Mycotoxins in Poultry Feed
Mycotoxins are toxic substances produced by molds and fungi on plants, in the field, or during storage.
The BIOMIN Mycotoxin Survey provides regular updates on the occurrence of mycotoxins in the raw commodities and finished feed based on thousands of samples collected from across the globe in addition to regional reports on US corn-based feed ingredients.
Mycotoxin contamination found in complete feed is often from multiple ingredients, regularly resulting in flock exposure to multiple mycotoxins over the course of their time in production.
Overall, mycotoxin risk management is critical to reduce the effects on bird health and performance, which when unaddressed, can lead to significant economic losses for producers.
General effects of mycotoxins on poultry
The presentation of mycotoxicosis is a culmination of factors, including the nature of the mycotoxin exposure (duration, concentration, types of mycotoxins), the environment (management, hygiene, other pathogens, and stressors), and the status of the bird itself (species, life stage, sex).
Compared to other livestock species, such as swine, poultry are generally considered more resistant. However, young birds and or those involved in breeding or producing eggs can be display higher sensitivity. Additionally, poultry have mixed sensitivity to mycotoxins, as different species suffer from different toxic effects. Ducks, geese, and turkeys seem to be more sensitive to mycotoxicoses than chickens and quails.
Mycotoxins in general have drastic effects on the gastrointestinal tract, where the mycotoxins make direct contact to the gastrointestinal mucosa. Once mycotoxins are taken up into the blood stream, various internal organs and systems can be impacted. The liver, kidneys, and immune system can also be affected by several different toxins. Clinical presentations involving the respiratory system, nervous system, and integument can be observed depending on the mycotoxins present, while the reproductive system can be impacted through direct and indirect effects depending on degree of challenge. Overall mycotoxin exposure can culminate in decreased performance and increased sensitivity to pathogens.
These toxins are commonly found in areas where crops are subjected to heat and drought stress, and can be found in sub-optimal storage conditions. The discovery of aflatoxins and aflatoxicosis in poultry began in England in the 1960’s when it was found that groundnut meal imported from Brazil was the source of an outbreak of disease of unknown etiology in turkeys, then known as Turkey X Disease. Since then, the source of aflatoxin has been elucidated as being the mold Aspergillus flavus.
Aflatoxins can cause death when administered at high levels, but the greatest impact comes from reduced reproductive and performance capabilities. In general, common aflatoxin symptoms in poultry include decreases in performance - reduced weight gain and feed conversion rate (FCR) -, as well as weight and size variation of the organs such as the liver, spleen, kidneys, bursa of Fabricius and thymus. Aflatoxins in poultry feed have been shown to suppress the immune system, cause hepatocellular damage and fatty liver syndrome in multiple poultry species, and are highly carcinogenic. Aflatoxins can carry over into eggs, meat, and organ tissue (kidney, liver, ova).
Type A-Trichothecenes (A-Trich) are of major concern to the poultry industry and can cause severe productivity losses. This group consists of a group of multiple toxins, the best known of which are T-2 toxin and HT-2 toxin. Type A-Tricothecenes are considered more potent compared to Type B-Trichothecenes and are so potent that they can cause contact lesions in the oral mucosa and throughout the gastrointestinal tract of poultry. T-2 toxin in poultry has been shown to cause reduced feed intake, body weight, egg production, and impaired nutrient absorption. These toxins have also been known to contribute to immune suppression.
Deoxynivalenol, acetyldeoxynivalenol, fusarenon X, and nivalenol, are all mycotoxins that are part of the Type B-Trichothecenes family. The most well-known is deoxynivalenol (DON).
Deoxynivalenol inhibits intestinal nutrient absorption and alters intestinal cell and barrier functions. These mycotoxins significantly affect the immune system, reducing lymphocyte proliferation, macrophage activity, and antibody response to certain vaccinations and influence immunoglobulin levels.
Additionally, numerous studies have indicated that DON, by itself or in combination with other mycotoxins, may be a predisposing factor for several diseases, including necrotic enteritis in broiler chickens.
Fumonisins (FUMs) are mycotoxins produced by Fusarium proliferatum and F. verticilloides. These mycotoxins occur worldwide and are predominant contaminants of corn and corn by-products. This group of mycotoxins mainly consists of fumonisin B1 (FB1), FB2 and FB3, with FB1 being the most toxic. FUMs disrupt the metabolism of sphingolipids (important components of cellular membranes and neural tubes) through the inhibition of the enzyme ceramide synthase, resulting in increased sphinganine to sphingosine (Sa/So) ratios. These mycotoxins are generally poorly absorbed by the gastrointestinal tract, hence intestinal cells are exposed to their toxic effects for longer periods of time and this can result in their damaging.
Main symptoms observed with fumonisin exposure in poultry are decreased body weight and average daily weight gain, mostly attributed to modulation of intestinal function and disruption of gut integrity. Although commonly thought to require high levels to impact bird health, chronic exposure can have profound impacts to gastrointestinal health, the immune system, and liver and lung function. Fumonisins are an important consideration in mycotoxin risk management programs as they act as predisposing factors for diseases in multiple ways, and amplify the impacts of DON.
Despite relatively low levels of acute toxicity, zearalenone (ZEN) can have a significant impact on reproduction. In comparison to other species, such as swine, poultry are less sensitive to ZEN. The negative effects are due to the interaction of ZEN and its metabolites with estrogen receptors. Due to this interaction, ZEN may have some negative effects on both fertility and hatchability of fertile eggs.
Young chicks and turkeys are very sensitive to ochratoxins. These nephrotoxins suppress feed intake, growth, egg production and have a negative influence on eggshell quality. Ochratoxin A exposure has also been shown cause immunosuppression in birds by negatively impacting cellular, humoral, and innate immune responses. Furthermore, ochratoxin A tends to accumulate in kidneys, liver, and muscle tissues, as well as in blood serum and, therefore, it represents a potential hazard in the human food chain.
Synergistic effects of mycotoxins
Toxicological interactions between mycotoxins enhance the toxic effects, even at low levels.
Fusarium graminearum and Fusarium culmorum are known to produce several different fusariotoxins, including zearalenone and deoxynivalenol, which are known to interact synergistically. In addition, the analysis of deoxynivalenol often indicates the co-occurrence of other fusariotoxins such as other trichothecenes (T-2 toxin, nivalenol, diacetoxyscirpenol), zearalenone, and fumonisins.
Diagnosis of mycotoxicosis
Mycotoxicoses are diseases caused by ingestion of mycotoxins, inhalation, or contact with the skin. The effects of mycotoxins in poultry species are diverse, varying from immunosuppression to death in severe cases, depending on various factors including those which are 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, biosecurity, hygiene, temperature). This complexity often impedes correct attribution of problems caused by mycotoxins.
There are multiple diseases in poultry species that are attributed to stress stimuli and are opportunistic infections. Mycotoxins have been shown to be sufficient to induce and exacerbate multiple diseases, and thus preventative health programs for flocks need to have a mycotoxin risk management plan in place.
Mycotoxin risk management
Robust mycotoxin risk management comprises three steps:
Reducing exposure to mycotoxins in feed is key. Regular analysis of feed and/or feed ingredients can help to uncover potential threats to birds. Identifying contamination can help to reduce exposure and determine what the best options are for prevention and mitigation. However, a highly contaminated sample does not mean the entire crop is bad and a ‘clean’ sample does not guarantee that all of the feed is mycotoxin-free.
Good storage practices, along with proper bin and feeder management, are essential to avoid further growth of molds and thereby prevent the production of additional mycotoxins.
When it comes to counteracting mycotoxins, the poultry industry tends to think of toxin binders or mycotoxin binders first. Regular application of mycotoxin binders is advisable; however, clay mineral binders are not an effective answer to all major mycotoxins. This is especially true when attempting to mitigate trichothecenes since their structures are not suitable for adsorbing by binders. Biotransformation, the use of microbes and enzymes to degrade mycotoxins, is the most effective strategy. This mode of action provides reliable protection against Fusarium mycotoxins by biodegrading mycotoxins into non-toxic metabolites.
In addition to biotransformation, a bioprotection strategy is also important. Feed additives are available that contain plant and algae extracts to provide support to the liver and the immune system.
A combination of different strategies can counteract the negative effects of mycotoxins in poultry more completely, especially in cases of multi-mycotoxin contamination with the poorly absorbed Fusarium mycotoxins in animal feed.
Mycofix® is not sold in the United States and Canada.