The Influence of Mycotoxins on Poultry Performance
Mycotoxins are a heterogeneous group of secondary fungal metabolites. Their formation in food and feedstuffs is influenced by many factors, including humidity, temperature, pH, oxgen concentration, type of substrate or presence of competitive micro flora.
Mycotoxins have been implicated in a range of human an/or animal diseases and occur in a variety of raw materials. The ingestion of mycotoxins can produce both acute and chronic toxicities ranging from death to chronic interference with the function of the nervous, cardiovascular, pulmonary and endocrine systems as well as the alimentary tract. Some mycotoxins are carcinogenic, mutagenic, teratogenic and immunosuppressive (Proctor, 1994).
The mycotoxins have attracted worldwide attention over the last few decades. This is due to three main reasons. Firstly the effect of mycotoxins on human health, secondly due to the huge economical losses associated with contaminated feeds and the loss of animal productivity, and thirdly due to the impact of mycotoxin contamination on international trade in commodities.
Limited information is available on the transmission of mycotoxins into poultry products, meat and eggs. The objective of this review is to determine to what extent mycotoxins are transferred into poultry eggs and meat.
2. Mycotoxin transfer to poultry eggs and meat
There are more than 300 known Mycotoxins. However, due to their presence and concentration in food, and toxic potential, only a few are relevant to consumer protection. These include the aflotoxins, ochratoxins and trichothecenes like deoxynivalenal, zearalenone and fumonisins (Blank, 2002).
It is important to consider to what extent mycotoxins might be carried over into the edible tissues like meat and eggs, when contaminated feed is fed to poultry. A review by Blank (2002) showed that the carry over of mycotoxins into edible tissues is relatively low and is dependent on the specific mycotoxins and animal species.
At the cellular level, the main toxic effect of the Trichothecenes mycotoxins appears to be primarily the inhibition of protein synthesis, followed by a secondary disruption of DNA and RNA synthesis. Trichothecenes influence the actively dividing cells such as the lining of the gastrointestinal tract, skin, lymphoid and erythoid cells. The toxic action of the trichotheneces results in: extensive necrosis of the oral mucosa and skin in contact with the toxin, acute effects on the digestive tract and decreased bone marrow and immune function.
Typical lesions caused by the trichotheneces in chickens are circumscribed poliferative yellous plaques occurring at the margin of the beak, mucosa of the hard palate, angle of the mouth and tongue. Growth retardation, abnormal feathering, regression of the bursa of Fabricius and anemia, are also observed in chickens exposed to toxic levels of trichotheneces. Laying hens show oral lesions and a decrease in feed intake, egg production, egg and shell quality.
Although the number of known trichotheneces is over 100, information on the natural occurrence in agricultural products indicates that the most important are T-2 toxin and deoxynivalenol (DON), which are all Fusarium produced toxins. The skin and subcutaneous fat apparently act as a reservoir for these toxins, delaying absorption and sustaining metabolism as well as excretion (Leeson et al. 1995). In chickens the absorption of the T-2 toxin appears to be much higher than that of DON, which accounts for its greater toxicity.
Orally or parenterally administered, trichotheneces do not accumulate in the body of animals to any extent and the residues are rapidly eliminated within a few days after exposure (Leeson et al. 1995). In chickens, DON is not significantly distributed into edible tissues. In the study of Lun et al. (1986) no DON residues could be detected in the egg yolk, albumen, or eggshell of laying hens fed on a diet containing 300ppm of DON. Subsequently no residues could either be detected in the breast muscle, thigh muscle, heart, liver or kidneys.
Prelusky et al. (1987) as quoted by Bergsjo et al. (1993) reported that DON and DON metabolite residues might be present in the eggs of laying hens. However, the concentration of these mycotoxins were too low to cause concern over food hygiene, but the effect on poultry reproduction could not be ruled out. Bergsjo et al. (1993) did not report any clinical signs of toxicosis in hens fed diets with 2500, 3100 and 4900 ppb of DON respectively. In the same study, a higher incidence of unabsorbed yolk sac was reported for the progeny of the hens fed the contaminated diet. This was however, not dose related. Cloacal atresia and cardiac abnomalies were also associated with feeding the contaminated feed. Thus when feeding diets contaminated with even moderate levels of DON to laying hens, it may adversely affect the foetal development of their offspring.
The Ochratoxins are a group of 7 fungal metabolites composed by an isocoumarin moiety linked to the amino acid L-�-phenylalanine. The main target organ for ochratoxin is the kidney. At the molecular level ochratoxin interferes with DNA, RNA and protein synthesis by inhibiting the enzyme phenylalanine-tRNA synthetase. Additionally, Ochratoxin also affects renal carbohydrate metabolism through an effect on the renal mRNA coding for phosphoenol pyruvate carboxykinase, which is a key enzyme in gluconeogenesis. Ochratoxin induced alteration of these metabolic pathways, results in damage to the epithelium of renal proximal convoluted tubules, decreased electrolyte absorption and increased water excretion through an osmotic diuresis.
In broilers, the major clinical signs of Ochratoxicosis are poor growth, reduced feed efficiency, increased water consumption, and therefore increased manure moisture. The major effects of Ochratoxins in laying hens are decreased feed intake and egg production, as well as reduced egg weight, specific egg gravity, and increased incidence of shell stains, blood and meat spots.
Residues of Ochratoxin in the edible tissues of poultry were reported in several studies as reported by Leeson et al. (1990). The level of residues is directly (dependant) on the level of Ochratoxin administered in the diet and the period it was fed to the animal. When Ochratoxin was administered to the diet at a level of up to 2.0 ppm Ochratoxin for 8 weeks. Residues were detected in the livers and white muscles of birds fed more than 1.0 ppm ochratoxin and in red muscles of birds receiving more than 1.5 ppm ochratoxin. Four days after the withdrawal of Ochratoxin from the feed, no residues could be detected. Long-term administration of 50 ppb dietary Ochratoxin in higher residues in the livers of broilers (up to 11.0 ppb) than in layers (1.5 ppb). However, the converse situation occurred in the kidney, up to 0.8 and 5.8 ppb in broilers and layers, respectively. Small amounts of Ochratoxin (0.8 ppb) were also detected in the thigh muscle of the hen but not in breast muscle.
Fuchs et al. (1988) demonstrated that Ochratoxin was retained in the egg, by using whole body autoradiography and labeled toxin. In albumen, radioactivity was homogeneously distributed and therefore hard to detect on the film, but in egg yolk clearly defined ring-shape areas of radioactivity were visible. Therefore, according to Fuchs et al. (1988), a permanent intake of Ochratoxin can lead to accumulation of this toxin in the egg, where it can express its teratogenic and embryotoxic effects. Laciakova et al. (2001) reported that mycotoxins, especially Ochratoxin, were able to penetrate the eggshell and accumulate in the egg yolk. This is mainly influenced by the temperature and air humidity in the storage rooms, as well as the contamination of the eggshell with the toxigenic strains of microscopic filamentous fungi producing these mycotoxins.
Aflatoxins are a group of heterocyclic metabolites produced by the fungi of the genus Aspergillus, particulary A. flavus and A. parasiticus. Even though 18 different Aflatoxins have been identified, only Aflatoxins B1, B2, G1 and G2 have been detected as natural contaminants of feeds and feed stuffs. The target organ for the toxic action of Aflatoxins is the liver. Poultry species vary in their susceptibility to Aflatoxins with ducklings being the most sensitive and chickens the most resistant Leeson et al. (1995). The adverse effects of Aflatoxin on broiler performance are both time and dose (dependent). In broilers, toxic levels of Aflatoxin cause a decrease in body (weigth) and feed intake, poor skin pigmentation, depletion of lymphoid organs such as the thymus and bursa of Fabricius, and macroscopic and histologic lesions in the liver. Reduced egg production, egg weight, antibody titers in disease challenged hens and increased liver fat are the most prominent manifestations of aflatoxicosis in layers (Leeson et al. 1995, Proctor 1994).
Asperigillus spp. can grow on a variety of substrates and most foods and feeds are susceptible to invasion by aflatoxigenic strains at any stage of production, processing, transportation and/or storage. The most important factors influencing Asperigillus spp growth and Aflatoxin production are relative humidity (around and in the substrate) and storage temperature. According to Leeson et al. (1995) the optimum conditions in feed mills for Aflatoxin formation are 19 to 27oC, 79 to 89% relative humidity, and 10 to 13% moisture. However, the presence of aflatoxigenic molds on grains does not necessarily mean the presence of Aflatoxin, just as the absence of molds does not mean the absence of Aflatoxins. Aflatoxins are extremely stable in grains and may persist long after mold growth has stopped.
According to Leeson et al. (1995) residues of Aflatoxins can be found in poultry meats and products, but results of a withdrawal trial showed that poultry could metabolize and eliminate Aflatoxin from their tissues in relatively short time (72 to 96h). Azzam & Gabal (1998) detected Aflatoxin in eggs at levels far higher than the permissible concentration, when a level of 200 ppb Aflattoxin were fed (on a daily basis) to hens for 22 weeks. Trucksess et al. (1983) found Aflatoxin B1 and the Aflatoxin metabolite Ro, in eggs after feeding Aflatoxin B1 at al level of 8 ppm for 8 days. The transfer of Aflatoxin and the metabolite occurred rapidly after initial administration and were found in eggs laid only one day after the hens received the contaminated feed. In this experiment the level of Aflatoxin and its metabolite increased until day 4 and 5 respectively, after which it remained constant for the remainder of the trial. After withdrawal of the contaminated feed, the level of Aflatoxin and it’s metabolite decreased rapidly. Low levels of Ro and no detectable levels of B1 were found in the eggs of the treated hens 7 days after the feeding of an Aflatoxin-free diet. From these results it was concluded that Aflatoxin could enter the egg at any stage of development. In this case the yolk was already developed before day 1, thus the Aflatoxin entered the egg with the albumen and diffused directly to the yolk. The distribution of toxin concentration between the albumen and yolk were similar. The same levels of toxin were found in both the ova and complete egg, which indicate that the transmission is relatively constant throughout the process of egg formation. According to Laciakova et al. (2001) Aflatoxin B1 accumulates in the genitals of chickens, turkeys and ducks, resulting in a transfer to the egg (albumen and yolk) as well as to their offspring (yolk sac and liver).
All tissues from the hens that were fed the contaminated diet, contained levels of Aflatoxin B1 and the metabolite Ro, but only Ro could be detected 7 days after the withdrawal of the contaminated feed. Laciakova et al. (2001) showed that the penetration of Aflatoxins through the eggshell, when eggs were stored at sub-optimal conditions, resulted in Aflatoxin concentration of much lower than the maximum concentration allowed (5ppb) within the egg.
The fungus Fusarium moniliforme, Fusarium proliferatum and Fusarium nygamai produces Fumonisins B1, B2 and B3 respectively (Henry & Wyatt 2001). The only commodities in which fumonisins have been detected so far are corn-based animal feeds and human foods. The mechanism of action of Fumonisins appears to be disruption of the synthesis of spingolipids. Exposure to toxic levels of Fumonisins result in an increase in the blood serum levels of sphinganine and sphingosine, while the blood serum levels of complex sphingolipids are decreased. According to Leeson et al. (1995) Fumonisin has a very low toxicity for poultry.
Broiler chicks fed Fumonisin contaminated feed showed an increase in the liver, kidney and proventriculus weights as well as an increased mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration (Henry & Wyatt 2001). Henry & Wyatt (2001) concluded that laying hens might be able to tolerate relatively high concentrations Fumonisins for long periods of time without effecting health and performance. No information on Fumonisin residue in poultry meat and products is currently available (Proctor 1994).
Zearalenone is a phenolic resorcyclic acid lactone with potent estrogenic properties, primarily produced by Fasarium roseum (Leeson et al. 1995). Zearalenone is regarded as not very toxic to laying hens and broilers. According to Allen et al. (1981) high dietary concentrations of Zearalenone up to 800 mg/kg of feed did not have any detrimental effects on layer performance.
However, the feeding of Zearalenone contaminated feed to laying hens might cause residues of the toxin in the yolk, which could have an influence on human health. Danicke et al. (2002) found that dietary levels of 1.1 mg/kg Zearalenone fed to laying hens does not result in detectable residues of either Zearalenone or its metabolites in the egg yolk, albumen, abdominal fat, breast meat or ovaries.
The carry over of mycotoxins in to the eggs and meat of poultry are relatively low. Furthermore, after a short withdrawal period combined with the feeding of non-contaminated diets, most of the mycotoxins except for Ochratoxin, are no longer detectable in the edible tissues of poultry. On the other hand the mycotoxins such as DON, Ochratoxin, Aflatoxins and Aurofusarin may have detrimental effects on embryo development and hatchability.
Date published: 2004-06-18
Dr. D. Barnard and