Mycotoxins are pervasive and dangerous fungal metabolites in feedstuffs formed in the field pre-harvest and under sub-optimal storage conditions post-harvest. Consumed by livestock and poultry, they can reduce performance and alter metabolism, possibly causing pathological states-mycotoxicoses-in both animals and humans. Mycotoxin contamination can result from a range of mycotoxin-producing fungi depending upon the feedstuff source, crop conditions, storage temperature, available moisture, etc. On a global basis, Fusarium mycotoxins are likely the most common mycotoxins (Wood, 1992)

Both the global frequency of mycotoxin contamination of feedstuffs and severity of mycotoxicoses in livestock and poultry appear to be increasing in recent years (see appendix of the article). However, increased international trading of feedstuffs contributes to the severoty of mycotoxicoses as this increases the chance that a given compound feed will contain components of widely varying geographical origins. Such blends of ingredients increase the chance of the feed containing mixtures of different mycotoxins. This can result in toxicological synergies that increase the severity of mycotoxicoses (Speijers and Speijers, 2004).

Synergy of multiple mycotoxins

One clue that toxicological synergy involving mycotoxins occurs is that symptoms typical of mycotoxicoses are seen despite analysis of the feed that indicates only very low concentrations of mycotoxins (Trenholm et al., 1983). In this situation, it is not clear if a mycotoxin problem really exists, or if poor performance is due to management or nutritional factors. It is now known that unexpected toxicity may be due to toxicological interactions between different mycotoxins that exaggerate the toxicity. The likelihood of this occuring is greatest for the Fusarium mycotoxins.

Other research shows that feeding naturally-contaminated feedstuffs produces grater toxicity than feeding of an equivalent amount of purified mycotoxin (Trenholm et al., 1994). Fusaric acid, the most common of the Fusarium mycotoxins (Bacon et al., 1996), can increase the toxicity of the trichothecenedeoxynivalenol (DON or vomitoxin) (Smith et al., 1997). Fusaric acid, however, is seldom analysed in feeds due to its low toxicity when consumed in the absence of other toxins (Smith and MacDonald, 1991; Smith and Sousadias, 1993).

Adsorbents against mycotoxicoses

A variety of approaches have been used to prevent and treat mycotoxicoses in livestock and poultry, but the use of speciality feed additives referred to mycotoxin adsorbents is the most common (Huwig et al., 2001); Romos et al., 1996). For example, alfalfa fibre can have protective effects against zearalenone (James and Smith, 1982; Stangroom and Smith, 1984) and T-2 toxin (Carson and Smith, 1983b) but alfalfa is also often a source of Fusarium contamination in diets.

Hydrated sodium calcium aluminosilicate (HSCAS) has been shown to have potential to reduce aflatoxicosis, but has been shown not to be effective against Fusarium toxicoses (Patterson and Young, 1993). Bentonite has been shown to be effective against T-2 toxin (Carson and Smith, 1983a), but only at levels that are not practical in animal feeds. Other types of clays also have some potential benefits against T-2 toxin, but again only at very high levels of dietary inclusion (Smith, 1984). The problem of high levels of dietary inclusion of adsorbents has been overcome with the development of polymeric glucomannan mycotoxin adsorbents (GMA), which are extracted from the cell wall of yeast.

Another approach for the prevention of mycotoxicoses is the use of feed additives containing enzymes selected to ‘detoxify’ mycotoxin molecules in the lumen of the digestive tract. The challenge to this approach is to identify enzymes non-specific enough to detoxify combinations of mycotoxins that might produce toxicological synergies, but also specific enough to not cause structural damage to the digestive tract or to interfere with digestive function. Van der Eijk (2003) described such an enzyme product that will compromise the effectiveness of ELISA mycotoxin assay kits when assaying feeds. This would imply a high degree of non-specificity which could impair digestive function. Thermal stability of enzymes in pelleted or extruded feeds is also a concern.

In-vitro and in-vivo testing of additives

Van der Eijk (2003) also addresses the comparison of in-vitro and in-vivo methods for determining the efficacy of mycotoxin detoxification technologies. Simple in-vitro systems (constant pH and duration of incubation) do not correlate well with in-vivo feeding trials. This was demonstrated by Rotter et al., (1989) in the testing of activated charcoal to overcome ochratoxin A toxicity in poultry. Similar conclusions were drawn by Diaz et al., (2002, 2004) in determining the efficacy of different adsorbents to reduce aflatoxin M1 in milk. Nonetheless, even the most sophisticated in-vitro models (Zeijdner and Havenaar, 2003) cannot account for environmental factors that can indirectly influence the severity of mycotoxicoses under field conditions.

To approximate field conditions it is necessary to conduct in-vivo demonstrations of the efficacy of mycotoxin adsorbents. While the body of research on pigs continues to grow, some of the most recent work focuses on poultry.

Broilers

A total of 360 broiler chicks of a commercial strain were fed 4 diets for 56 days (Swamy et al., 2002a). The diets included: (1) control; (2) low level of contaminated grains (4.7 ppm deoxynivalenol + 20.6 ppm fusarc acid + 0.2 ppm zearalenone); (3) high level of contaminated grains (8.2 ppm deoxynivalenol + 21.6 ppm fusaric acid + 0.56 ppm zearalenone); and (4) high level of contaminated grains + 0.2% GMA (9.7 ppm deoxynivalenol + 21.6 ppm fusaric acid + 0.8 ppm zearalenone). Weight gain and feed intake were determined weekly. Blood and biliary samples were collected after 3 and 8 weeks and were analysed for hematology and serum chemistry.

The feeding of increasing levels of contaminated grains to broilers resulted in a linear decrease in growth rates and feed intake (P<0.05, Table 1).

Table 1.

Broilers: Effect of feeding blends of grains naturally-contamined with Fusarium mycotoxins on weight gain and feed consumption

This was not seen, however, until birds were in the grower phase. Elevations in red blood cell count and in serum hemoglobin and uric acid concentrations were noted at the end of the study (Table 2).

Table 2.

Broilers: Effect of feeding blends of grains naturally-contamined with Fusarium mycotoxins on hematology, serum chemistry and breast meat colouration

Most of these effects were prevented by the feeding of GMA.

In this work, the feeding of contaminated grains to broilers resulted in reduced growth only in the grower and finisher phases, which supports the concept that broilers do not exhibit feed refusal in manner similar to swine fed Fusarium mycotoxin contaminated diets (Smith et al., 1997). The absence of this protective behaviour in broilers results in numerous adverse metabolic changes that progress with the consumption of contaminated materials. The reason for this species difference has been shown to be differences in the effects on brain neurochemistry (Swamy et al., 2004b). The feeding of contaminated grains to pigs elevated brain serotonin concentrations. In broilers, such treatments elevated both serotonin and catecholamines, thereby canceling the effect of serotonin on appetite suppresion.

It is likely that mycotoxin-induced growth suppression in the broilers in these trials was due to gradual alternations in metabolism that occured with extended feeding of contaminated grains. The alterations in red blood cell counts and hemoglobin contrentrations were similar to blood changes seen in ascites. In the current study, this may have been partially due to the hypotensive effect of fusaric acid. Reduced blood flow to the lungs may have constituted a stress which resulted in an adaptation and increased oxygen trapping capacity of the blood. The elevations in serum uric acid concentrations may be a reflection of the reduction in hepatic protein synthesis caused by the trichothecene mycotoxins deoxynivalenol and 15-acetyldeoxynivalenol. Elevated free amino acid concentrations would result in increased amino acid oxidation and increased nitrogen excretion in the form of uric acid.

Layers

For 12 weeks, a total of 145 laying hens (45 weeks old) were fed diets including: (1) control; (2) contamined grains + 0.2% GMA (Chowdhury and Smith, 2004). The diets including contaminated grains were found to contain 12 ppm deoxynivalenol, 0.5 ppm 15-acetyldeoxynivalenol and 0.6 ppm zearalenone. Parameters measured after 4, 8 and 12 weeks included feed consumption, rate of lay, egg and egshell quality and plasma chemistry.

The feeding of contaminated grains to laying hens decreased feed intake relative to controls in the first month, but increased feed intake relative to controls in the first month, but increased feed intake thereafter (Table 3).

Table 3.

Layers: Effect of feeding blends of grains naturally-contamined with Fusarium mycotoxins on feed consumption and feed efficiency

This resulted in a large deterioration of feed efficiency in the latter months of the experiment. Egg production  also declined in months 1 and 2 (Table 4).

Table 4.

Layers: Effect of feeding blends of grains naturally-contaminated with Fusarium mycotoxins on organ weights and plasma uric acid concentrations