Mould, poisons and other toxins
Warfarin (rat bait)
Warfarin and other anticoagulants are commonly used to control rodents. In piggeries, they can kill both rodents and pigs by interfering with their blood-clotting mechanisms.
Pigs affected by warfarin bleed in a variety of sites. Most commonly they bleed under the skin and develop haematomas. A haematoma is an accumulation of blood under the skin like a bruise. Purplish-blue in colour, haematomas can be quite vast and will distort the pig's appearance. They commonly appear behind the shoulder blade. Pigs affected by warfarin may also bleed from small wounds, such as at injection sites and there will be a continual loss of blood as it does not clot. Pigs may bleed from the rectum, producing dung with blood on the outside, and internally into body cavities. Pigs will appear pale due to the blood loss.
Vitamin K is the specific treatment for pigs affected by warfarin. It can be given in the feed but it is better to give it to severely affected pigs by injection using a fine needle. Anaemic pigs need to be given extra iron.
Care should be taken to ensure warfarin baits do not fall into areas where pigs can eat them or into feed storage or mixing areas. There have been cases when warfarin has been accidentally included in a batch of feed and caused widespread poisoning. If warfarin poisoning is suspected, the source should be identified as soon as possible and removed.
Warfarin poisoning can be confirmed by laboratory testing of specially treated blood samples.
Although there may be a risk of poisoning pigs with rodent control, do not abandon your rodent control program. Piggeries attract rodents and they need to be controlled as they can spread disease and eat large quantities of pig feed.
Mycotoxins may cause similar signs of illness to those produced by warfarin.
Salt poisoning or water deprivation
Salt poisoning or water deprivation occurs when weaner, grower or finisher pigs are deprived of water for more than 24 hours. The same syndrome is seen when pigs consume excessive salt in either the feed or water or both. The worst clinical signs and most deaths occur if unlimited water is reintroduced to pigs after a period with no water. The higher the salt level in the feed the worse the poisoning in cases of water deprivation.
Salt poisoning or water deprivation can occur following pump breakdowns, blockage of water lines and nipple drinkers or when pigs do not drink because the water is too hot. Drinking water becomes too hot when it is delivered to pigs by pipes that are exposed to the summer sun for about 30 m or more.
Clinical signs are initially thirst, constipation, skin irritation and lack of appetite. Nervous signs follow, especially when unrestricted water is suddenly available after a period without water. Nervous signs include: ear twitching; aimless wandering; bumping into objects; dog-sitting; falling over sideways; and apparent deafness and blindness. Affected pigs may move around in a circle using one foot as a pivot and may convulse. Convulsions re-occur with remarkable regularity at approximately seven-minute intervals.
Water should be reintroduced gradually to pigs that have been without water for more than 24 hours. Severely dehydrated animals need to be rehydrated gradually so that they do not ingest large quantities of water quickly. Electrolytes in water can be used for rehydrating affected animals. Pigs showing nervous signs need to be placed in a darkened area with bedding material to help prevent injuries.
Salt poisoning can be diagnosed at post-mortem by characteristic microscopic changes in the pig's brain.
Organophosphates are widely used in agriculture as insecticides. Some are registered for use in pigs for the control of mange and lice. They vary in their toxicity. Those used in pigs have low toxicity so poisoning rarely occurs. Overdosing, particularly of very young piglets, leads to poisoning so directions for use should be followed and dose rates carefully calculated. Pigs should not come in contact with insecticidal organophosphates, but mistakes do occur and there have been cases where insecticidal organophosphates have poisoned pigs.
Clinical signs include excessive salivation, urination, defaecation, vomiting and general uneasiness. Later there may be hind-limb paralysis and colic. Prompt veterinary treatment will reduce the mortality rate in a group of poisoned pigs.
Heavy metal poisoning
Heavy metal poisoning in pigs is due to excessive quantities of copper, selenium, lead, arsenic (inorganic, a totally different poisoning to organic arsenical poisoning), iron or mercury in the diet. Poisoning usually follows a feed mixing error or use of a contaminated ingredient.
Each metal affects pigs in a different way. Clinical signs vary from reduced growth rate to nervous signs and death. Diagnosis is confirmed by the analysis of tissue samples from dead pigs and samples of the offending feed.
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 feedstuffs 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.
The fungi that produce aflatoxins (Aspergillus flavus and A. parasiticus) most commonly grow during storage of summer crops such as 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°C. Aflatoxins can be produced within two to six weeks and signs of poisoning in 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, which has been stored moist and heated in a 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.
Ochratoxin A is produced by a number of Aspergillus and Penicillium 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 not been identified in Australia, as at 2005.
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 prolapsed 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 Fusarium graminearum) produce it in grains, particularly maize, grown in cool, wetter (upland) regions, such as the Atherton Tableland in north Queensland. The fungus 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 New South Wales. 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 only been known to occur on a few occasions in Australia. Diagnosis is confirmed by analysing the feed. Zearalenone can also occur at high concentrations in wheat and barley hays, and can affect pigs if the hay is used as bedding in free-range systems and consumed by the pigs.
This group of mycotoxins includes deoxynivalenol (DON), which is occasionally detected in wheat and triticale in northern New South Wales and southern Queensland. Pigs initially reject their feed, and thereafter eat barely enough 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, and has been found in districts near the Queensland-New South Wales 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 has not been detected in grain in Australia (as at 2005).
Fumonisins are common in maize infected with Fusarium verticillioides in most temperate regions of the world, including Queensland and New South Wales, 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 US, but this syndrome has not been detected in Australia (as at 2005). Our research has found some reductions in performance (20% worsening of feed conversion) when fumonisin-containing maize from southern Queensland was fed, but problems are extremely unlikely to occur on piggeries unless pigs are raised on all-maize diets.
The most dramatic effect of these substances is the 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 g) 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 it 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 two or three 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.