1. Background

Mycotoxins are known to affect human and animal health since 1370s BC. Ergotism or St. Anthony's fire is one of the oldest known mycotoxins. The mysterious deaths of archeologists are also considered due to the prevalence of ochratoxin A (OTA) in certain Egyptian tombs [1]. In 1673, the disease was linked to consumption of grains infected with ergot (sclerotia of

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and eproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Claviceps purpurea) in France. An epidemic resulted in first ergotism control measures in 1770. In 1952, an outbreak of "moldy corn toxicosis" was caused by the consumption of mold contaminated corn-based feed for swine in southern USA [2]. In the early 1960s, over 100,000 turkey poults and 20,000 ducklings, pheasants and partridges poults in England died with clinical signs of liver necrosis and biliary hyperplasia. This incidence brought together world renowned scientists under the umbrella to resolve the puzzle related to turkey "X" disease [3, 4]. Brazilian peanuts used in formulating feeds for these domesticated animals were found to be heavily infected with aflatoxin B1 (AFB1) were found to be the main reason for this huge fatality after a series of analyses in England [3] and was named after Aspergillus flavus in 1962. A year later (in 1963), its complete structure was characterized by Prof. Buchi's team [1] and subsequently, aflatoxins (AFs) were further categorized as AFB and AFG because of blue and green fluorescence under UV light, respectively [3]. The most extensively publicized case came under the spotlight with an outbreak in humans in western India in October 1974 [5]. Unseasonal rainfall resulted in extensive mold production of extremely high AFs (6.3– 15.6 mg/kg) in corn crops [6]. In 2004, several hundreds of Kenyans became severely ill and almost 125 casualties were reported during an acute aflatoxicosis outbreak [7]. Since the identification of Aflatoxins (AFs) in 1965, the momentum of scientific paper publication toward mycotoxin is an increasing trend where 16,821 papers are recorded in Scopus and is an indicative of its importance [8].

countries with mycotoxins regulations should have at least regulatory limits for AFB1 or the sum of AFB1, AFB2, AFG1, and AFG2 in foods and/or feeds [11]. Mycotoxins exposure includes both pure mycotoxins and also masked mycotoxins which are formed when plants protect

Aflatoxins: Their Toxic Effect on Poultry and Recent Advances in Their Treatment

http://dx.doi.org/10.5772/intechopen.80363

127

Cereals and their products are susceptible to fungal invasion that may be accompanied by mycotoxin production [17]. Approximately 25–40% of cereals produced worldwide are directly or indirectly contaminated with mycotoxins especially AFs with annual losses of around 1 billion MT of food products [9, 18]. A. flavus and A. parasiticus are responsible for producing AF during storage particularly in hot and humid countries in the tropics as com-

A. flavus is commonly found in energy rich concentrates (corn, rice etc.) and protein rich concentrates (peanuts, cottonseed etc.) but are not commonly found in tree nuts. A. parasiticus occurrence in South East Asia is rare and has the same hosts as those of A. flavus [20]. A. flavus is generally responsible for AFB1 and AFB2 production, whereas A. parasiticus produces AFB1, B2, G1 and G2 [3]. AFB1 ranges 77% of total AFs as major contaminant in cereals [21]. In the grains, the germ is the main site for Aspergillus sp. development which leads to greater

The on-going global warming is going to be an alarming condition for the aflatoxins contamination [8]. Williams et al. [23] observed that improperly dried stored food is commonly

temperatures that range between 24 and 35C and moisture content >7% (10% with ventilation). About 4.5 billion people are chronically exposed to AFs in developing countries. Tropical and sub-tropical regions have favorable environment for AFs production as compared to

Binder et al. [11] found low concentrations of Deoxynivalenol, T-2 toxin and Zearalenone as major contaminants in European (temperate areas) feed samples while AFs, DON, FUM and ZON tended to be dominant in Asia and Pacific (tropical areas) significantly. Elzupir et al. [25] found a total of 64.29% animal feed (130.63 μg/kg) and 87.50% manufactured animal rations (54.41–579.87 μg/kg) followed by 69.32% groundnut samples (4.07–79.85 μg/kg) contaminated with AFs in Khartoum State of Sudan. Summer was found to be the most favorable for AFs growth (78.95% samples) followed by autumn (66.67% samples) and winter season (43.37% samples). AFB1 was found the most common contaminant followed by AFG1, AFB2 and AFG2.

N and 40

S of the equator with

themselves by conjugating mycotoxins to biopolymers [8].

pared to those in the temperate regions of the world [9, 19].

invaded by fungus (Aspergillus sp.) in areas within latitude 40

potential of AF accumulation [22].

temperate region [19, 24].

4. Mycotoxin occurrence

3. Factors affecting mycotoxin production

## 2. Mycotoxins

Mycotoxins (MW 700 Da) are secondary metabolites produced by mycelial filamentous structures, specifically called molds [4, 9, 10]. Aspergillus, Penicillium and Fusarium species are responsible for the production of most prevalent mycotoxins, i.e. AFs, ochratoxin, zearalenone, deoxynivalenole, trichothecene-2, etc. [11]. Cereals are more prone to mycotoxins contamination by fungal growth on plants in fields or fungi growing saprophytically during storage. Not all fungal growth results in mycotoxins production (e.g. penicillin, is widely used an antibiotic) or the detection of fungi implies necessarily the presence of mycotoxins [12, 13]. All the secondary metabolites from molds do not impose toxic effects [4].

In response to the environment, five different mechanisms are involved in the production of mycotoxins viz. secondary fungal metabolism, bioconversion of plant compounds (dicoumarol), defense mechanism of plants to fungal aggression and plant-fungus associations [9]. Among the environmental conditions, agronomic practices including harvesting technology as well as the health status of the plant are the most approachable factors for fungal contamination in plants and ultimately mycotoxin production. Humans and animals can be exposed to mycotoxins by various routes like ingestion, aerosol and placental routes [14], which may lead to different fatal consequences as these toxins can be carcinogenic, neurotoxic and immunotoxic, mutagenic, teratogenic, esterogenic and/or hepatotoxic [15]. The severity of health effects posed by mycotoxins depends on species, sex, age, nutritional status, etc. [16]. AFs, OTA and possibly fumonisin B1 (FB1) have been classified as being carcinogenic [9]. All countries with mycotoxins regulations should have at least regulatory limits for AFB1 or the sum of AFB1, AFB2, AFG1, and AFG2 in foods and/or feeds [11]. Mycotoxins exposure includes both pure mycotoxins and also masked mycotoxins which are formed when plants protect themselves by conjugating mycotoxins to biopolymers [8].
