Animals come into contact with mycotoxins via pasture, preserved forages, grain, other feedstuffs, complete commercial feeds and bedding. Many toxins have now been classified by their impact on animal health, performance and welfare. The variety of toxins that may be present within forage, feed or bedding depends on the number and types of mould and fungal growth on these materials, which in turn dictates the symptoms that may be observed. The presence of several fungi and their toxins within natural materials means that symptoms can often be multiple and confusing in character, making mycotoxicosis diagnosis rather difficult. Some animals are more readily affected than others by specific toxins.
It is generally assumed that feed-borne mycotoxins are the sole source of contamination. However this is not always the case. Housing pigs on straw is common in many countries, because of its perceived benefits to animal welfare and environmental concerns. The consumption of straw by these animals can be considerable and has been estimated to be between 10 and 15% of total feed intake in weaned pigs, and even higher in sows. If the straw is contaminated with mycotoxins, then pigs on straw bedding may be at risk of increased mycotoxin ingestion. In a recent Australian study (Moore, 2005) over 80% of straw samples examined were positive for mycotoxins. In one study, adding a mycotoxin binding agent to the diet of pigs kept on straw bedding, improved growth rate. This highlights the potential risk that straw and other material used for bedding poses to pigs and the urgent need for appropriate preventative action.
Main moulds and mycotoxins found in feed and bedding materials
Field origin |
Storage origin |
|
Fusarium |
Penicillium |
Aspergillus |
Deoxynivalenol |
Ochratoxin |
Aflatoxin |
Zearalenone |
PR |
Ochratoxin |
T-2 |
Patulin |
Sterigmatocystin |
Fumonisin |
Penicillic acid |
Fumintremorgens |
Moniliformin |
Citrinin |
Fumigaclavins |
Nivalenol |
Penitrem |
Fumitoxins |
Fusaric acid |
Cyclopaizonic acid |
Gliotoxin |
Certain circumstances can result in increased susceptibility of animals to mycotoxins:
- Higher performing animals are more sensitive to toxins
- Animals fed larger amounts of preserved forages, high risk pasture or grain-based feeds are more likely to come into contact with fungal toxins
- Climate change may increase opportunities for fungal growth on plant material
- Increased reliance on prepared and stored, rather than fresh feed materials will increase potential for fungal contamination.
Common symptoms of mycotoxicosis include:
- Poor performance,
- Infertility,
- Lameness,
- Inadequate immunity/vaccination failure
- Disease
- Behavioural problems
- Undiagnosable changes in character, behaviour or performance of an animal
Limiting mycotoxin exposure
Several strategies are available to limit exposure of animals to mycotoxins. The most obvious one is to apply strict quality control measures on all feed, bedding and forage materials to minimise the potential for the toxins to enter the food chain. However, toxin contamination may not always be accompanied by visible fungal growth, and laboratory analysis can be used to check for specific or indicator toxins for control purposes.
Prepared, lower volume bagged compound feeds (e.g. horse feed and dry pet foods) should be kept in cool, dry conditions, and used up within the recommended shelf-life of the individual product. Only purchase feed that you can use up within this timeframe. Part-used bags of old feed should be discarded.
Mouldy hay or forage should never be fed to animals. It is a prime source of mycotoxins contamination, and many moulds may also cause respiratory disease in mammals. When feeding small numbers of animals, any ensiled forages must be consumed within one week of being opened. Only feed out the amount that will be consumed within this timeframe.
If endophyte rye grass pasture is exposed to drought, the concentration of toxins will become large at the base of the plant. If the grass then is exposed to rain, facilitating rapid growth, this will translocate the toxins up the stem, exposing grazing animals to high doses of toxins, resulting in symptoms such as ‘staggers’.
In order to ensure the negation of toxic effects of any mycotoxins that may be in feed or forage, a proven effective sequestering agent, such as Mycosorb™, should be made available within the animals daily diet.
Synergy of Mycotoxins
The toxic responses and clinical symptoms observed when more than one mycotoxin is present in feed are complex and diverse. The combined negative effects on productivity and health of mycotoxins are considered to be greater than the sum of their individual effects.
The worldwide trading of feedstuffs may have contributed to the proliferation of mycotoxins and increasing incidence of mycotoxicosis. Mixing different feed ingredients from various parts of the world increases the risk that the feed will contain mixtures of different mycotoxins. Synergies between mycotoxins may increase the severity of the attack. In addition, the threshold level at which symptoms occur may be lower. Indeed, it has also been shown that feedstuff contaminated naturally with mycotoxins produces higher toxicity than equivalent amounts of purified toxins, probably due to the multiple toxins in naturally contaminated samples. For example, fusaric acid, the most common of the Fusarium mycotoxins, increases the toxicity of DON in piglets.
In general, animal responses are more affected by a combination of mycotoxins than by individual mycotoxins. This response can be described as either cumulative or synergistic, depending on the specific combination of mycotoxins. It may well be that the severity of the symptom is dependent upon the different sensitivities to the combination of mycotoxins rather than to the differing effects on brain neurochemistry.
Toxicity thresholds vary between classes of pigs and their health status. Individual mycotoxins seldom occur in isolation and there are additive or synergistic interactions which markedly decrease the threshold levels at which toxicity occurs. Consequently, there are no safe levels of mycotoxins.
Mycotoxins & Immunity
The toxic responses and clinical symptoms observed when more than one mycotoxin is present in feed are complex and diverse. The combined negative effects on productivity and health of mycotoxins are considered to be greater than the sum of their individual effects.
The worldwide trading of feedstuffs may have contributed to the proliferation of mycotoxins and increasing incidence of mycotoxicosis. Mixing different feed ingredients from various parts of the world increases the risk that the feed will contain mixtures of different mycotoxins. Synergies between mycotoxins may increase the severity of the attack. In addition, the threshold level at which symptoms occur may be lower. Indeed, it has also been shown that feedstuff contaminated naturally with mycotoxins produces higher toxicity than equivalent amounts of purified toxins, probably due to the multiple toxins in naturally contaminated samples. For example, fusaric acid, the most common of the Fusarium mycotoxins, increases the toxicity of DON in piglets.
In general, animal responses are more affected by a combination of mycotoxins than by individual mycotoxins. This response can be described as either cumulative or synergistic, depending on the specific combination of mycotoxins. It may well be that the severity of the symptom is dependent upon the different sensitivities to the combination of mycotoxins rather than to the differing effects on brain neurochemistry.
Ttoxicity thresholds vary between classes of pigs and their health status. Individual mycotoxins seldom occur in isolation and there are additive or synergistic interactions which markedly decrease the threshold levels at which toxicity occurs. Consequently, there are no safe levels of mycotoxins.
Poultry and immunity
- Fusarium toxins decrease white blood cells and cause impaired titres to the Newcastle disease virus in vaccinated poultry.
- Aflatoxin in growing broilers (up to 42 days old) caused significantly lower antibody titres, reflecting a reduction in the responsiveness of the immune system to exposure to pathogens, either from invading organisms or vaccination (Azzam and Gabal, 1997).
- Feeding diets naturally contaminated with Fusarium to broilers from day old for 56 days resulted in significant reductions in antibody (IgA) levels. IgA forms the first line of defence against environmental pathogens in exposed mucosal surfaces, e.g. the respiratory tract, which is particularly important in intensively housed poultry (Swamy et al, .2002).
- Kamalavenkatesh et al., (2005) demonstrated that T2 and CPA toxins, consumed either singly or in combination, had an immunosuppressive impact on 1-28 day old vaccinated broilers to Newcastle disease.
Mycotoxins interfere with various immune tissues, including lymphoid organs. Studies have shown that mycotoxins caused a reduction in mitotic cell number in the Bursa organ in broilers. Feeding contaminated diets has also been shown to reduce humoral immune responses to Newcastle disease virus (NDV) vaccine (Santin et al., 2002). In a commercial situation, this effect would reduce vaccine efficiency. In broiler breeders, a reduction in the transfer of maternal immunity to the chick can cause lower liveability of hatchlings.
Fumonisins inhibit the activity of the enzyme sphinganine N-acyl transferase, showing that cellular membranes can be directly affected by toxins in vivo, which in turn dictates the integrity and function of immune cells. Ledoux et al. (1992) found that that fumonisin ingestion in chickens decreased humoral immunity, suppressed lymphocyte proliferation and reduced bacterial clearance. Other studies (Santin, personal communication) found an increasing linear relationship in the interference of fumonisin on vaccine titres against NDV in broilers.
Petska et al. (2004) showed that the mycotoxin DON and other tricothecenes affected the genetic modulation of immune cells (either up- or down-regulation). Low doses of trichothecenes have been associated with immune stimulation. Conversely, high levels of toxin ingestion increased leukocyte cell death and immune suppression. Over or inappropriate stimulation of the immune system is not desirable, as it diverts energy and nutrients away from growth performance (Koutsos and Klasing, 2001).
Immune suppression in commercial poultry flocks, whether growing or breeding farms, cause reductions in vaccine titres, increases in infections (e.g. E. coli or Clostridium spp.) and more carcass downgrades due to lesions. In cases where toxins over-stimulate immune responses, a strong vaccine reaction and poorer feed conversion rate may result.
Prevention of damage and poor functionality of the immune system due to toxin exposure can be addressed by using a proven, effective mycotoxin binder, such as Mycosorb™. The table below shows how the negative impact of two different mycotoxins, in relation to immunity can be reversed.
Effects of in-feed protective agents on the antigen-specific immune response in mycotoxin-induced immuno-compromised animals
Compound |
Mycotoxins |
Species |
Observations |
Mycosorb™ |
|
|
|
Glucomannans |
AFB1 - 0.4, 0.9 |
Pig |
Restore the OVA-specific lymphocytes proliferation after the immunization (Meissonnier et al., 2009) |
Glucomannans |
T2-toxin - 1.2 |
Pig |
Restore the OVA-specific IgG production after the immunization (Meissonnier et al., 2009) |
Pigs and immunity
- Trials have shown that piglets exposed to the toxin Fumonisin type B1 had increased susceptibility to an oral infection of E. coli strain 28C at the ileal, caecal and colonic parts of the intestines (Oswald et al., 2003).
- Bouhet et al. (2006), showed a decrease in interleukin (IL-8) concentrations was reported in pigs exposed to E. coli and fed increasing levels of FB1 (see graph below). This drop in IL-8 results in decreased cellular recruitment in other aspects of the immune system, which increases the ability of the invading E. coli organism to colonise the intestine, hence worsening the infection.
Impact of increasing FB1 exposure on IL-8 immune response (* indicates significant reduction P<0.05)
- Administering a challenge with Pasteurella multocida type A following exposure to FB1 resulted in a much higher pulmonary inflammation response and increased coughing in piglets. This demonstrated a poorer immune response when compared to piglets exposed to the P. multocida alone.
- When sections of the gut were examined, the epithelial structure in the piglets exposed to FB1 underwent major damage, which impairs the barrier function of the gut against infective organisms (Bouhet et al., 2004).
- Piglets exposed to 8 ppm FB1, showed a reduction (graph below) in the efficiency of vaccination against Mycoplasma administered at days 9 and 25 of age (Taranu et al., 2005).
Effect of FB1 on Mycoplasma vaccination efficacy
in piglets
- Oswald et al. (2008) examined the impact of exposing piglets to FB1 on lymphocyte proliferation with FB1 exposure maximised at 1912 ppm (graph below), and showed that FB1 exposure reduced lymphocyte response significantly, especially when the pigs were younger. However, adding Mycosorb™ to the feed caused no significant loss of lymphocyte activity, even immediately after exposure to the toxin.
Protective effect of Mycosorb™ on lymphocyte proliferation in piglets exposed to FB1 toxin
