Mycotoxins and poultry production
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.
Immunosuppression… 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).
Abnormal behavior… wet litter… strange occurrences? That could be mycotoxins!
Other impacts related with the presence of mycotoxins are: toxicity related with the nervous system (neurotoxicity); effects related with the production of blood cells (hematopoietic effects); kidney problems (nephrotoxicity); gastro-intestinal effects; problems related with feathering and mucous membranes (dermal effects) and birth defects of the offspring (teratogenic effects). The impact in all this different systems can often be recognized as animals show abnormal behavior or the daily routine of the farm is disturbed. Birds standing together in groups can be a sign of nervous syndrome caused by aflatoxins (Leeson et al., 1995)(Figure 2). Other signs of neurotoxicity include lack of reflexes and abnormal wing positioning caused by T-2 toxin (Wyatt et al., 1973). Pale bird syndrome is expressed in the animal by the paleness of the mucous membranes and legs. This syndrome is caused, amongst other factors, by aflatoxins intake (Tyczkowski, 1987) and may lead to the downgrading of the carcasses due to improper colouring. Although expressed by the color of the skin, jaundice (yellow skin) is actually a reflex of the hepatic alterations and hepatotoxic effects also caused by this toxin (Dalvi, 1986). Along with this, impaired feathering may also be observed, either by the ingestion of aflatoxins or trichothecenes (Leeson et al., 1995; Wyatt, 1975). The ingestion of these two groups of mycotoxins and fumonisins may also lead to the occurrence of hemorrhages, anemia or other hematological disorders (Weidenbörner, 2001; Kidd et al., 1997; Jand et al., 2005). Birth hatch defects caused by aflatoxins (Cilievici, 1980) will increase the number of chicks which are rejected at the beginning of the production cycle, with clear economic impacts. Diarrhea has been associated with the ingestion of trichothecenes (mainly DON) and fumonisins (Jand et al., 2005; Satheesh et al., 2004). This condition, as well as the increased water consumption and renal dysfunction caused by ochratoxins (Elling et al., 1975; Hamilton et al., 1982; Leeson et al., 1995) have serious impacts of the daily management of a production unit. In general, poultry are quite resistant to zearalenone; however, enhanced secondary sex characteristics and vent enlargement are stated in literature as effects caused by this toxin (CAST, 2003).
Figure 2: Nervous syndrome cause by aflatoxins
And moneywise… what are the effects?
Decreased feed intake and feed refusal, reduced daily weight gain and inhomogeneous flocks, impaired FCR, lower slaughter weight, decline on egg production, egg size, egg weight, egg shell quality, egg hatchability and higher mortality rates. These are the numerous effects which are observed in poultry fed mycotoxin-contaminated diets. Type A trichothecenes (T-2 toxin, HT-2 toxin, diacetoxyscripenol) are of major concern to poultry industries and cause economic losses in productivity. They are highly toxic to poultry, especially broiler chickens as they have very low LD50 values (2 mg/kg for diacetoxyscirpenol and 4 mg/kg for T-2 toxin) (Leeson et al., 1995). An outbreak of a disease associated with the presence of T-2 in moldy barley was observed in poultry (ducks, geese). Lesions in the geese included necrosis of the mucosa of the oesophagus, proventriculus, and gizzard. (Greenway & Puls, 1976). T-2 toxin reduces feed intake, body weight, egg production and causes oral lesions (Wyatt et al., 1975). Young chicks and turkey poults are highly sensitive to ochratoxins (Leeson et al., 1995). These nephrotoxins can suppress feed intake, growth, egg production and additionally, they cause poor egg shell quality (CAST, 2003). Fumonisins are associated with spiking mortality in poultry (Jand et al., 2005). Signs of dietary fumonisin are decreased body weight and average daily weight gain as well as increased gizzard weight (Ledoux et al., 1992; Weibking et al., 1993). Other effects which can mean lower carcass value are, for example, the occurrence of higher number of bruises and bruised broilers caused by the increased capillary fragility due to aflatoxins ingestion. According to Tung and his team at 0.625 ppm AfB1 the minimum force required to bruise a broiler was lowered (Tung et al., 1971). His experiment was done in 1971, without the stress of modern production systems.
Pathological changes – another prove of mycotoxins presence
Changes in the organs weight, texture and/or coloration may be observed in the carcass after slaughtering if animals were fed mycotoxin-contaminated diets. Weight variations have been reported after ingestion of aflatoxins: positive for liver, spleen and kidneys (organs' enlargement) and negative for bursa of Fabricius and thymus (organs' reduction). Other pathological changes related with the ingestion of this mycotoxin comprehend the change in texture and coloration of liver and bursa of Fabricius (Espada et al., 1992; Jand et al., 2005; Leeson et al., 1995; Virdi et al., 1989). However, these alterations are not only related with aflatoxins ingestion; other groups of mycotoxins have been associated with necrosis of lymphoid and hematopoietic tissues, gizzard lesions (trichothecenes) and kidney and liver weight increase and liver necrosis (fumonisins) (Hoeww et al., 1981; Huff et al., 1988; Lun et al., 1986; Ledoux et al., 1992; Leeson et al., 1995; Satheesh et al., 2004). In some countries, in case livers are expected to be sold, special attention should be taken regarding this aspect, as they might be rejected after inspection due to pathological changes.
Residues in animal products – food safety in risk?
Unfortunately, when mycotoxins in animal production are referred to, problems do not end with the slaughtering of animals. The carry-over of these compounds is known to occur for some of them, namely for aflatoxins, ochratoxins (Micco et al., 1987; CAST, 2003; Petersson, 2004) and FUM (Vudathala et al., 1994). Aflatoxin B1 and aflatoxicol - a carcinogenic metabolite of the carcinogen aflatoxin B1 (Wong and Hsieh, 1978) were found in eggs and tissues of laying hens consuming aflatoxin contaminated feeds (kidneys, liver, muscle, blood and ova). Aflatoxin M1 – classified by International Agency for Research on cancer (IARC) as a possible human carcinogen – was found only in the kidneys (Trucksess et al., 1083). Micco and his team studied the long-term administration of low doses of mycotoxins in poultry and reported that OTA residues in liver were higher in broilers (up to 11.0 ppb) than in hens (1.5 ppb), whereas the reverse occurred in kidney (up to .8 and 5.8 ppb, respectively) when animals were fed 50 ppb OTA contaminated feed from 14th day of age onward. IARC has evaluated OTA and included it in "Group 2B: Possibly carcinogenic to humans" (IARC, 1993). Although found at very low levels to, alone, represent a danger to human health, these might be other concerns for producers who care about the quality of products they deliver.
Mycotoxin Risk Management
Binders have been used throughout the years allegedly to counteract mycotoxins in animal feeds. This solution has been proved efficient against aflatoxicosis, but regarding other mycotoxins such as zearalenone and ochratoxin it was shown to be very limited or practically zero in the case of trichothecenes (Huwig et al., 2001). The problem is that due to their different nature and diverse chemical structures not all mycotoxins can be effectively adsorbed; therefore the successful approach to manage a diverse range of mycotoxins must comprehend not only adsorption but also biotransformation. Biotransformation stands for the conversion of mycotoxins into non-toxic metabolites by the action of enzymes or life microbes. It is known for years that some microorganisms are able to degrade some mycotoxins. However, only certain microorganisms, e.g., Biomin® BBSH 797 and Biomin® MTV, which have the potential to degrade trichothecenes (namely deoxynivalenol), ochratoxin A and zearalenone, meet the prerequisites for use as animal feed additives (Schatzmayr et al., 2006). Mycofix® gathers adsorption, biotransformation and bioprotection (plant and algae extracts for immune- and hepatoprotection) in one product – the most complete tool for a proper Mycotoxin Risk Management!
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