Mycotoxicosis is the consequence of ingestion of grains or forage containing toxic metabolites produced by certain fungi. Fungi that produce toxins often do so only under specific conditions of warmth, moisture and humidity. Factors that adversely affect plants or their seeds (grains) often influence mycotoxin production. Mycotoxins can develop in field grains, damaged grains or improperly stored feeds.
Of the over 200 mycotoxins identified to date, at least seven have been reported to cause disease in swine. Some fungi produce more than one mycotoxin. Several different fungi can produce different mycotoxins in a single mixed feed. The toxins may be additive or may potentiate one another. When metabolized, they may be converted into other toxic substances. While toxicologic effects are numerous and often confusing, one should be careful not to implicate mycotoxins in disease processes without credible evidence.
Mycotoxins produce their toxic effects in several ways, including impairment of metabolic, nutritional or endocrine functions. Many mycotoxins damage the liver, reduce average daily feed intake, growth and feed efficiency. Some are teratogenic or carcinogenic. Some are immunosuppressive and predispose pigs to secondary diseases. Several mycotoxins decrease the reproductive performance of sows. Metabolites sometimes are passed in the milk of sows to their litters. The effect of mycotoxins may vary with the amount ingested, the time over which it is consumed, and the age of exposed swine. Young pigs usually are much more susceptible than adults. Within a herd there can be great variability in response to a mycotoxin.
Mycotoxicoses can present with either chronic or acute onsets. Most exposures are probably chronic or subacute as a result of consuming small amounts of toxin over a long period of time. In these instances, there may be few signs of toxicosis other than decreased appetite, slow growth, and increased susceptibility to secondary diseases. Acute outbreaks may have more obvious signs and will vary for each of the different mycotoxins. Diagnosis of chronic mycotoxicosis is often difficult because clinical signs are seldom overt and lesions are not specific. By the time a mycotoxicosis is considered, the suspected feed has often already been consumed with none having been collected and stored properly for analysis.
Prevention of mycotoxicosis is largely through careful selection and proper storage of high quality grains and other feed ingredients and the careful maintenance and cleanliness of feed preparation equipment. It often is worthwhile to properly dry and store samples of representative batches of grain that are used on a farm in the event they are needed for analysis later. Producers anticipating problems should locate a competent laboratory and get information on appropriate sample collection and storage techniques.
This mycotoxicosis is caused by mycotoxins produced by Aspergillus flavus, Aspergillus parasiticus or Penicillium puberulum. Four major toxins (B1, B2, G1, G2) are produced. B1 is of greatest significance and is a potent hepatotoxin. Fungi growing on peanuts, corn, wheat and several other cereal grains commonly produce the toxins. Maximum aflatoxin formation occurs under conditions related to the specific grain, its moisture content, storage temperature and humidity.
There is a marked age-related difference in susceptibility to aflatoxicosis. Young nursing or weaned growing pigs are much more susceptible than adults. When aflatoxin is ingested by a lactating dam, toxic metabolites are passed in her milk and serve as a source of exposure to the nursing pigs. These toxins reduce feed intake, average daily gain and feed efficiency. Since aflatoxins are immunosuppressive, signs of toxicosis often include an increase in previously controlled secondary diseases.
Acute aflatoxicosis is uncommon in swine. It is usually a subacute to chronic disease caused by daily ingestion of smaller amounts of aflatoxin over several weeks. Lesions often vary noticeably among pigs in the same affected group but are predominantly those of a hepatopathy. In the more acute cases there are sudden deaths, hemorrhages in multiple tissues, and icterus. The liver may be swollen, fatty, and have areas of necrosis. There may be a prolonged clotting time. With subacute to chronic hepatotoxicosis, the liver may be reduced in size, fibrotic, and ascites may be present.
Diagnosis is usually based on some combination of a history of slow growth (often accompanied by secondary diseases that seem unresponsive to treatment), an elevation of serum enzymes associated with hepatocellular damage, and gross lesions related to liver pathology. Microscopic hepatic lesions include bile duct hyperplasia and enlargement of hepatocytes. In swine, chronic aflatoxin toxicity can occur with at levels as low as 300 ppb in the feed; acute toxicity usually doesn’t occur until concentrations beyond 1000 ppb. Aflatoxin is considered to be carcinogenic in humans.
Claviceps purpurea is a fungus of many grasses and several cereal grains, especially rye, oats and wheat. The sclerotium of the fungus is a dark, elongated body and often can be seen on cereal grain heads and in processed grains. The fungus produces three major alkaloids that cause ergotism. The primary lesions caused by the alkaloids include arteriolar vasoconstriction and endothelial cell injury that often leads to thrombosis. When present in low levels, the alkaloids can result in reduced growth rates. Larger amounts lead to ischemic necrosis followed by a dry, gangrenous sloughing of parts of extremities, especially tails, ears and hooves. Symptoms of ergotism are exacerbated by cold weather. In pregnant sows, ergotism can inhibit mammary development, reduce litter size, reduce birth weights, and cause a profound post-farrowing agalactia. The agalactia is believed to be related to inhibition of prolactin secretion.
Diagnosis of ergotism is based on lesions coupled with the gross or microscopic identification of significant numbers of ergot sclerotia in grains or the ground feed. Doubtful results may be verified by laboratory confirmation of significant amounts of alkaloids in the feed.
The fumonisins include two principal toxins produced by Fusarium moniliforme. Signs of acute toxicity in growing and adult pigs are primarily related to the respiratory system and include dyspnea, cyanosis, weakness and death within four to ten days. Pulmonary lesions include marked pulmonary edema and hydrothorax. Pregnant sows that survive acute toxicity frequently abort in the days following their recovery. Growing pigs that survive the acute syndrome suffer from clinical signs related to a hepatotoxicosis. Their lesions may include icterus, hepatic necrosis, and megalocytosis. Differences in lesions and clinical presentation seem to be dose related.
Recent research has demonstrated that fumonisins decrease the ability of intravascular macrophages to clear blood-borne bacteria in swine, thereby potentially increasing susceptibility to respiratory disease. Fumonisin is a well known cause of leukoencephalomalacia in horses and is carcinogenic in humans at high concentrations.
There are numerous structurally related toxic compounds produced by certain Fusarium species that are classified as trichothecene mycotoxins. At least three of these are of importance in pig production. Trichothecenes are cytotoxic to many cell types and are strongly immunosuppressive. Signs of trichothecene toxicity usually include feed refusal, salivation and, sometimes, vomiting. With chronic exposure there may be paresis, paralysis, or seizures. Lesions often include gastroenteritis, hemorrhagic diathesis, skin irritation, and necrosis.
Diagnosis of trichothecene-related toxicosis can be difficult. The presence of moldy or caked feed, along with a reluctance to consume it, may suggest the presence of a trichothecene toxicosis. Improvement following a change in feed suggests the original feed was contaminated.
In swine, the experimental administration of T-2 toxin, alone and with aflatoxin, has resulted in crusting and ulceration of the skin of the snout, lips, buccal commissures, and prepuce.
Deoxynivalenol is a commonly occurring mycotoxin in corn and wheat. Despite its common name of “vomitoxin,” swine only rarely consume a large enough dose to produce vomiting; reduced feed intake is often the only sign present.
This mycotoxin is produced by Fusarium graminearum and may be present in moldy corn, standing corn, other grains, and in pelleted cereal feeds. It has an estrogenic effect that results in vulvovaginitis and precocious mammary development in prepuberal gilts. Swelling and enlargement of the vulva sometimes lead to tenesmus with prolapse of the rectum. Similar estrogenic effects in gilts have occurred as a result of consuming estrogens from other sources, including alfalfa.
There are few, if any, highly effective treatments for most mycotoxicoses. A ration suspected of being toxic should be replaced with good quality feed. If a large quantity of the feed remains, it sometimes can be fed to less susceptible species or diluted with good quality feed so that the mycotoxin no longer is being fed at a toxic concentration. There are several mycotoxin “binders” on the market that can be used to prevent the absorption of some mycotoxin from the pig’s gut.
Mycotoxins have been suggested as a cause of abortion in swine but none have shown the effect in an experimental setting. Astute practitioners should be reluctant to implicate mycotoxins as a cause of ill-defined maladies without evidence.