The major effects of fungal deterioration of grains include decreased germination, discoloration, development of visible mold growth, musty or sour odors, dry matter loss and nutritional heating, caking, and the potential for production of mycotoxins in the grain. Decreased germination of the grain occurs when storage fungi invade the germs or embryos of the grain kernel. The embryos are weakened and die as the storage fungi attack and parasitize the embryo to utilize its oils and other nutrients. Decreased germination caused by storage fungi usually precedes discoloration. However, discoloration can be caused by both field and storage fungi and can result in brown to black germs in wheat and corn and “blue eye” in corn, due to the presence of blue Aspergillus and Penicillium species. Musty odors may become apparent before mold growth becomes visible and is an early warning of mold activity, as is heating.
Heating often starts in the fine materials or dust associated with the grain and is due to the growth of storage fungi. If sufficient heating occurs, the grain becomes dark and blackened. Further growth of storage fungi may result in surface growth and binding of the grain kernels together by mold hyphae, which is manifested as caking of the grain (i.e., large masses of the kernels bound together). By the time caking occurs, mold growth has become extensive and the grain is in advanced stages of decay. At this point the moisture content of the grain is increasing due to the respiration of the molds, and growth of yeasts and bacteria may also occur.
Mycotoxins
The word mycotoxin is derived from the Greek word mykes, meaning fungus or mold, and the Latin word toxicum, poison or toxin. Thus, mycotoxin is a general term meaning fungus poison or mold toxin. Mycotoxins are toxic secondary metabolites produced by filamentous microfungi or molds. These secondary metabolites are distinguished from primary metabolites because they are not required for the growth of the fungus and have no apparent purpose in the metabolism of the organism. It has been speculated that mycotoxins are waste products or defense mechanisms. Mycotoxins are toxic and harmful in varying degrees to humans and animals, and may contaminate cereal grains in the field and in storage. Mycotoxins are stable compounds that resist destruction by food-processing methods and may carry through and contaminate finished processed foods.
There are numerous specific mycotoxins that may contaminate cereal grains, such as aflatoxins, ochratoxin, fumonisins, moniliformin, deoxynivalenol, T-2 toxin, and zearalenone. Mycotoxin research began in 1960 with the outbreak of Turkey “X” disease in England, where thousands of turkey poults and other young farm animals were lost due to poisoning by a fungal metabolite produced by Aspergillus flavus in peanut meal. The toxic substance was called aflatoxin (A. flavus toxin). Since 1960, many other toxic mold metabolites have been described. Those mycotoxins currently thought to be most important in cereal grains are listed in Table 2 (see p. 28) along with the molds that produce them.
Mycotoxins exhibit a range of toxicological properties, including acute toxicity or poisoning, which often results in death, and subacute or chronic toxicity, which may not result in death directly but which gradually weakens and lowers the general health of an animal or human due to effects on the immune system. Chronic toxicity may result in greater susceptibility to secondary bacterial infections. Some mycotoxins are carcinogenic and may cause cancers; some are mutagenic and are capable of causing mutations; they may also be teratogenic and embryo toxic, causing deformities and death in developing embryos.
Media, Methods for Molds and Mycotoxins
There are a variety of media and methods for detection and enumeration of molds in cereal products. Many media are recommended by the International Commission on Food Mycology (ICFM) as well as given in the Compendium of Methods for the Microbiological Examination of Foods.
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