Open access peer-reviewed chapter - ONLINE FIRST

Animal Feeds Mycotoxins and Risk Management

Written By

Zacharia Waithaka Ng’ang’a and Eric Niyonshuti

Submitted: December 8th, 2021 Reviewed: December 13th, 2021 Published: March 14th, 2022

DOI: 10.5772/intechopen.102010

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Mycotoxins and Food Safety - Recent Advances Edited by Romina Alina Marc

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Mycotoxins and Food Safety - Recent Advances [Working Title]

Dr.Ing. Romina Alina Marc

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Abstract

The demand for livestock products is the main factor affecting the demand for livestock feeds worldwide. However, animal feed safety has gradually become more important, with mycotoxins representing one of the most significant hazards. Mycotoxins are toxic secondary metabolites produced naturally by fungi that grow on various agriculture commodities. Aflatoxin, fumonisin, ochratoxin, trichothecene, and zearalenone are the more prevalent mycotoxins in animal feeds. Some of mycotoxins impacts include; loss of animal and human health, reduced animal productivity, increased veterinary service costs, feed disposal and increased research costs which enhance the importance of mycotoxins detoxification. Contamination of feeds may occur both during pre-harvest and post-harvest. The purpose of this chapter is to review the most prevalent mycotoxins in animal feeds, reveal the origin of mycotoxins contamination and the possible risks they pose to feeds and livestock. This chapter also gives an overview of the most important factors that influence mold growth and mycotoxin production as well as the economic impacts of mycotoxins. To the end of this chapter, mycotoxins preventive methods, both preharvest and postharvest, are well discussed.

Keywords

  • mycotoxins
  • mold
  • animal
  • nutrition
  • prevention
  • detoxification

1. Introduction

The demand for livestock products is the main factor affecting the demand for livestock feeds worldwide. The world-wide demand for animal feed is expected to increase as a result of the global demand for animal sourced food which is expected to increase due to growth of the world population. The United Nations Food and Agriculture Organization (FAO) estimates that food demand will increase by 60% by 2050, and animal protein production will increase by 1.7% per year between 2010 and 2050, with meat production expected to increase by nearly 70%, aquaculture by 90%, and dairy by 55% [1, 2]. However, animal feed safety has gradually become more important, with mycotoxins representing one of the most significant hazards [3]. Mycotoxins are secondary metabolites produced naturally by filamentous fungi, which are considered toxic substances when present in food for humans and feed for animals [4]. They are small and quite stable molecules which are extremely difficult to remove or eradicate, and which enter the feed chain while keeping their toxic properties.

More than 500 mycotoxins have been identified, the majority of which have been either regulated or tested [5]. These chemically different mycotoxins formed by more than 350 fungal species and causing diseases to living organisms have been researched [6] but only a few have been extensively researched and even fewer have good methods of analysis [7]. The primary classes of mycotoxins are aflatoxins (B1, B2, G1, G2) of which aflatoxin B1 (AFB1) is the most prevalent, zearalenone (ZEA), trichothecenes such as deoxynivalenol (DON) and T-2 toxin (T-2), fumonisins (FUM: FB1, FB2, FB3) and ochratoxin A (OTA) [8]. With regard to animal feed, aflatoxins, fumonisins, ochratoxins, trichothecenes, and zearalenone are the more prevalent ones hazards [3]. The majority of mycotoxins in these groups are produced by three fungal genera: Aspergillus, Penicillium and Fusarium [9]. Many species of these fungi produce mycotoxins in animal feedstuffs. Because a given mold species can produce many types of mycotoxins in a single food item, multiple contaminations are possible. Multiple varieties of mycotoxins can also be discovered in the same feed if it contains a variety of contaminated products or raw materials. Several studies and surveys that revealed concurrent contamination were mentioned in a review on mycotoxins in the human food chain by Galvano et al. There is therefore a risk of simultaneous contamination in animal feed since raw cereals can also be employed as raw materials in animal feed preparation [10].

Mycotoxin contamination usually occur in the field as well as during processing and storage of feed products as long as the conditions allow fungal colonization with moisture content and ambient temperature being the key determinants of this mycotoxin production [11]. Mold growth in feeds is undesirable because they secrete toxins which impair with animal health and productivity [12]. Direct consequences of consumption of mycotoxins-contaminated livestock feed include reduced feed intake, feed refusal, poor feed conversion, diminished body weight gain, increased disease incidence, and reduced reproductive capacities [13]. Furthermore, mycotoxins could potentially impose large costs on the economy [14]. The addition of adsorbents to feeds is the most widely applied way of protecting animals against mycotoxins.

However, it is quite relevant to understand possible sources of mycotoxins that contaminate animal feeds and the various available preventive methods that can be explored. This review is intended to explore and provide information about most prevalent mycotoxins in animal feeds. The review also highlights the origin of mycotoxins in feeds, the possible risks they pose to feeds and livestock production in general. To the end of this article, mycotoxins preventive methods and mycotoxins risk management methods both before and after harvesting animal feeds are well discussed.

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2. Mycotoxins and fungi classification

Mycotoxins are toxic secondary metabolites produced naturally by filamentous fungi that grow on various agriculture commodities [4, 15]. The main factors influencing fungi growth and mycotoxin production are temperature and moisture [14]. The mycotoxin contamination can occur during pre-harvest and post-harvest, this is why researchers have divided fungal species into two main groups: field fungi and storage fungi [12].

Field fungi invade the seeds while the crop is still in the field and require high moisture conditions (20–21%). These include species of Fusarium, Alternaria, Cladosporium, Diplodia, Gibberellaand Helminthosporium.On the other hand, storage fungi are those that invade grain or seeds during storage and require less moisture than field fungi (13–18%). Storage fungi include species of Aspergillusand Penicillium[12]. It’s important to remember that not all fungal growth results in the production of mycotoxins, and that the detection of fungi does not always suggest the presence of mycotoxins.

Mycotoxigenic species may be further classified based on their geographical prevalence. Aspergillus flavus, A. parasiticusand A. ochraceusreadily proliferate under warm and humid conditions, while Penicillium expansumand P. verrucosumare essentially temperate fungi. Fusarium fungi are more ubiquitous, but toxigenic species from this genus are less likely to be associated with cereals contamination from warm countries [11].

Mycotoxins are classified according to their chemical structures and biological activities as; carcinogenic (e.g. aflatoxin B1, ochratoxin A, fumonisin B1), oestrogenic (zearalenone), neurotoxic (fumonisin B1), nephrotoxic (ochratoxins, citrinin, oosporein), dermonecrotic (trichothecenes) and immunosuppressive (aflatoxin B1, ochratoxin A, and T-2 toxin) [16].

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3. Major mycotoxins in animal feeds and toxicity

According to different reports, more than 400 mycotoxins have been identified. Mycotoxins can occur under natural conditions in animal feeds. Most mycotoxins of concern in the area of animal nutrition are produced by three genera of fungi, namely, Aspergillus, Penicillium, and Fusarium (Table 1) [19]. Biomin, a feed additive manufacturer, conducted a two-year assessment to assess the incidence of mycotoxins in feed and feed raw materials in several of the key animal production locations. AFB1, OTA, DON, T2 toxin, ZEA, and fumonisins were determined in a total of 2753 assays on 1507 samples collected from European and Mediterranean markets. Mycotoxins were found in 52% of these samples, demonstrating that the prevalence of mycotoxins in animal feed is relatively significant [20].

MycotoxinMolds/fungal species
AflatoxinAspergillus flavus, A. parasiticus
DeoxynivalenolFusarium culmorum, F. graminearum, F. sporotrichioides
Ochratoxin AA. ochraceus, A. Alliaceus, A. melleus, A. ostianus, A. sulphureus, Penicillium viridicatum, P. palitans, P. commune, P. variabile, P. cyclopium, P. verrucosum, P. purescens
T-2 toxinF. acuminatum, F. equiseti, F. poae, F. semitectum, F. sporotrichioides
ZearalenoneF. culmorum, F. graminearum, F. sambucinum, F. semitectum, F. sporotrichioides
FumonisinsF. proliferatum, F. verticillioides

Table 1.

Some key species of molds producing some of the most important mycotoxins in animal husbandry [17, 18].

3.1 Aflatoxin

Aflatoxins are produced by strains of Aspergillus flavusand A. Parasiticusand they are a prominent cause of disease in animals. Naturally occurring aflatoxins are B1, B2, G1 and G2. Aflatoxin B1 is the most prevalent of the aflatoxins and occur in a couple of important animal feeds. It is one of the most potent hepatocarcinogens and causes acute hepatotoxicity as well as growth retardation in animals. Aflatoxin contaminates most agricultural commodities. The highest levels of contamination have been recorded in groundnuts, tree nuts, other oilseeds and corn. Corn, cottonseed, and peanuts are some of the most important sources of aflatoxin in animal feeds [21]. Small cereal grains (barley, oats, and wheat) are also occasionally colonized by the causative molds, which produce low to moderate quantities of aflatoxin. Soybeans do not support significant levels of aflatoxin B1 production [22].

Worldwide aflatoxins have been reported to be prevalent in both feedstuffs and finished feeds [23]. Aflatoxin is posing a dangerous problem for animal industry and human health [24]. Concerning livestock health, Aflatoxins cause acute death to chronic disease. Chronic aflatoxins poisoning causes a wide range of symptoms that aren’t always visible clinically; a slow rate of growth in young animals is a sensitive clinical indicator of chronic aflatoxicosis. Aflatoxicosis is characterized by a decrease in total production, greater vulnerability to stressors, and clinical manifestations such as gastrointestinal problems [3]. Long-term consumption of aflatoxin contaminated feeds results in negative effects on the liver (primary target organ), such as hepatic cell and tissue injury, as well as gross abnormalities [25, 26].

3.2 Ochratoxin

Ochratoxin is a dangerous mycotoxin, produced by Aspergillus species in warmer climates and Penicillium species in cold areas. Ochratoxin contaminates various raw agricultural commodities and has dangerous effects on animals and humans [27]. Ochratoxin predominantly affects the kidneys of all animal species, but it can also harm the liver at high concentrations. Because of its strong protein affinity, especially for albumin, ochratoxin A (OTA), a primary ochratoxin, accumulates in animal tissues. OTA has been proved to be a potent nephrotoxic, immunotoxic, neurotoxic, hepatotoxic, and teratogenic compound. The intake of feed contaminated with OTA affects animal health and productivity [28]. The kidneys are the most affected by OTA-acute toxicity, and pigs have the highest susceptibility, developing nephropathy following exposure [29]. Many animal studies, including chick, quail, rabbit, hamster, rat, and mouse research, indicated teratogenic effects, with craniofacial deformities and lower birth weight being the most prevalent [30, 31]. The most relevant effects of ochratoxins in animal cells are the inhibition of protein synthesis, lipid peroxidation, DNA damage and oxidoreductive stress [32].

3.3 Zearalenone

Zearalenone is one of the well-known mycotoxins produced by Fusarium mold species [33]. The fungi that produce zearalenone are distributed worldwide, particularly in cereal grains and derived products [34]. Zearalenone is a stable compound during storage and can resist high temperature during processing of food [35]. Furthermore, it was observed that during feed processing (e.g., milling, extrusion, storage and heating) zearalenone was not decomposed [36]. It can be found in all products intended for animal feeding [33]. It is recommended that the overall amount of zearalenone in the diet should not exceed 250 ppb [37]. It has been concluded that zearalenone interacts with estrogen receptors and causes an oestrogenic response in animals [38]. Among its estrogenic effects includes decreased fertility, increased embryo lethal resorptions, reduced litter size, change in serum levels of progesterone and teratogenic effects in pigs and sheep [35].

At higher doses, zearalenone interferes with conception, ovulation, implantation, fetal development and the viability of newborn animals [37]. Large doses of zearalenone toxin are associated with abortions in dairy cattle as well as reduced feed intake, decreased milk production, vaginitis, increase vaginal secretions, poor reproductive performance and mammary gland enlargement in heifers. Swine have been shown to be the most sensitive to zearalenone among farm animals; some consequences in pigs include swelling of the vulva and mammary glands, stillbirth, prolonged estrus intervals, vulvovaginitis, vaginal and/or rectal prolapse, ovarian atrophy, disrupted conception, abortion and infertility [39, 40, 41]. In male pigs, zearalenone induces feminization, decreases spermatogenesis, testicular weight, decreases libido, and decreases testosterone levels [37].

3.4 Fumonisins

Fumonisins are neurotoxic and possible carcinogens. Fumonisins are hydrophilic, unlike other known mycotoxins, which are soluble in organic solvents, making them challenging to study. Different fumonisins have been previously identified (FA1, FA2, FB1, FB2, FB3 and FB4) [42]. Fumonisins causes liver and kidney damage, decreases weight gains, impairs immune function and increases mortality rates in most animals. FB1 and FB2 were isolated from F. moniliformecultures and were found to promote cancer in rats [42]. Fumonisins occur naturally in corn, and they have been linked with equine leukoencephalomalacia which results in softening of white tissue in the brain [41]. Interference with the enzyme N-acyltransferase, which is involved in sphingolipid metabolism, is the principal mechanism of fumonisins toxicity. This mainly results in the disruption of processes involved in liver functioning as well as affecting other biological functions such as protein metabolism and the urea cycle [41, 43].

3.5 Trichothecenes

Trichothecenes are produced mainly, but not only, by Fusarium species. With a basis on the chemical structure, more toxic but less prevalent type A trichothecenes (T-2) and widely occurring type B trichothecenes (deoxynivalenol, DON) are well defined [44]. Trichothecenes are mostly found in cereals, commercial cattle feed and mixed feeds. They affect livestock animals, pets and humans [14]. Trichothecenes can be easily absorbed via the skin and gastrointestinal tract [5]. Ingestion of feeds contaminated by trichothecenes results in decreased feed intake and weight gain, bloody diarrhea, hemorrhaging, oral lesions, low productivity, immunosuppression, abortion, and sometimes death [3, 45].

Trichothecenes have several action mechanisms, including DNA, RNA, and protein synthesis inhibition, neurotransmitter alterations, lipid peroxidation, apoptosis, mitochondrial function inhibition, and cytokine activation [46, 47]. Through microbial degradation of trichothecenes in the gastrointestinal system, monogastric animals, particularly young pigs, are very sensitive, although poultry and ruminants appear to be less sensitive to some trichothecenes [46]. Because of inadequate absorption following oral exposure, extensive metabolism, and rapid removal from the body, poultry have a higher tolerance to trichothecenes [48, 49].

3.5.1 T-2 toxin

T-2 is the most lethal of the trichothecene mycotoxins, and its toxicity in animals varies depending on age, dosage, and species. The T-2 toxin, which is mostly produced by Fusarium tricinctum, was the first trichothecene to be discovered as a naturally occurring grain contaminant in the United States, where it was linked to a deadly toxicosis in dairy animals fed moldy corn [50]. T-2 toxin was found to inhibit protein and DNA synthesis and weaken cellular immune responses in animals [51]. T-2 toxin has been linked to feed refusal, output losses, diarrhea, intestinal hemorrhages, and death in dairy cattle. In poultry, the T-2 toxin has been linked to oral and intestinal lesions, as well as immune system impairment, hematopoietic system destruction, decreased egg production, thinning of eggshells, feed refusal, weight loss, altered feather patterns, and incorrect wing positioning [52, 53]. Cells that divide rapidly are more vulnerable to T-2 toxin thereby explaining why the immune system and the gastrointestinal tract are two of T-2’s primary targets. Carcinogenesis, immunological depression, neurotransmitter abnormalities, weight loss, growth retardation, oral lesions, diarrhea, and vomiting are among indications of chronic and acute T-2 toxicity in animals [5, 47, 54].

3.5.2 Deoxynivalenol (vomitoxin)

Deoxynivalenol (DON) is one of the most frequently detected trichothecenes in grains [55] and the most common producing species of deoxynivalenol (DON) is F. graminearum[56]. DON is stable and it can survive processing, milling. Therefore, it easily occurs in feeds prepared from contaminated corn and wheat.

Swine are the most vulnerable of all livestock species to deoxynivalenol (DON) toxicity. The main symptoms for DON are vomiting (hence known as “vomitoxin”), feed refusal, skin damage and hemorrhage especially in swine [44]. DON has been associated with reduced milk production in dairy cattle, reproductive performance inhibition and immune function inhibition in several animal species [56]. Low intakes of DON causes nausea, diarrhea, gastrointestinal tract lesions, decreased nutritional efficiency, and weight loss in animals while higher doses of DON intake induces vomiting and feed refusal with severe reduction in weight, severe damage in the hematopoietic systems and immune dysregulation [57, 58, 59]. Dogs and cats can be affected as well, and sensitivity to DON mainly vary with gender and age [5, 60].

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4. Factors influencing mold growth and mycotoxin production

The production of mycotoxins requires molds growth [18]. The production of these compounds, especially in grains, is highly dependent on environmental factors pre and/or postharvest (Table 2) [61]. Temperature, relative humidity strains of toxigenic organisms and occurrence of competitive growth are the most factors responsible for mold outbreaks in the field [62]. Temperature, water activity, and oxygen are the most significant elements for growth and mycotoxin generation, aside from the presence of nutrients. Physical and chemical features of substrates affect their ability to support fungal growth. Physical qualities include water activity, oxygen availability, and surface area, while chemical characteristics include carbohydrates, lipids, protein, trace elements, and amino acid composition [63].

MycotoxinTemperature (°C)Water activity
Aflatoxin330.99
Ochratoxin25–300.98
Fumonisin15–300.9–0.995
Zearalenone250.96
Deoxynivalenol26–300.995

Table 2.

The optimum temperature and water activity for mycotoxins production in grains [61].

According to [64], a minimum water activity of 0.70 will sustain growth of storage molds, though for field molds that produce mycotoxins water activity should be above 0.85. Most fungi require the relative humidity to be above 70% for them to develop. At a moisture level of 14–15%, in equilibrium with a relative humidity of 70–75%, Aspergillus glaucuswill develop and thrive on cereals, pulses, pellets, and defatted oilseed meals [65]. At the same relative humidity, the moisture levels of the whole oilseeds such as rapeseed, sunflower, or flax will be only 6–7%, but the fungi will still develop.

Many researchers have reported that pre-harvest fungal invasion is influenced by in-field damage caused by insects, birds, rodents, husbandry practices and adverse weather. Stress caused by drought, nutrient deficiency and untimely or excessive fertilizer application may also predispose towards fungal establishment. Airborne fungal spores can easily infect cracked grain, whereas soil-borne spores can easily infect pods and cobs of crops that fall to the ground. Mold is encouraged and fungal infection is favored by repeated planting of the same crop in the same field, poor harvest handling, poor storage, and post-harvest pest attack.

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5. Overview of mycotoxin effects in animals

Intake levels, duration of exposure, toxin species, modes of action, metabolism, and defense systems all influence the harmful effect of mycotoxin ingestion in animals. The presence of multiple mycotoxins in feed probably have at least an additive, if not synergistic, effect. In animals, mycotoxins have a wide range of biological consequences, including liver and kidney damage, neurological effects, immune-suppressive effects, carcinogenic, estrogenic and teratogenic effects, to mention a few. Carcinogenic examples of mycotoxins include AFB1, OTA, and FB1. When mold and mycotoxins are present together, it can lead to infection risk, as well as reproductive issues. Animals that consume mycotoxin-contaminated feed may experience appetite loss, reduced feed efficiency, immunosuppression (leading to increased disease incidence), poor weight gain, and mortality [7, 39, 66].

It should be noted that toxicity may vary considerably within a structural group of mycotoxins and that the danger may not always be due to the toxin itself but to its metabolites. Chronic intoxication can adversely affect animal health, leading to problems with reproduction, increased susceptibility to infectious diseases, and altered performance. According to a review by [5], mycotoxins exhibit their cellular/molecular effects via several mechanisms including metabolic enzyme inhibition, ribosomal binding, DNA effects, protein interaction, ionophore activity, effects on hormones, epigenetic properties, necrosis and apoptosis, RNA polymerase effects, and mitochondrial interactions. Mycotoxins have varied impacts on various organ systems and cellular pathways. Aflatoxin, ochratoxin, and T-2 toxin, for example, all inhibit protein synthesis, but in distinct ways: aflatoxin binds to both RNA and DNA and stops transcription, T-2 toxin inhibits translation initiation, and ochratoxin inhibits phenylalanine-t RNA synthetase and hence translation [67].

Mycotoxins are capable of inducing both acute and chronic effects. The effects observed are often related to dose levels and duration of exposure. Acute primary mycotoxicosis occurs if high to moderate amounts of mycotoxins are consumed. Specific, overt, acute episodes of disease ensue, which include hepatitis, hemorrhage, nephritis, necrosis of oral and enteric epithelium, and death. Chronic primary mycotoxicosis, resulting from moderate to low levels of mycotoxin intake, often cause reduced productivity in the form of slower rate of growth, reduced production and inferior market quality. Consumption of low levels of mycotoxins through the feeds do not cause serious mycotoxicosis, but often predisposes to various infectious diseases and especially to secondary bacterial infections [68, 69], because of the suppression in both humoral and cell mediated immune response in such animals [68].

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6. Economic impacts of mycotoxins

Mycotoxins are estimated to affect as much as 25% of the world’s crops each year [70]. In the United States and Canada alone, the cost of mycotoxins is estimated to be more than $5 billion each year [7]. In developing countries, many foods and feeds which otherwise can be available for consumption or trade are lost in production or storage [71]. The mycotoxins in animal feeds are one of the leading causes of output losses and increased management expenses in animal husbandry around the world [72].

Mycotoxin-contaminated products cause significant economic and trade problems at almost every marketing stage, from the producer to the consumer. Many importing countries have placed restrictions without following the Codex Alimentarius Commission’s guidelines for risk assessment and acceptable methodologies thereby negatively impacting developing countries’ economies [73]. Mycotoxins in ethanol co-products (dry distiller’s grain and soluble) have an annual economic impact of about $18 million on the swine sector in the United States. Mycotoxins create economic losses because of their effects on cattle production, crop losses, and the costs of regulatory programs targeting mycotoxins. Depending on the toxicity of each mycotoxin and the country, regulation limits for mycotoxins in animal feedstuffs vary whereas in some countries the limits might not even exist [7, 74, 75].

Mycotoxins significantly impact both the productivity and the nutritional value of cereal and forage [70]. Molds use nutrients from the feed to grow. This results in reduced energy content of the feeds, decreased feed palatability and increased feed refusal by animals [64]. Consumption of feeds contaminated by mycotoxins cause organ damage, immune suppression and health disorders, limiting growth and performance of farm animals [76] and thereby directly leading to economic losses [77]. The economic impact of mycotoxins includes loss of animal and human life, increased health care and veterinary care costs, reduced livestock production, disposal of contaminated foods and feeds, and investment in research to reduce severity of the mycotoxin problem [78].

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7. Risk management: prevention of mycotoxins in feeds

Because of the harmful consequences of these mycotoxins, several strategies have been developed to assist prevent the production of mycotoxigenic fungus, as well as detoxify mycotoxin-contaminated animal feeds. These includes:

  • Mycotoxin contamination prevention.

  • Mycotoxin detoxification in feed.

  • Mycotoxin absorption inhibition in the gastrointestinal tract.

There are physical, chemical and biological treatment methods as well as commercially available products that can be added to the diet to reduce the harmful effects of mycotoxin-contaminated animal feed, in addition to pre- and postharvest prevention procedures to control mycotoxin contamination in feedstuffs and feed. Some of the new techniques for controlling mycotoxicosis in animals include enzymes, microbes, antibodies, aptamers, and transgenic crops although binders are the current widely used mycotoxin detoxifiers with varying results [7]. Therefore, to lessen the harmful and economic impact of mycotoxins in feeds, any detoxification technique must meet an essential criteria [63, 79]: The technique must either inactivate or remove the mycotoxins in feeds, avoid producing or leaving toxic residues, not alter the nutritional and technological properties of feed, be capable of destroying fungal spores to prevent the formation of new toxins, and be technically and economically feasible.

Contamination mainly occurs or is encouraged before harvest and during harvesting [80]. Currently researchers worldwide are keen on developing effective methods to prevent preharvest mycotoxin contamination. Preharvest preventive measures include breeding resistant crops, good agronomic practices such as irrigation to prevent plant stress and crop rotation to reduce soil population of mycotoxin producing fungi and harvesting at the optimum stage of maturity [81].

The control of insect infestation in kernels may help to prevent A. flavusand A. parasiticusproliferation and subsequent aflatoxin production [82]. The introduction of non-toxin producing isolates of A. flavusto competitively replace aflatoxin producers is one of the most promising strategies for reducing preharvest contamination of crops with aflatoxin [83]. A good quality product is obtained only when the crop is harvested at the optimum stage of maturity, particularly if it is to be stored subsequently for protracted periods [71]. İt is desirable to harvest early in the day, in the same cases, at the sunset to avoid excessive field heat leading to rapid deterioration and fungal colonization. Where harvesting is done in dry weather, mycotoxin contamination does not prove problematic, it does however pose a problem when harvesting is done in very humid weather [84]. Delayed harvest particularly favors contamination with Fusarium.Mechanically damaged and shriveled grains are regularly contaminated by molds, and moldy grains can partially be removed by separators [85].

Unless the moisture content is safe below the grain-moisture content, which is in equilibrium with humidity of the air component of the grain, the development of fungi and other spoilage organisms is almost inevitable. The easiest and cheapest way of ensuring safe storage is to reduce moisture content before storage. Thus, where natural reduction is prevented by natural conditions at harvest time, the grain must be dried before storage [65]. Mold problems only occur if silage is exposed to oxygen for instance if the silage is not tightly covered, in case of damaged covers or when silage is being fed out to the livestock. İt is recommended to use airtight containers during the ensiling process of forage and if these containers are damaged in any way, repairs must be made as quickly as possible to stop the development of mold [64].

While it is sensible to store feedstuffs under conditions of temperature and humidity that minimize fungal growth, it is often the case that the product has been spoiled before harvest and already contains a considerable amount of mycotoxins [86]. Thus, detoxification processes including biological, chemical and physical methods are often necessary to remove, destroy or reduce toxic effects, without producing or leaving toxic residues or carcinogens in the food and animal feed materials.

7.1 Physical strategies

Irradiation and thermal processing techniques like cooking, boiling, baking, frying, roasting, microwave heating, and extrusion are some of the physical techniques used for reducing or inactivating mycotoxins in feeds [45]. These physical methods including sorting, flotation, and extraction remove mycotoxins from contaminated grain products and/or eliminate the bioavailability of mycotoxins in the gastrointestinal system [87]. Heat treatments are applicable in degrading mycotoxins in feedstuffs. Of the toxins isolated from fungi, more than 90% melt at temperature above 100°C, and 70% have melting point above 150°C and 250°C. However, heat may destroy vitamins and denature proteins and so reduce nutritive value especially at the temperature required for degradation of mycotoxins [88].

7.2 Extraction with solvents

Mycotoxins can be extracted from contaminated food materials like oilseed peanuts and cottonseed using a variety of solvents. 95% ethanol, 90% aqueous acetone, aqueous isopropanol, 80% isopropanol, hexane-methanol, methanol-water, acetonitrile-water, hexane-ethanol-water, and acetone-hexane-water are the most often used solvents [84]. While solvent extraction can efficiently remove aflatoxin from oilseed meals without the creation of hazardous byproducts or a deterioration in nutritional properties, the technique’s large-scale implementation is limited by its high cost and concerns with toxic extract disposal [84, 89].

7.3 Adsorption

One strategy for decreasing mycotoxin exposure is to reduce their bioavailability by incorporating various mycotoxin-adsorbing agents into the compound feed, which reduces mycotoxin uptake and transport to the blood and target organs. Adsorbing agents are substances of high molecular weight that, upon reaching the gastrointestinal system (aqueous medium), can bind mycotoxins, preventing their absorption, and allowing fecal excretion of this adsorbent–toxin complex [90]. They do not dissociate in the gastrointestinal tract of the animal thus preventing or minimizing exposure of animals to mycotoxins.

Mycotoxin-adsorbing agents can be silica-based inorganic compounds or carbon-based organic polymers. Some of the inorganic adsorbing agents utilized include natural clay products as well as synthetic polymers. Activated carbons, hydrated sodium calcium aluminosilicate (HSCAS), zeolites, bentonites, and certain clays are the most studied adsorbents, they possess a high affinity for mycotoxins, and they have shown immense potential for use in animal feeds to overcome aflatoxicosis [77, 84]. Adsorption agents are quite successful in preventing aflatoxicosis, although they are not as effective against other mycotoxins [91]. The main mycotoxins are adsorbed sufficiently by at least one type of adsorbent, but a few adsorbents may be used for various mycotoxins and none of them have been shown to be effective against all toxins (Table 3) [93].

CompoundsAffected mycotoxins
Hydrated sodium calcium aluminosilicate (HSCAS)Aflatoxin B1
ZeolitesAflatoxin B1 and zearalenone
BentonitesAflatoxin B1 and T2 toxin
Specific clays (kaolin, sepiolite and montmorillonite)Aflatoxin B1
Active carbonsOchratoxin and aflatoxin B1
ColestiralamineOchratoxin and zearalenone
Poly-vinyl polypyrrolidone polymers (PVPP)Aflatoxin B1

Table 3.

Some adsorbents and mycotoxins on which they are effective [92].

When supplemented at a concentration of 10 g/kg feed, most of them have been shown to be effective aflatoxins binders. Their effectiveness against mycotoxins such as zearalenone, fumonisins, and trichothecenes, on the other hand, is very limited or non-existent [77]. T-2 toxin can be adsorbed by bentonite, however its inclusion rate in the diet must be 10 times higher (100 g/kg) than the effective amount for aflatoxins [94]. Phyllosilicates such as kaolin and sepiolite, like most clays, are ineffective against mycotoxins other than aflatoxins [95, 96]. Because clay binders are relatively ineffective against mycotoxins other than aflatoxins, natural organic binders have been highly proposed. Organic binders are more effective against a wider spectrum of mycotoxins than inorganic binders, making them better suited to multi-contaminated diets. They’re also biodegradable, which means they will not end up in the environment after being expelled by animals. Clays, on the other hand, which are assimilated at a faster pace than organics, collect in manure and then spread in the field, causing harm to the environment [96].

7.4 Chemical techniques

Mycotoxins have been found to be reduced, destroyed, or inactivated by a variety of chemicals. Acids (e.g., formic and propionic acids), bases (e.g., ammonia, sodium hydroxide), oxidizing compounds (e.g., hydrogen peroxide, ozone), reducing agents (e.g., bisulphite), chlorinating agents (e.g., sodium hypochlorite, chlorine dioxide, and gaseous chlorine), and miscellaneous reagents (e.g., formaldehyde) are some examples of these chemicals which have undergone testing before for their efficacy in mycotoxin decontamination [84, 85, 97]. Even though most of these chemical treatments can remove mycotoxins in feeds, chemical detoxification does not meet the FAO requirements, because they often reduce the nutrient quality of the treated feeds, and some compounds leave behind their toxic metabolites that have unfavorable side effects [84, 85]. This is the fundamental reason why their extensive use in the animal feeds sector is severely constrained.

7.5 Biological techniques

Biological detoxification implies the biotransformation or degradation of a toxin, by bio-transforming agents such as endogenous enzymes to a metabolite that is either non-toxic when ingested by animals or less toxic than the original toxin and readily excreted from the body. Because it works under mild, ecologically favorable circumstances, biological decomposition of mycotoxins has showed promise [98].

A variety of bacteria, yeasts, and molds can degrade aflatoxins. The idea is to utilize enzymes that precisely breakdown each mycotoxin, or class of mycotoxins, into a non-toxic molecule. With recent developments in molecular biology, genetic engineering, and microbial genomics, as well as the discovery of microbial populations’ catabolic capacities, research in this area has expanded. It has been widely proven that microorganisms, such as fungus and bacteria, may breakdown mycotoxins in feed (Table 4) [99, 100, 101]. Saccharomyces cerevisiaeis one of the most successful developing bacteria at binding to AFB1. Strains such as Phomasp., Mucorsp., Trichoderma harzianum, Trichodermasp. 639, Rhizopussp. 663, Rhizopussp. 710, Rhizopussp. 668, Alternariasp. and some strains belonging to the Sporotrichumgroup are some of the fungal strains that have been demonstrated to degrade AFB1 to levels ranging from 65–99% [102].

MycotoxinBinding capacity (%)
Lactobacillus rhamnosusspecies (G.G.)Aflatoxin B180
PropionibacteriumAflatoxin B180
Bifidobacterium bifidumspeciesAflatoxin B2, G1, and G274, 80 and 80
Saccharomyces cerevisiaeZearalenone52
Glucomannan obtained from the cell wallAflatoxin95
Fumonisin45
Deoxynivalenol10

Table 4.

The toxin binding capacity of biological products obtained from yeast cell walls with different bacterial species [92].

Flavobacterium aurantiacumalso shown the ability to effectively remove aflatoxin B1 [103]. Based on a European Food Safety survey, Trichosporon mycotoxinivoranswas found to be the only microorganism that shows the potential to degrade OTA and meets the prerequisites for use as an animal feed additive [104]. Therefore, as endogenous oxidation control systems may be more desirable, extensive research is needed in identifying, characterizing and purifying enzymes involved before this approach becomes more practical [97, 103].

Enzyme-linked immunosorbent assays, thin layer chromatography, high performance liquid chromatography, gas chromatography, near-infrared spectroscopy, and liquid chromatography-mass spectrometry are some of the current analytical methods for detecting and quantifying mycotoxins. Some of these techniques can be applied to samples that contain numerous mycotoxins [7].

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8. Conclusion

Mycotoxins are toxic secondary metabolites produced naturally by fungi that grow on various agricultural commodities. Mycotoxins significantly impact both the productivity and the nutritional value of cereal and forage. Mycotoxin contaminated feeds impact animal health and productivity. Contamination of feeds may occur during pre-harvest and post-harvest. Every year, mycotoxins cause massive economic losses in the animal feed sector and animal husbandry. As a result, measures to remove or inactivate mycotoxins in diet and feed are critical. Different measures to prevent mycotoxin production and its drawbacks are being applied worldwide. On farm measures are efficient in terms of products safety and costly feasible, but there are not enough to completely prevent fungi growth in crops. Therefore, detoxification processes including biological, chemical and physical methods are often used to remove, destroy or reduce toxic effects in feeds or food contaminated in the field. However, traditional physical and chemical procedures have several drawbacks, including limited efficacy, safety concerns, palatability losses, and the high cost of the equipment required to perform these techniques. They have also been criticized to reduce nutritive value of the feeds, and to have side effects on animal and human health. Adsorbents and microorganisms/enzymes use may be more desirable and are currently used as feed additives in many parts of the world. Further research work is needed to weigh out their potential compared to the other methods of detoxification.

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Written By

Zacharia Waithaka Ng’ang’a and Eric Niyonshuti

Submitted: December 8th, 2021 Reviewed: December 13th, 2021 Published: March 14th, 2022