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Mycotoxins and poultry production

by 5m Editor
20 January 2009, at 12:00am

Mycotoxins are substances produced by fungi imperfecti which, in some cases, do protect plants or plant seeds against parasites (Schardl et al., 1996). However, upon ingestion, inhalation or dermal contact, these mold-produced substances are poisonous to vertebrates. Even with more than 100.000 species of fungi known, only some of them are active mycotoxin producers. The fungi species which are known to produce the most hazardous mycotoxins in agriculture and in animal production are Fusarium, Aspergillus and Penicillium sp.

Mycotoxins vary greatly regarding their toxicological effects as they do not belong to a single class of chemical compounds (Jewers, na). The environmental conditions in which they are preferably produced also differ. Fusarium toxins, such as trichothecenes, zearalenone and fumonisins are commonly produced on the field, whereas aflatoxins and ochratoxins are produced by Aspergillus and Penicillium sp mainly after harvest and during poor storage conditions.


It is not easy to detect and to diagnose problems related to mycotoxins once their effects in animals are diverse, varying from immune suppression to death in severe cases, depending on toxin-related (type of mycotoxin consumed, level and duration of intake), animal-related (species, sex, age, breed, general health, immune status, nutritional standing) and environmental (farm management, hygiene, temperature) factors. Moreover, there is a drastic difference between scientific reports and field observations. In scientific feeding experiments animals are usually fed a known quantity of mycotoxins since the objective is to understand the impact of one or two mycotoxins in different parameters. Moreover, animals involved in research have a disease-free status and are kept under controlled conditions in order to minimize the influence of external factors in the results. In the field, however, animals are exposed to a wider range of mycotoxins and are subject to a broader variety of stressing factors. They may be in poor health conditions and fragile immune status and subjected to problematic management practices. All these factors contribute a great deal to the final susceptibility of animals to the presence of mycotoxins. So, it is not surprising if animals exhibit mycotoxicoses even at apparent “low levels” of mycotoxins present in the feed.

mmunosuppression… the hidden enemy

Some effects of mycotoxins cannot be immediately detected by visual examination; nonetheless they are revealed when animals are, for instance, faced with infectious agents. Immunosuppression is one of these effects, as confirmed by several scientific works. Aflatoxins, ochratoxins and trichothecenes – all these toxic compounds are known to decrease the resistance of animals rendering them more susceptible to diseases (Ghosh et al., 1990; Sharma, 1991; Dwivedi and Burns, 1984; Leeson et al., 1995; Singh et al., 1990; Harvey et al., 1991; Kidd et al., 1997).

In general, aflatoxins are the most immune suppressive (CAST, 2003). Aflatoxin B1 intoxication in broilers impacts the cell-mediated immunity by decreasing the albumin and globulin (Ghosh et al., 1990) which is in accordance with the knowledge that aflatoxin exerts an important role in the inhibition of protein synthesis. As for OTA, in 1984, Dwivedi and Burns investigated immunoglobulin concentration in birds’ sera and found out that this was lower in OTA fed birds than in control sera. OTA combination with Salmonella increased by 13.2% the mortality rate of the challenged broiler chicks (Elissalde, 1994). Layers were more susceptible to typhimurium colonization (Fukata et al., 1995). In 2003, the presence of OTA increased mortality and the severity of an E. coli infection in broiler chicks (Kumar et al., 2003) and S. gallinarum infection in the absence of OTA caused 11.5% mortality, which increased to 28.8% in the presence of OTA in broiler chicks diets (Gupta et al., 2005). Trichothecenes were also reported to impact the immune system. DON reduced Newcastle Disease humoral titers of 18 week old pullets and decreased the stimulation index of splenocytes of broiler pullets (Harvey R. B., 1991). T-2 was also shown to be cytotoxic to chicken macrophages in vitro (Kidd et al., 1997).

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