The purpose of this review is to present information about raw materials that can be used in pig and poultry diets and the factors responsible for variations in their mycotoxin contents. The levels of mycotoxins in pig and poultry feeds are calculated based on mycotoxin contamination levels of the raw materials with different diet formulations, to highlight the important role the stage of production and the raw materials used can have on mycotoxins levels in diets. Our analysis focuses on mycotoxins for which maximum tolerated levels or regulatory guidelines exist, and for which sufficient contamination data are available. Raw materials used in feed formulation vary considerably depending on the species of animal, and the stage of production. Mycotoxins are secondary fungal metabolites whose frequency and levels also vary considerably depending on the raw materials used and on the geographic location where they were produced. Although several reviews of existing data and of the literature on worldwide mycotoxin contamination of food and feed are available, the impact of the different raw materials used on feed formulation has not been widely studied.

Fungal species and toxin contamination were determined in 110 cereal samples (54 maize, 35 wheat, and 21 barley) collected in the southeastern part of Romania from 2002 to 2004. The most frequent fungal contaminants belonged to Aspergillus and Fusarium, and maize was the most contaminated cereal. The main toxigenic species identified were Aspergillus flavus, Aspergillus fumigatus, Fusarium graminearum, and Fusarium culmorum in all cereals and Fusarium verticillioides in maize. The presence of aflatoxin B1 (AFB1), deoxynivalenol (DON), zearalenone (ZEA), fumonisins, and ochratoxin A was determined by enzyme-linked immunosorbent assay. More than 90% of the samples were contaminated with at least one toxin. Around 30% of maize samples were contaminated with AFB1, and in 20% of these samples the level of toxin exceeded that allowed by European Union regulations. In 48 and 42% of samples, levels of DON and ZEA, respectively, exceeded those allowed by the European Union. Neither fumonisins nor ochratoxin A were found in samples from any year or cereal. These results indicate that cereals produced in Romania have a particular pattern of mycoflora and mycotoxin contamination because DON and ZEA in addition to AFB1 were found.

The interactions between mycotoxins and gut microbiota were discovered early in animals and explained part of the differences in susceptibility to mycotoxins among species. Isolation of microbes present in the gut responsible for biotransformation of mycotoxins into less toxic metabolites and for binding mycotoxins led to the development of probiotics, enzymes, and cell extracts that are used to prevent mycotoxin toxicity in animals. More recently, bioactivation of mycotoxins into toxic compounds, notably through the hydrolysis of masked mycotoxins, revealed that the health benefits of the effect of the gut microbiota on mycotoxins can vary strongly depending on the mycotoxin and the microbe concerned. Interactions between mycotoxins and gut microbiota can also be observed through the effect of mycotoxins on the gut microbiota. Changes of gut microbiota secondary to mycotoxin exposure may be the consequence of the antimicrobial properties of mycotoxins or the toxic effect of mycotoxins on epithelial and immune cells in the gut, and liberation of antimicrobial peptides by these cells. Whatever the mechanism involved, exposure to mycotoxins leads to changes in the gut microbiota composition at the phylum, genus, and species level. These changes can lead to disruption of the gut barrier function and bacterial translocation. Changes in the gut microbiota composition can also modulate the toxicity of toxic compounds, such as bacterial toxins and of mycotoxins themselves. A last consequence for health of the change in the gut microbiota secondary to exposure to mycotoxins is suspected through variations observed in the amount and composition of the volatile fatty acids and sphingolipids that are normally present in the digesta, and that can contribute to the occurrence of chronic diseases in human. The purpose of this work is to review what is known about mycotoxin and gut microbiota interactions, the mechanisms involved in these interactions, and their practical application, and to identify knowledge gaps and future research needs.