Barry Blaney, DPI&F
Mycotoxins are poisons produced by moulds (microscopic fungi) growing in feedstuffs. Moulds such as ergot (Claviceps species) can grow on grain and produce mycotoxins before harvest. Other moulds infect grain before harvest but produce most mycotoxins during storage. The moulds that produce mycotoxins are not always visible, but feed stuffs that become visibly mouldy during storage are very likely to reduce productivity.
There are several key questions that should be considered when faced with options on either the purchase of fungus-infected (often weather-damaged) grain or the use of feed that has become mouldy in storage. Some are:
- whether fungal toxins (mycotoxins) are present in concentrations sufficient to affect pig health and performance;
- whether the palatability and nutrient content has been altered for better or worse, and the most important question of all;
- whether the lower price of the grain or other feed component, compensates for these effects and the risks involved.
Many moulds cause only a slightly reduced growth rate or poor feed conversion, but some mycotoxins with more drastic effects are aflatoxins, ochratoxins, zearalenone, trichothecenes (deoxynivalenol, nivalenol), fumonisins and ergot alkaloids. These mycotoxins do occur in particular regions and in particular situations, so that prior knowledge of these circumstances will greatly reduce the risk of poisoning.
Aflatoxins
The fungi that produce aflatoxins (Aspergillus flavus and A. parasiticus) most commonly grow during storage of summer crops (maize, peanuts and sorghum) but wheat and barley can also be affected.
Typically, aflatoxin poisoning occurs on small farms that mix their feeds from home-grown grain. Failure to dry grain, or moisture condensation and accumulation during storage favour the growth of moulds, which is accompanied by heating - these moulds grow best at 30-40 degrees. Aflatoxins can be produced within 2-6 weeks and signs of poisoning of pigs may be noticed within a week of it being introduced to the diet.
The clinical signs of aflatoxin poisoning are not characteristic. Pigs go off their feed and some may die, some are anaemic (pale) and jaundiced (yellowish in colour). Characteristic damage is caused to the liver, that can be detected when it is examined post mortem, and a diagnosis of aflatoxin poisoning is confirmed when the feed and tissues from dead animals are analysed at a laboratory.
There is no specific treatment for affected pigs. Replace or dilute the mouldy feed with clean feed containing adequate protein, as the effects of aflatoxin poisoning are made worse by low dietary protein. Pigs may take several weeks to recover and never reach their normal growth potential.
Overall, the main risks are peanut waste, and grain has been stored moist and heated in the silo. Mouldy peanuts and waste from failed peanut crops have caused sudden and serious mortalities. One spectacular case of aflatoxin poisoning in Queensland followed the feeding of mouldy bread to a group of 380 pigs. Within two hours, 50 pigs were dead and another 30 died over the next three days. Failure to dry sorghum grain before storage has led to aflatoxin poisoning in piggeries in southern and central Queensland - heating in the silo is a result of mould growth (the mould causes the heating), and the resultant mouldy lumps and encrusted grain can contain high concentrations of aflatoxins. Although less frequent, mouldy maize, barley and wheat can on occasion contain enough aflatoxins to poison pigs.
Ochratoxins
Ochratoxin A is produced by a number of Aspergillus and Penicilllum fungi, and causes kidney damage. Depressed appetite and reduced growth rate may result. Ochratoxin A is a common contaminant of barley infected with Penicillium verrucosum and grown in cool and wet conditions in northern Europe and Canada. However, this fungus does not occur in barley grown in southern Australia. Ochratoxin A occurs in Queensland occasionally, almost invariably at concentrations too low to effect pigs, and the source is Aspergillus ochraceus in mouldy sorghum or maize. Ochratoxin can also be produced by Aspergillus carbonarius in grapes. However, ochratoxin poisoning of pigs has never yet been identified in Australia.
Zearalenone
Zearalenone is a mycotoxin with some properties of the female sex hormone oestrogen. When fed to female grower pigs, zearalenone causes swelling and reddening of the vulva similar to that seen at natural heat (oestrus). This can progress to straining and prolapse of the rectum and vagina. Zearalenone also causes slight development of the teats of gilts and occasionally swelling of the prepuce of boars. Several Fusarium moulds (mainly F. graminearum) produce it in grains, particularly maize, grown in cool, wetter (upland) regions, such as the Atherton Tableland in north Queensland. The fungus actually grows on the grain before harvest when rainfall is high and insect damage prevalent, but damp, cool storage after harvest increases the hazard. A dark purple discolouration of maize may be an indication of infection with zearalenone-producing mould. Wheat (or triticale) affected with head blight (scab) also can contain zearalenone, but occurs infrequently, usually in northern NSW. Affected wheat has a bleached appearance, and some grains have red tips. Zearalenone can also be present in weather-damaged sorghum. Zearalenone poisoning of pigs has occurred on only a few occasions in the past 30 years in Australia. Diagnosis is confirmed by analysis of the feed. Zearalenone can also occur at high concentrations in wheat and barley hays, and can affect pigs if the hay is used as beeding in free-range systems and consumed by the pigs.
Trichothecenes
This group of mycotoxins includes deoxynivalenol, which is occasionally detected in wheat and triticale in northern NSW and southern Qld. Pigs initially reject feed, and thereafter eat barely sufficient for survival. If the pigs are hungry when the feed is first offered, they may eat and then vomit, which is why deoxynivalenol is also called vomitoxin. This is a rarely diagnosed form of mycotoxicosis in Australia, so far found only in districts near the Qld/NSW border ranges. The closely related substance nivalenol also causes feed rejection. It occurs in maize grown on parts of the Atherton tableland, but this has not been associated with lost pig production. A dark purple mould (Fusarium graminearum) infecting wheat, maize and triticale before harvest produces these mycotoxins, often in conjunction with zearalenone. There are a few other trichothecenes, including T2-toxin, which could potentially affect pigs, but have never been detected in grain in Australia.
Fumonisins
Fumonisins are common in maize infected with Fusarium verticillioides in most temperate regions of the world, including Queensland and NSW, and fumonisins can be produced before harvest. Drought stress is a contributing factor in increased contamination. Fumonisins have been associated with pulmonary oedema (fluid in the lungs) of pigs in the USA, but this syndrome has never been detected in Australia. DPI&F experiments have found some reductions in performance (20% worsening of feed conversion) when fumonisin-containing maize from southern Qld was fed, but problems are extremely unlikely to occur on piggeries unless pigs are raised on all-maize diets.
Ergot alkaloids
The most dramatic effect of these substances is cessation of milk production by sows, often leading to starvation of piglets. Ergot fungi come in different species: rye ergot (Claviceps purpurea) infects rye grass, wheat and barley; and sorghum ergot (Claviceps africana) infects sorghum. Infection of grain occurs when the crop is flowering - the fungus spores enter the pollen tube, especially when pollination is impaired by cool, wet weather. As the grain head matures, the fungus produces an ergot where the seed would usually be, and these ergots contain mycotoxins called ergot alkaloids. Rye ergot has occasionally affected pigs in southern Australia, and sorghum ergot caused serious losses in piggeries around Monto and Biloela in central Queensland in 1997 and a few problems also occurred in the Downs and Burnett in 2002.
Sorghum ergots can be detected in grain as follows: Dissolve a tablespoon (20 gm) of table salt in a cup (200 ml) of water. Slowly add about half a cup of the grain, stirring constantly. Ergots will tend to float while clean seed sinks. Remove the floating material and examine under a magnifying glass. After removing stalk and immature grains, look for ergots. These are of similar size to the grain but are slimmer, with a rough, scaled surface. Often they can be seen just emerging from the glumes, and sometimes they are surrounded by a larger mass of black sooty fungus called Cerebella that is often associated with ergot. If the sample contains more than 2 or 3 of these ergots, do not feed to sows without having it checked in a laboratory. However, grower and finisher pigs are more tolerant to ergot, and test-feeding a few pigs would reduce the risk to the whole herd. For more detail see DPI&F Note on Ergot in sorghum-biology, management and toxicity to livestock (Agdex 115/637).
Effects of moulds on palatability and nutrients
The only mycotoxins that have so far been shown to affect pigs in Australia are aflatoxins, zearalenone, deoxynivalenol and ergot alkaloids. As described above, these occur in particular circumstances, and knowledge of those circumstances will help to reduce risk of poisoning.
Mould growth before harvest
In general, changes in palatability and nutrient content of grain infected with mould before harvest (weather-damage) is slight, and there may even be some improvement in nutritive value as a result of starch hydrolysis similar to that seen in early germination. Deteriorated grain will be lighter in weight, be discoloured and darkened if mould invasion is extensive and the endosperm is likely to have a chalky appearance due to the partial hydrolysis of the nutrient stores. Gross energy on a weight basis may be unaffected, but fibre and non-protein nitrogen may be increased. The minor nutritional deficiencies of weather-damaged grains can generally be ignored in dietary formulation, but if desired, increasing the digestible energy with fat can easily compensate. An example of this situation arose when wheat grown on the Darling Downs in 1999 was bleached white as a result of infection with the fungus Botryosphaeria zeae. Young pigs fed this grain performed equally as well as pigs fed normal grain. Another common fungus that appears to have no adverse effects on pigs is 'covered smut' of barley, which is infection by the fungus Ustilago hordeii.
Mould growth in storage
Many moulds can grow in stored feed when hygiene is poor. Mould spores are always present in feed and the main factor stopping mould growth is lack of moisture. Condensation, leaks, rodent and insect damage all lead to mould growth. When this has occurred, the main affects are reduced palatability and worsening of feed conversion. These effects should not be ignored, as the effects on profits can be severe. Mould infection of grain decreases its feed value for pigs through the removal of storage starch and the hydrolysis of protein and losses in fat content also occur. Consequently, in material with extensive mould invasion during storage, the relative amount of fibre in the grain will increase in proportion to the decline in starch, protein components and fats, leading to reductions in digestible energy content. Vitamins and other essential nutrients can also be affected. The result of these changes is poor conversion of feed into pigmeat. Regular cleaning of silos and feed handling equipment, and rapid feed turn over are very important to maintain feed quality.
Sometimes in times of high humidity, feed may become slightly mouldy despite good hygiene and there is a need to use this material. Damaged feed that has undergone fungal growth during storage may exhibit 'off' aromas and flavours and be unpalatable when first offered to pigs. Usually, this poor palatability lasts only a few days before pigs become accustomed to the taste and smell. If it persists longer than this, it might indicate infectious disease or dietary imbalance, although mycotoxins are a possibility.
Economic factors
The decision whether or not to feed weather-damaged grain or mouldy feed is a matter of balancing the risk of reduced growth with lower feed costs. Avoid feeding any unpalatable feed to young pigs, as reduced intakes when young will compromise later performance. For example, at 1990 prices for the Queensland pig industry, a 15% decrease in feed intake by young pigs produced a 7% decrease in profit margin, although this could be compensated for by a 22% decrease in the price of grain. Finishers are a better proposition for unpalatable feed as slightly reduced intakes may be desirable to reduce fat deposition, and actually improve feed conversion slightly. Should feed conversion be adversely affected, as will happen if nutrients are unbalanced or if there are toxins in the feed, profits will reduce substantially. For example, in 1990 in Queensland, a 15% decrease in feed conversion efficiency by pigs would reduce profits by 10%, and the break-even point would not be reached until the cost of the grain was reduced by 24%. However, these examples are extreme cases that are not often purely the result of moulds and mycotoxins. Providing that the particular situations where mycotoxins are known to occur are avoided, pig farmers are in a good situation to take advantage of discounts offered for weather-damaged grain. Risks can also be minimised by blending different sources of grain and by test-feeding to small numbers of pigs where possible.
Further information
For further information:
DPI&F Business Information Centre from 8 am to 6 pm weekdays: Phone 13 25 23 (Queensland residents), non Queensland residents phone +61 7 3404 6999; e-mail callweb@dpi.qld.gov.au
DPI&F's web site www.dpi.qld.gov.au
As well as being published on DPI&F's pig industry web site atwww.dpi.qld.gov.au/pigs/, this DPI&F Note will be published on the DPI&FPrimeNotes CDROM and will be published on DPI&F's national Pig Technotes CD.
Information contained in this publication is provided as general advice only. For application to specific circumstances, professional advice should be sought. The Department of Primary Industries and Fisheries has taken all reasonable steps to ensure the information in this publication is accurate at the time of publication. Readers should ensure that they make appropriate inquiries to determine whether new information is available on the particular subject matter.
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Last revised October 2004
