
Affected birds are depressed, dehydrated, usually pass more urine and die from kidney failure. Those that survive are stunted, poorly feathered and have anaemia and immune-suppression (Ochratoxin level more than 0.6 ppm). There may be reduced weight or develop wet dropping causing increased numbers of stained eggs. There is also a decrease in egg production and hatchability (at ochratoxin level more than 2.0 ppm) and poor performance in progeny derived from affected hens.
Mycotoxin binding agents include activated charcoal, yeast cell wall products, synthetic Zeolites and mined mineral clays such as aluminosilicates, sodium bentonite. Effectiveness of these compounds depend upon the adsorptive capacity, their structure, their purity and the characteristics of the targeted mycotoxin.
a) Zeolites (Sodium Zeolites A) and aluminosilicates have strong affinity to aflatoxin and form a stable complex.
i) Hydrated Sodium Calcium Aluminosilicates (HSCAS) and nutrients with antioxidant capabilities (Selenium, Methionine and Vitamin E)
ii) HSCAS and Virginiamycin
b) Mannan Oligosaccharides, developed by esterifying yeast cell wall glucomannans, can specifically adsorb Aflatoxins, Ochratoxin and Fusariotoxins.
c) Dietary supplementation of activated carbon reduces the toxic effects of many insecticides, pesticides and other toxins by adsorption and elimination in the faeces.
i) Toxic feed should be removed and replaced with uncontaminated feed. Poultry usually recover from most mycotoxicosis soon after an uncontaminated feed is available.
ii) Increase the dietary levels of protein. The mycotoxins affect the protein and amino acid metabolism. Increasing the dietary level of proteins can minimize the ill effects especially when uncontaminated with aflatoxin. Increase also the vitamin supplementation.
iii) Supply of methionine and other sulphur containing amino acids, over and above the requirement can protect the chicks from growth depressing effects of aflatoxin.
iv) Treatment of bacterial or parasitic diseases.
v) Poor management is particularly harmful to poultry stressed by mycotoxins and should be improved.
vi) Liver tonics may be given. Additional amount of lipotropic agent like choline helps in minimizing liver damage.
vii) Vitamin D3 supplementation can minimize the adverse effect of aflatoxin, such as leg weakness and poor egg shell quality.
viii) Mycotoxins are free radical generators and therefore challenge the antioxidant responses within the poultry. Therefore, increase the supplementation of vitamin E, vitamin C and selenium.
Occurrence of mycotoxins in grains is extremely common and therefore requires a programme for controlling their ill effects in poultry.
i) Purchase a clean feed stuff
ii) Discard the grains suspected of contamination (i.e. mouldy and caked feed).
iii) Keep the moisture of grain less than 12%.
iv) Sun drying is the best method to prevent mould growth. But, it does not destroy the toxin.
v) Store the feed and ingredients in well ventilated dry place; which is water, insect and rodent proof.
vi) Adequate ventilation of poultry house to reduce humidity (removes moisture available for fungal growth and mycotoxin formation in feeders).
vii) Avoid storage of feed for more than a week.
viii) Mycotoxin may form in decayed, crusted feed in feeders, feed mills and storage containers. Therefore, regular inspection of feed containers is essential.
ix) Withdraw toxin contaminated feed immediately.
x) Pelleting feed destroys fungal spores and decreases fungal burden. The combination of pelleting and antifungal agent has additional effectiveness.
xi) However, despite all the precautions, mycotoxins do get into the feed. Therefore, to deal with this difficult problem, the most practical way is to use effective mould inhibitors and scientifically tested broad spectrum toxin.
xii) The most effective method of neutralizing mycotoxins already in feed is binding them to an inert compound therefore they can.?? cannot be absorbed from the intestines.
The most appropriate practices for mycotoxin control are:
i) Prevention of fungal growth on crops in the field, at harvest time, during storage of feedstuffs and processing of feed.
ii) Application of appropriate mycotoxin binder in order to achieve good productivity and economy.
iii) As with most poultry diseases, prevention is more economical than treatment.
Dr. Suraj Amrutkar, SKUAST-J, Jammu, Dr. Suhas Amrutkar, MAFSU, Parbhani, Maharashtra, Bharti Deshmukh, NDRI, Karnal