1. Drugs and antibiotics are not effective in treatment.
2. The symptoms can be traced to foodstuffs or feed.
3. Testing of said foodstuffs or feed reveals fungal contamination.
4. The symptoms are not transmissible person to person.
5. The degree of toxicity is subject to persons age (more often in very young and very old), sex
(more often in females than males) and nutritional status.
Zearalenone often occurs with DON in naturally-contaminated cereals. Zearalenone is responsible for reproductive disorders due to its oestrogenic effect at high concentrations. However, in general ZEA has limited toxicity to birds.
Aspergillus and Aflatoxin:
- Aflatoxicosis: caused by high doses in short intervals or low doses in high intervals.
- 1961, caused the deaths of over 100,000 turkey poults: “Turkey X disease”.
- Toxin was traced to contaminated Brazilian peanut meal in poultry feed.
- Grows best between 80-90 0 F
- Aflatoxins are of concern in warm and humid climatic conditions.
- Damage to grain increases likelihood of fungal growth
- Definite link to cancer in animals.
- Possible link to cancer in humans. Studies done in Africa and Asia show a correlative link, but not a causative one.
- Primarily attacks the liver, in cases of cirrhosis, necrosis, and carcinomas with a secondary affect of immune suppression.
- Risk factor for neonatal jaundice, in areas of maternal consumption.
- Does not stay in the body for long periods of time, usually excreted within 96 hours, in animals.
- In milk, for human consumption, advisory level is 5 ppb.
Among poultry, ducks are the most susceptible to aflatoxin, followed by turkeys, broilers, laying hens and quail. In all species, aflatoxins are hepathotoxic with fatty changes, causing hepathocyte degeneration, necrosis, and altered liver function. Suppression of hepatic protein synthesis is the main factor resulting in growth suppression and reduced egg production. Aflatoxin is also known to interfere with vitamin D metabolism, contributing to reduced bone strength and leg weakness. By reducing bile salt production, aflatoxin negatively affects lipid and pigment absorption. Additionally, the metabolism of other minerals including iron, phosphorus and copper are also affected by aflatoxin. Aflatoxin increases the fragility of capillaries, reducing prothrombin levels thereby drastically increasing the incidence of bruising in carcasses and carcass downgrading. Due to the transfer of aflatoxin into edible products and its carcinogenic effects, most countries have set upper legal limits for aflatoxin in feed
Clinical signs of Aflatoxin Toxicity:
- Embryo toxicity
- Specific visceral haemorrhage
- Increased susceptibility to environmental and microbial stressors
- Leg weakness and reduced bone strength
- 'Pale bird syndrome'
- Fatty liver
- Liver necrosis
- Bile duct hyperplasia
- Increased incidence of bruising and downgrading
- An increase in the size of the liver, kidneys and spleen,
- Liver becoming friable, pale in colour and extremely fatty with increasing severity of the outbreak.
- Lymphoid tissue, including the bursa of Fabricius and thymus glands, undergo astrophy.
- The gall bladder is usually enlarged and filled with bile that appears dilute.
- An increased susceptibility to bruising, resulting from increased capillary fragility, is often observed.
- This effect is manifested by an increased incidence of Petechial haemorrhages of the musculature
- Decreased egg production and diminished interior and exterior egg quality is typical.
- In breeders, increased embryonic mortality, decreased hatchability and an increased incidence of malformed embryos will be evident.
- These effects occur from the transfer of aflatoxin or its metabolites to the egg during the time of dietary intake of toxin.
- Within 7 days after the cessation of aflatoxin feeding, marked improvement in hatchability can be observed
Prevention and Control:
Use clean eggs free of cracks and fresh litter free of hard wood, dusty rice hulls and peanut hulls. Maintain a clean environment in the hatchery and during brooding.
Treatment is very difficult as soon as the infection has been established, although enilconazole, sprayed in the house, is known to aid in preventing new infection. There is a regulatory issue here, as disinfection of the environment in presence of animals could be illegal in European conditions. Several disinfectants are used for prevention, but care should be given to the claimed activity and safety in use. Several producers claim a sporocidal activity, but when taking a closer look at the activity, the sporocidal activity is only evident after a very long contact time and/or high concentration. Fungal spores are extremely difficult to destroy by disinfection. Some of these compounds work on the metabolism, so when spores are not sporulating, they cannot exert their activity. When these compounds are washed away from the spores, they will be able to sporulate again. These compounds should be called anti-sporulant instead of sporocidal.
- Large genus with over 150 species.
- Discovered antibacterial properties within genus, causing production of penicillin.
- 100 species have mycotoxins.
- Nine specific toxins affecting human health are citreoviridin, citrinin, cyclopiazonic acid, ochratoxin A, patulin, penitrem A, PR toxin, Roquefortine C, and, Secalonic acid D.
- Separated into two groups: those that affect liver and kidneys, and those that are neurotoxic.
- Liver and kidney toxins are asymptomatic and cause overall animal debility.
- Neurotoxins cause visible trembling.
Ochratoxin A and Citrinin:
- Affects kidney function.
- Causes Balkan nephropathy and Yellow Rice Fever in humans.
- Chickens, turkeys, and ducklings are affected by ochratoxicosis, causing poor weight gain, egg output, and poor shell quality.
- Ochratoxin sources are peanuts, pecans, beans, dried fruit and dried fish.
- Citrinin sources are in wheat, rice, corn, and flour.
- Citrinin is most associated with horses, pigs, dogs, and poultry.
Ochratoxins are important storage toxins. They are produced by different fungi and are prevalent in temperate as well as in tropical regions.
Ochratoxin A is the most important of the ochratoxins. The primary effect of ochratoxin A in all poultry species is nephrotoxicity. In poultry, the proximal tubules are mainly affected and the kidney is pale and grossly enlarged. As with aflatoxin, fatty liver can also occur due to ochratoxin exposure. In acute cases, mortalities can occur due to acute renal failure. In young chicks, ochratoxin A is approximately three times more toxic than aflatoxin.
Clinical signs of ochratoxin toxicity include:
- Mortality due to acute renal failure
- Poor eggshell quality and higher incidence of eggs with blood spots
- Reduced embryo viability and decreased hatchability
- Reduced feathering
- Polyurea with large volumes of wet faeces
- Pale and grossly enlarged kidney
- Fatty liver
- Urate deposition in joints and abdominal cavity (at high exposure levels)
Depletion of lymphocytes and with it strong suppression of cellular immunity, thus enhanced susceptibility to viral infections
Cyclopiazonic Acid (CPA):
- Found in corn and peanuts in Georgia.
- Chief species from Penicillium causes cheese spoilage.
- Causes fatty degeneration in liver and kidneys in animals, chickens are very susceptible.
- May act synergistically with aflatoxin.
Future Fight against Mycotoxins:
- Have farmers select strains resistant to contamination.
- Scientists hope to genetically engineer plants resistant to fungal infection.
- Use feed additives that sequester the toxins and prevent absorption from the gastrointestinal tract
Economic losses associated with mycotoxicosis include:
- Poor growth
- Reduced egg production
- Reduced feed conversion
- Increased mortality
- Poor egg shell quality
- Reduced fertility
- Leg problems
- Carcass condemnation
- Increased susceptibility to disease
Broilers relatively resistant to acute toxic effects of fumonisins. Fumonisin mycotoxicosis leads to a very specific increase in sphiganine:sphingosine ratio. However, as sphinganine and sphingosine analyses are quite complex this ratio is seldom used as a biomarker in field situations.
Clinical signs of fumonisin toxicity include:
- Spiking mortality (paralysis, extended legs and neck, wobbly gait, gasping)
- Reduced growth rate
- Increased organ weights
- Hepatocellular hyperplasia
- Poor vaccination response
- Increased liver sphinganine: sphingosine ration (biomarker)
As the risk, if mycotoxicosis is very difficult to predict or evaluate, prevention strategies should be initiated when assessing even a low-risk situation. Prevention strategies must primarily aim at minimising mycotoxin formation in the field and during storage.
A significant reduction in mycotoxin formation can be achieved by good agronomic practices, for example:
- Selection of crop varieties that are more resistant to fungal foliar diseases
- Ploughing up harvest residues
- Avoiding no-till soil management practices
- Proper crop rotation
- Avoiding monoculture
During storage of dry feed ingredients, mycotoxin formation can be successfully controlled by monitoring the moisture content of the feed. If the moisture content is below 12%, moulds become metabolically inactive, and the risk of mycotoxin formation is strongly reduced. To avoid mycotoxin formation, be aware of the following:
- Moisture content below 12%
- Relative humidity below 60%
- Storage temperature below 20 °C
- Clear grain, avoid broken kernels
- Control insects and rodents
- Avoid stress (frost, heat, pH changes)
Mycotoxin adsorbents and binders:
As we know mycotoxins are usually found in combinations in complete animal feeds. A broad substrate binding capacity will ensure at least some fraction of all the mycotoxins will be rendered non-bioavailable and the bioavailable mycotoxins will be below the threshold of biological activity. Broad substrate binding capacity of a binding agent will also minimise the potential for toxicological synergy between mycotoxins.
Speciality feed additives, known as mycotoxin adsorbents or binding agents are the most common approach to prevent and treat mycotoxicosis in animals. It is believed that the agents bind to the mycotoxin preventing them from being absorbed. The mycotoxins and the binding agent are excreted in the manure.
The effective level of dietary inclusion for mycotoxin adsorbents will depend on the mycotoxin binding capacity of the adsorbent and the degree of contamination of the feed in question. A high binding capacity will minimise the level of inclusion and minimise the reduction in nutrient density caused by the feeding of the adsorbent. High levels of inclusion of adsorbents can also alter the physical properties of the feed which might impair feed processing such as pellet formation, in addition to altering the actual diet specification.
Mycotoxin binding is achieved through both:
- Physical adsorption
- Relatively weak bonding involving van der Waals interactions and hydrogen bonding
- Chemical Adsorption: (Chemisorption) is a stronger interaction which involves ionic or covalent bonding.
An effective binder or sequestering agent is one that prevents or limits mycotoxin absorption from the gastro-intestinal tract of the animal. In addition, they should be free from impurities and odours. Be aware that not all are equally effective. Many can impair nutrient utilisation and are mainly marketed, based on in-vitro data only.
There are two types of mycotoxin adsorbent/binder:
- Inorganic binders
- Organic adsorbents
Inorganic mycotoxin binders are silica-based polymers. Examples could include:
- Bleaching clays from the refining of canola oil
- Hydrated sodium calcium aluminosilicates (HSCAS)
- Diatomaceous earth
- Numerous clays
They can be grouped into two categories: Phyllosilicates and Tectosilicates
Phyllosilicates: bentonites/montmorillonites :
- Phyllosilicates are characterised by alternating layers of tetrahedral silicon and octahedral aluminium coordinated with montmorillonite oxygen atoms
- Isomorphous substitution leads to a net negative charge which must be satisfied by the presence of inorganic cations (Na, Ca, Mg, K)
- Applications: Adsorbents for heavy metals, suspension-stabilising agents in coatings, bonding agents for foundry sands and washes, binder in pelletisation processes, desiccants in feed products.
Tectosilicates: Zeolites :
- Tectoalumosilicates of alkali and alkaline earth cations that have an infinite three-dimensional cage-like structure
- Isomorphous substitution leads to a net negative charge which is satisfied by the presence of inorganic cations (Na, Ca, Mg, K)
- Applications: Adsorbents for ammonia, heavy metals, radioactive cesium and mycotoxins.
Organic mycotoxin adsorbents are carbon based polymers. Examples could include:
Fibrous plant sources such as:
- Oat hulls
- Wheat bran
- Alfalfa fibre
- Extracts of yeast cell wall
Such materials are biodegradable but can, in some cases, also be vectors of mycotoxin contamination. Benefits of yeast cell wall are low inclusion, high surface area and certainly no toxic contaminants. The efficacy of glucomannan-containing yeast products as mycotoxin adsorbents in feeds has been investigated globally with several studies with all animals
Mycotoxin adsorbents offer an attractive short-term solution to the challenge of mycotoxin-contaminated animal feeds. The only complete solution to the mycotoxin challenge will be the long-term goal of eliminating mycotoxins from the food and feed chains through improved quality control based on better analytical techniques coupled with genetic advances in plant resistance to fungal infestation.
Mycotoxin adsorbent should be:
- Proven efficacy in vivo as well as in vitro
- Low effective inclusion rate
- Stable over a wide pH range (This is necessary so that the mycotoxin stays attached to the adsorbent throughout the gut and is excreted.)
- High affinity to adsorb low concentrations of mycotoxins
- High capacity to adsorb high concentrations of mycotoxins
- Ability to act rapidly before the mycotoxin can be absorbed into the bloodstream.