Mycotoxins - Mycotoxicosis - Fungi producers in digestive tract samples of animals, grains, feed, plants, soil, ..., - Fungal cultures; Molecular diagnosis of genes codifying for mycotoxins (PCR and sequencing).
The term mycotoxins derives from mycotoxicosis, used for the first time in 1955 to describe the diseases caused in animals by fungal toxins. Mycotoxins are only toxic chemicals formed as secondary metabolites of fungi, which may be present in the grains or in the feed infected with fungi (molds). These toxins are not always produced by fungi, but are secondary non-essential metabolites, formed when fungi, or the host plant of them, are under stress. Being stable chemical compounds cannot be destroyed during most of the processing done during the preparation of food or feed. The presence of mycotoxins in grain feeds can cause toxic effects in animals when they are ingested in very small amounts. Its toxic effects are manifested as diseases that affect one or several organs depending on the type of mycotoxins, and may even cause the death of animals. Depending on the specific substances and concentration, some may become carcinogenic, mutagenic, teratogenic and immunosuppressive. Those mycotoxins that are immunosuppressive allow viruses, bacteria or parasites to develop a secondary infection that may be more evident than the affectation caused by the mycotoxin itself.
The basic characteristics that characterize mycotoxicosis are:
- The cause is not identified immediately.
- Mycotoxicosis is not transmitted from one animal to another.
- The treatment with drugs or antibiotics, has no effect unless there is a secondary infection due to the immunosuppressive effect of some mycotoxins.
- Outbreaks of mycotoxicosis are usually seasonal, since climatic conditions that favor the growth of the fungus and the production of the toxin are required.
- There is usually a specific association with the ingestion of a particular feed or grain.
- The presence of a large number of fungi or their spores in the feed does not necessarily indicate that toxin production occurs.
- Similarly, the absence of fungi does not exclude mycotoxicosis, because the conditions of storage or preparation of the feed can destroy the fungus, while the thermotolerant mycotoxins persist and can exert their effect.
Mycotoxins also pose a potential danger to human health when they eat foods that contain them. Even the dust generated when handling the contaminated grain can contain mycotoxins, so it also poses a risk to people who inhale these pollutants.
Among the mycotoxins, aflatoxins, are the most notable for having been the first discovered and for the considerable research that has been done with them, compared with others. These mycotoxins were isolated and identified in 1961, following an incident in which 100,000 turkeys died in the British Islands when they ate feed containing contaminated hazelnuts. Feed producers and manufacturers are often less familiar with other mycotoxins such as ochratoxin, zearalenone, deoxynivalenol, trichothene T-2 and fuminosin.
Mycotoxins can cause considerable economic loss for farmers and grain handlers because they must reduce the costs of the products when they are contaminated, and even in the worst case they have to eliminate intensely contaminated products. Feed manufacturers that incorporate grains contaminated with mycotoxins as feed ingredients in their products can cause health problems in livestock or poor performance of animals that ingest them.
Potential economic losses include a loss of business, the claim of customers, and responsibilities for the supply of the product that contains them. Farmers who feed their own grains contaminated livestock can have economic losses, due to the poor reproduction of animals, the decline of their growth, or the death of animals.
Mycotoxins are produced by saprophytic or phytopathogenic fungi that may be present in cereals, hay, grass straw, and other forages. The most frequent fungi in animal feed are Aspergillus spp., Fusarium spp. and Penicillium spp.
Traditionally, toxigenic fungi in crops have been divided into two classes: field fungi (or plant pathogens), which invade and produce their toxins before harvesting, and storage fungi (or saprophytes) that invade or produce their toxins after the harvest. However, the original source of both kinds of fungi is in their own field. In addition, some fungi can belong to both classes and colonize the beans before and after harvesting.
As an example, Aspergillus flavus infects the grain crops in the field, but also contaminates the conserved grains when the conditions of temperature and humidity are favorable. The interactions between environmental stress factors, such as water activity and temperature, influence the expression and biosynthesis generated by the regulatory genes for the production of mycotoxins by fungal mycotoxigenic species.
The measures taken after the harvest, avoiding the high temperatures during the storage and realizing the fast drying of the grains, can diminish the quality of the grain, but they reduce the risks for the health due to the negative effect for the growth of molds and as a consequence, reduce potential contamination with these toxins.
As the most frequent fungi are Aspergillus spp., Fusarium spp. and Penicillium spp., the most important mycotoxins are those produced by these fungi: deoxynivalenol (DON), zearalenone, tricothecene T-2 or fuminosin produced by Fusarium spp.; the aflatoxins produced by Aspergillus spp.; ochratoxin produced by Penicilium spp.; and the ergotamine produced by Claviceps purpurea (the ergot of rye), among others.
The FAO (The Food and Agricultural Organization) of the United Nations estimates that each year, approximately 25% of the world's crops are contaminated with mycotoxins, causing annual losses of about one billion metric tons of food products.
The early detection of these contaminants and the identification of the main toxigenic fungal species is important, to evaluate the food quality, and also to develop control strategies that ensure it.
Cereals are the main source of mycotoxins that enter the food chain, but other foods such as fruits and peanuts may also be contaminated.
Of the approximately 400 known species of mycotoxins, corresponding to very different kinds of chemical compounds, about 25 are relevant, because of their frequency and because of the concentration they reach in the products contaminated with the producer fungi.
The monitoring of mycotoxin and mycotoxin fungi is critical to maintain a high quality of the grains and the products derived from them.
To detect the presence of mycotoxins, the complexity of the matrix of the grains must be taken into account, as well as the wide range of physical and chemical properties of the mycotoxins, so very selective and sensitive techniques are required to even detect the presence, plus a variety of them, in the same product.
To simultaneously extract several toxins, it must be taken into account that they can come from products of different types and that the toxins correspond to very different chemical products. To overcome these problems, solid phase chemical extraction methods have been developed to analyze them from food. The biggest disadvantage of these solid phase chemical methods is the time required for their realization, especially when a large number of samples must be analyzed. One of the most recommended methods for the extraction are the immunoaffinity columns since they are very selective and specific, but have the drawbacks of high cost and cannot be reused.
Traditionally, the analyzes to determine the presence of mycotoxins have been made by high performance liquid chromatography (HPLC), liquid chromatography/mass spectrometry (LC/MS), after having separated them by means of a solid extraction procedure or by column of affinity. These methods usually allow the determination of different classes of mycotoxins, provided that they correspond to a limited number of molecules.
Molecular methods, such as the polymerase chain reaction (PCR), can be an alternative to conventional methods to detect the fungi capable of producing them (mycotoxigenic), but not the mycotoxins themselves. In this sense, multiple PCR tests have been proposed, which allow the simultaneous amplification of several genes specific to the fungal species and/or the regulatory or structural genes involved in their biosynthesis. These tests have been successfully applied to detect mycotoxigenic fungi in a variety of foods or feeds.
Animal foods that can contain them: grains, feed, pet food.
General clinical signs (manifestations) to suspect a mycotoxicosis:
- Decreased growth (several).
- Rejection of food (several).
- Decrease in food efficiency (do not gain weight) (several).
- Decrease in egg production (poultry).
- Decrease in fertility.
- Presence of hemorrhages (several mycotoxins that cause liver damage).
- Presence of areas of ischemia due to deficiency of vascular irrigation due to vasoconstriction, mainly in legs (Claviceps purpurea – ergot, ergotism).
- Estrogenic effect (increase of mammary glands in males) (zearalenone).
- Secondary infections due to viruses or bacteria (several that have an immunosuppressive effect: aflatoxins, ochratoxins, ...).
- Unusual mortality.
Signs in necropsy of deceased animals:
• Hepatic impairment (several).
• Renal involvement (ochratoxins, which is why they have been called nephrotoxins).
• Bone marrow involvement.
Main mycotoxins / mycotoxicosis
Some of the characteristics of the main groups of mycotoxins are as described in the following paragraphs:
Aflatoxins are toxic metabolites of Aspergillus flavus, A parasiticus and other Aspergillus species. These fungi are present in the soil and in decaying vegetation, cause heating and decomposition of stored grains and can invade the corn in the field. The most susceptible crops and derivative products, among other products, for the development of these fungi are corn, hazelnuts, hazelnut flour, cotton seeds and cottonseed meal. The conditions that favor the invasion of corn by Aspergillus flavus in the field include the stress of the plant due to dryness or the damage caused in the corn ears by the maggots of the corn ears or other insects, the birds, the hail or the early frosts. The elevated temperatures together with a humidity of 18% of the grain are ideal conditions for the fungal invasion of the grains. The optimum temperature for the production of aflatoxin in storage is from 25ºC to 32ºC. Grains with a moisture content below 15% have a lower risk for mold growth and the production of aflatoxin, while an optimum moisture of the grain of around 18% and an external relative humidity at the level of 85% or higher favor it.
Clinical signs of aflatoxicosis:
The clinical signs of aflatoxicosis are very varied. In pigs it is fundamentally a liver disease, although other organs may be affected. Decreased growth and lower feed efficiency (feed conversion rate) occur when aflatoxin is consumed at levels of 100 to 400 ppb. Young animals and breeding females are the most sensitive to aflatoxins. Liver damage, bleeding, and death can occur when aflatoxin levels exceed 400 ppb. At these levels the sows can abort or give birth to dead pigs. In birds, the size of the liver, kidneys and thymus, and Fabricius bursa decrease.
Aflatoxins decrease the concentration of albumin and globulins, so it is deduced that they exert an inhibition of protein synthesis. At the same time, they are immunosuppressive in that they affect the immune response mediated by cells and the humoral response to antibody production, causing symptoms such as abnormal behavior (birds standing in groups) and other signs related to the nervous syndrome.
Aflatoxicosis in poultry mainly affects the liver, but may involve immunological, digestive and haematopoietic functions. Aflatoxin can negatively affect weight gain, food intake, feed conversion efficiency, egg production, as well as male and female fertility. Some effects are directly attributable to toxins, while others are indirect, such as reduced food intake. The susceptibility to aflatoxins varies, but in general, ducklings, turkeys and pheasants are susceptible, while chickens, Japanese quail and guinea fowl are relatively resistant. Clinical signs vary from bloating to high morbidity and mortality. At necropsy, the lesions are mainly found in the liver, which may redden due to necrosis and congestion or appear yellowish due to the accumulation of lipids. Hemorrhages can occur in the liver and other tissues. In chronic aflatoxicosis, the liver turns yellow to gray and atrophies. Aflatoxins are carcinogenic, but tumor formation is rare with the natural disease, probably because the birds do not live long enough for this to happen.
Aflatoxins are a problem for milk producers who must use feed with a very low aflatoxin level. Chronic symptoms include liver and kidney damage, decreased growth, decreased feeding efficiency, kidney damage, anemia, interference with the immune system, increased sensitivity to bruising and interference with the normal metabolism of proteins and fats. Clinical signs of acute aflatoxicosis include depression, nervousness, abdominal pain, diarrhea, rectal prolapse and death.
Aflatoxin M1 has been classified by the International Agency for Research on Cancer (IARC) as a group 1 carcinogen (highly carcinogenic to humans).
Deoxinivalenol (DON) (Trichothecenes, T-2)
Deoxynivalenol (DON) belongs to a class of mycotoxins referred to as trichothecenes, which also includes mycotoxins identified by the name of T-2, commonly known as vomitoxin. It is produced by Fusarium species. Fusarium graminearum, is a species of Fusarium that causes rotting of roots, stem and corn ears, although it also causes crust in wheat and produces DON mycotoxin in all grains.
Field conditions that favor the invasion of crop grains include heat and humid climate. The symptoms of the affectation can develop 3 days after the infection of the plants, when the temperatures are between 25ºC and 30ºC and the humidity is continuous. The plants seem to be more sensitive when they are infected in the phase of their flowering.
The DON is not known to increase in corn stored with the corn ears or in the small grains that come contaminated from the field since the growth of Fusarium requires a minimum of moisture own of the grain of 19 to 25%.
T-2 toxins are also produced by Fusarium species and can occur under the conditions described.
Clinical signs of DON (Trichothecenes, T-2):
General signs of the toxicity of trichothecenes in animals include weight loss, decreased feed conversion, feeding rejection, vomiting, bloody diarrhea, severe dermatitis, hemorrhage, decreased egg production, abortion and death. Pigs seem to be the most susceptible animals. Feed containing more than one part per million (ppm) of DON can cause a decrease in feed intake and reduce weight gain. In some cases there is vomiting. Cattle and poultry appear less susceptible to DON.
T-2 toxins in poultry can cause lesions on the tips of the beaks, anomalies in their plumage, reduction of egg production, egg laying with thin shells, reduction of weight gain and mortality. In the calves that consume feed contaminated with T-2, moderate enteritis with diarrhea may appear.
The trichothecenes type A (toxin T-2, toxin HT-2, diacetoxyscirpenol) are of great concern for the poultry industry as they can cause significant productivity losses. These mycotoxins are highly toxic to poultry, especially chickens, as suggested by the very low values required for the 50% lethal dose (LD50 of 2 mg / kg for diacetoxyscirpenol and 4 mg / kg for toxin T-2). In particular, the T-2 toxin causes a reduction in food intake, body weight (CP) and egg production, oral lesions and impaired nutrient absorption. In addition, the T-2 toxin can reduce egg production and increase the incidence of cracked eggs. The T-2 toxin is cytotoxic for chicken macrophages in vitro. Of trichothecenes type B, deoxynivalenol (DON) was recognized for the first time for its proinflammatory and immunomodulatory activities. This mycotoxin is capable of damaging the intestinal function and the integrity of the barrier, by affecting the area of the intestinal surface and the function of the intercellular junctions. When the barrier function is affected, it is associated with an increase in epithelial permeability and the translocation of pathogens and other toxic entities, as well as a non-specific inflammatory response and an overstimulation of the immune system associated with the intestine. In this context, several studies have shown that DON is a promoter factor for the development of necrotic enteritis and coccidiosis in poultry, even at concentrations below the permitted levels.
The administration of food contaminated with DON can cause decreases in the yield caused by a deteriorated food consumption and a minor weight gain, the mucous membrane of the gizzard presents erosions and injuries, altered hematological parameters, such as serum minerals and glucose levels. According to the literature, DON can significantly influence the weight and thickness of the eggshell. Trichothecenes also suppress cellular and humoral responses.
In poultry the trichothecenes cause a rejection of the feeding, caustic injury of the oral mucosa and areas of the skin in contact with the mold, acute digestive disease and injury to the bone marrow and the immune system. The lesions include necrosis and ulceration of the oral mucosa, reddening of the gastrointestinal mucosa, liver spots, atrophy of the spleen and other lymphoid organs and visceral hemorrhages. In laying hens, the decrease in egg production may be accompanied by depression, rejection of food and evident cyanosis in the crest and chins. Ducks and geese develop necrosis and pseudomembranous inflammation of the esophagus, proventriculus, and gizzard.
Zearalenone is typically produced by the fungus Fusarium graminearum. However, it can also be produced by other Fusarium species. Corn is the main source of this toxin. The field conditions described for the production of DON are also applicable to zearalenone. Exposure to conditions that maintain grain moisture between 22 and 25%, such as a delay in harvesting for several weeks, favor the growth of the producer fungi and the production of zearalenone. The production of toxin during storage is unlikely, unless the humidity of the grain exceeds 22%.
Clinical signs of zearalenone poisoning:
Zearalenone is best known for its estrogenic effect in pigs. When consumed at levels of a few parts per million, this toxin causes the estrogenic syndrome characterized by a swelling of the vulva in females and tenderness of the mammary glands in young males. Zearalenone can cause the death of embryos, inhibition of fetal development and decrease in the number of fetuses in sows.
In comparison with other species, poultry are less affected. However, zearalenone may have some negative effects on the fertility and development of fertile eggs.
Ochratoxin (Ochratoxin A)
Ochratoxins are produced by several species of Aspergillus and Penicillium. They can be found in cereal grains, dried beans, and hazelnuts. Likewise, they can exist in the storage of grains with high own humidity (greater than 25%). Therefore, the only recommended control is to keep the beans in cold and dry environments.
Clinical signs of ochratoxin A:
These toxins are often called nephrotoxins because of the kidney damage they can cause. Ochratoxin A can affect kidney function in pigs. In poultry the symptoms include growth retardation, decreased feed conversion, impaired renal function and mortality. Ochratoxin A can decrease the quality of eggshell and egg production.
Chicks and turkeys are very sensitive to ochratoxins, suppressing feed intake, growth, egg production and have an effect on shell quality. The administration of ochratoxin A (OTA) can reduce the concentration of immunoglobulins in the serum of birds and alter the innate natural defenses and the cellular and humoral responses of the immune system. In addition, OTA can enhance inflammation at target sites, primarily in the kidneys, while reducing the ability of immune cells to respond to inflammation.
Ochratoxins are quite toxic to poultry. These nephrotoxins are produced mainly by Penicillium viridicatum and Aspergillus ochraceus in grains and feed. Ochratoxicosis mainly causes kidney disease but also affects the liver, the immune system and the bone marrow. Severe poisoning causes reduced spontaneous activity, hypothermia, diarrhea, rapid weight loss and death. Moderate intoxication impairs weight gain, feed conversion, pigmentation, carcass yield, egg production, fertility and embryo development.
Fuminosins are produced by Fusarium verticilloides, F proliferatum and other Fusarium species that exist in corn. These fungi infect the roots of corn, leaves, stems and grains. F. verticilloides survives on crop residues on land and under favorable conditions, it can infect corn stems directly or through incisions caused by hail or insects. Fuminosins may be present in healthy grains. Of the fuminosin described, B1, B2 and B3 are the most abundant in contaminated food and feed and fuminosin B1 (FB1) generally accounts for 75% of the total content.
Clinical signs of fuminosins:
Horses seem the most sensitive animals to fuminosins. This mycotoxin when ingested by horses, causes a neurotoxic syndrome, called leukoencephalomalacia. This alteration is characterized by the liquefaction of the horse's brain. Neurotoxic symptoms include decreased feed intake, lameness, oral and facial paralysis, seizures and occasionally death. It has been shown that the toxin is carcinogenic and is associated with pulmonary edema in pigs. In humans, F. verticilloides has been associated with high rates of esophageal cancer in areas of the world where maize is the main source of food, such as in the Transkei region of South Africa and Linxian in China.
Ergotism (Claviceps purpurea) - Ergot
Ergotism is a disease of farm animals of worldwide distribution due to the ingestion of sclerotia (sclerotia) of the parasitic fungus Claviceps purpurea. Claviceps spp. are fungi that attack cereal grains. Rye is especially affected, but also wheat and other grains of cereals. The fungus invades and replaces the content of the grain or seed of rye and other small grains of forage plants. The hard and elongated sclerotes may contain variable amounts of ergot alkaloids of which ergotamine and ergonovine (ergometrine) are the most important pharmacologically. Cattle, pigs, sheep and poultry can suffer sporadic outbreaks and many other species are susceptible. Intoxication is due to the ingestion of seed heads or infected grains in important concentrations.
Mycotoxins are formed in the sclerotium, a visible, dark, hard mass of mycelium that displaces the grain tissues. Within the sclerote are the alkaloids produced. These alkaloids affect the nervous system causing seizure and sensory neurological alterations; to the vascular system causing vasoconstriction and gangrene of extremities; and the endocrine system, including neuroendocrine control of the pituitary gland.
Ergot alkaloids cause vasoconstriction by direct action on the arteriole muscles and repeated doses damage the vascular endothelium. These actions initially reduce blood flow and eventually cause terminal necrosis of the extremities due to thrombosis. A cold environment predisposes to gangrene of the extremities. In addition, these alkaloids cause stimulation of the central nervous system followed by depression, inhibit the release of pituitary prolactin in many species of mammals with failure for breast development at the end of gestation and delayed initiation of milk secretion, with agalactia after Birth. They have also been associated with heat intolerance, dyspnea, and reduced milk production in dairy cows. The most considerable lesions at necropsy are observed in the skin and subcutaneous tissue of the extremities. The superficial skin may be normal, but below it is cyanotic and hardened in advanced cases. In the areas near the necrotic area there are subcutaneous hemorrhages and edema. In pigs, the ingestion of infected grains can reduce food intake, reducing weight gain. Occasionally, pigs may show necrosis of the tips of the ears or tail. If they are ingested by pregnant sows it leads to a lack of breast development with agalactia after delivery and the piglets may be smaller than normal. The majority of the litter dies in a few days due to malnutrition. In sheep the signs are similar to those of cattle. In addition, the mouth may be ulcerated and there is marked intestinal inflammation. A convulsive syndrome has also been observed.
In the chicks the toes of the legs are discolored due to vasoconstriction and ischemia. In older birds, vasoconstriction affects the crest, barbels, face and eyelids that atrophy and disfigure. Vesicles and ulcers on the legs can develop. In the laying hens, the ingestion of feed and the production of eggs are reduced.
The diagnosis is based on the finding of the causal fungus (sclerotes) in the grains, hay or pastures supplied to the cattle that show signs of ergotism.
Mycotoxicosis by citrinin (Citrinin Mycotoxicosis):
The citrinina is produced by several species of Penicillium (Penicillium citrinum, Penicillium hirsutum, Penicillium verrucosum, Penicillium camemberti), Aspergillus (Aspergillus terreus, Aspergillus niveus, Aspergillus oryzae, Aspergillus carneus) and Monascus (Monascus ruber and Monascus purpureus), Natural contaminants of rice, wheat, barley, corn, rye and oats rice, wheat, barley, corn, rye, oats and other grain cereals.
Citrinin causes a diuresis that results in watery fecal stools and reduced weight gain. At necropsy, the lesions are moderate and affect the kidneys.
Mycosporein mycotoxicosis (Oosporein Mycotoxicosis):
Oosporein is a mycotoxin produced by Chaetomium spp., which causes gout and high mortality in poultry. Chaetomium spp. is found in feed and grains, including corn, rice, hazelnuts. Mycosporein mycotoxicosis manifests as a visceral and articular gout related to impaired renal function and elevated plasma concentrations of uric acid. Chickens are more sensitive to oosporein than turkeys. Water consumption increases during intoxication and faecal droppings are liquid and formless.
Mycotoxicosis by cyclopiazonic acid (Cyclopiazonic Acid)
Cyclopiazonic acid is a metabolite of Aspergillus flavus. In chickens, cyclopiazonic acid causes feed conversion problems, decreased weight gain and mortality. The lesions develop in the proventriculus, the gizzard, the liver and the spleen. The proventriculus dilates and the mucosa thickens and sometimes ulcerates.
Mycotoxicosis by sterigmatocystin (Sterigmatocystin)
Sterigmatocystin is a precursor of aflatoxin, produced by Aspergillus flavus, A. parasiticus, A. versicolor and A. nidulans, hepatotoxic and hepatocarcinogenic, but less frequent than aflatoxin.
Mycotoxicosis should be suspected when the history, signs and lesions are suggestive of food poisoning, and especially when molds on the grains, ingredients or feed are evident. Exposure to toxins associated with the consumption of a new batch of feed may cause subclinical or transient disease. Chronic or intermittent exposure can occur in regions where grain and feed ingredients are of poor quality or when feed storage is deficient or prolonged.
The definitive diagnosis involves the detection and quantification of the specific toxin(s). Feed and recently diseased or dead birds should be sent for analysis. The necropsy of the birds and the diagnostic tests should also be carried out in the feed if mycotoxicosis is suspected.
Samples of feed and ingredients should be collected properly and sent quickly for analysis. The formation of mycotoxins can be located in a batch of feed or grain. Several samples should be taken from different sites to increase the probability of confirming a mycotoxin formation zone.
Samples should be collected at ingredient storage sites, feed manufacturing and transport, feed depots and feed bins. Samples of 500 g should be obtained in separate containers. Clean paper bags, properly labeled, are adequate. However, closed plastic or glass containers are only suitable for a short period of storage and transport, because the feed and grain deteriorate rapidly in the airtight containers.
Crop grains should be maintained in clean, dry warehouses to control the development of fungi, reduce storage time, or add to feed additives inhibiting the development of fungi such as propionic acid.
The prevention of mycotoxicosis should focus on the use of food and ingredients free of mycotoxins and conservation measures that prevent the growth of molds and the formation of mycotoxins during transport and storage of food. Mycotoxins can be formed in decomposed and scabby foods in feeders, feed mills and storage tanks, so by cleaning and correcting the problem immediate benefits can be obtained.
Ventilation of bird pens to avoid high relative humidity also decreases the moisture available for fungal growth and the formation of toxins in feed. Antifungal agents added to feed to prevent fungal growth have no effect on the already formed toxin, but can be cost-effective in conjunction with other feed management measures. Organic acids (propionic acid, 500-1,500 ppm [0.5-1.5 g / kg]) are effective inhibitors, but the effectiveness can be reduced by the size of the particles of the feed ingredients and the buffer effect (neutralizer) of certain ingredients. Absorbent compounds such as sodium and calcium hydrated aluminosilicate (HSCAS) bind and effectively prevent the absorption of aflatoxins. Esterified glucomannan, derived from the cell wall of the yeast Saccharomyces cerevisiae, is protective against aflatoxin B1 and ochratoxins, reducing toxicity through binding and reducing the bioavailability of fumonisins, zearalenone and T-2 toxin. Several other fermentation products, algae, plant extracts and microbial feed additives have demonstrated their ability to bind or degrade mycotoxins and may be applicable and appropriate.
There are no specific antidotes, so the treatment is based on the elimination of the toxin source (see Prevention).
Mycotoxicosis is not generally treated with a therapy after diagnosis. A preventive approach is needed, recognizing the risk factors to avoid exposure to them. The most practical measures are the inactivation of the preformed toxin in the grain or feed, and the adsorption or inactivation of the toxin in the gastrointestinal tract.
The toxic food must be eliminated and replaced by an undisturbed food. Some mycotoxins increase the requirements of vitamins, trace elements (especially selenium), proteins and lipids and can be compensated with food supplements and water-based treatment. Non-specific toxicological therapies that use activated charcoal (adsorption of the digestive tract) in the diet have a conservative effect but are not practical for the larger production units.
The way in which samples are taken and processed is an important consideration when testing for mycotoxins. Grain samples should be representative of the entire lot and of sufficient size to compensate for the unequal distribution of the contaminant throughout the whole, as well as the low levels to be detected. The variability in the samples of grains used for the mycotoxin analysis is due to the fact that not all grains are contaminated and their distribution in the lot may not be uniform.
Tests carried out in IVAMI:
- Cultivation of fungal enrichment (molds) of samples.
- Cultivation of fungal insulation insulation (molds).
- Microscopic identification of fungi present compatible with mycotoxin-producing genera.
- Molecular detection of genes coding for mycotoxins.
- Sick or dead animals: in the case of birds extract the crop and send complete with the nutritional content it contains. In the case of other dead animals obtain content of the small intestine.
- Grains or feed: send a sample taken from various parts of storage: approximately 500 g of each.
Conservation of samples:
- • Animal samples (craw with its content, intestinal content): refrigerated for less than 48 hours; frozen for more than 48 hours.
• Samples of grains or feed: room temperature.
Delivery of results:
• 10 to 15 working days, according to the time required for the development of the fungi.
Cost of the tests:
• According to the type of study: consult firstname.lastname@example.org