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.
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.
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.
Cockleburs (Xanthium spp.) are widely distributed in the midwestern US and grow as weeds in fencerows, ditches, and low or marshy areas. The toxic principle, carboxyatractyloside, is present in the seeds and young seedlings of the plant, especially during the cotyledonary (“two-leaf”) stage of growth. Seedlings may be ingested by pigs on pasture especially after spring rains when burs sprout in low-lying areas. Also, seeds may be ingested in mixed or ground feeds. Pigs may be found dead after consuming only modest number of seedlings. Because the clinical course of disease is only several hours, signs may not be observed and lesions may be absent from dead pigs. Mortality is sporadic unless plants are numerous.
In experimentally poisoned pigs, signs include depression, hypoglycemia, occasional nausea, incoordination, convulsions, and death. Lesions include serofibrinous effusions in body cavities and subcutaneous edema. There sometimes can be edema of the gall bladder wall and mild gastroenteritis. Microscopic lesions include centrilobular hepatotoxicosis with centrilobular accentuation of the liver pattern.
Diagnosis is often difficult unless cocklebur seedlings can be found in significant numbers in the pasture or seeds can be found in the feed. An “on-the-knees” search for the two-leaf stage sometimes reveals seedlings deep within lush pasture. Cocklebur poisoning must be differentiated from poisonings caused by ingestion of clay pigeons, aflatoxin, and gossypol.
In pigs showing clinical signs, mineral oil administered per os may delay absorption of the toxic principle until it can be eliminated. Injecting physostigmine has been reported to be of value in affected pigs.
Roxarsone and arsanilic acid are used to promote growth and to treat swine dysentery and eperythrozoonosis. Roxarsone is more toxic than arsanilic acid but most features of poisoning are similar in both cases. Poisoning is dose-related. Chronic poisoning may occur when low doses are given over a long period of time. Acute poisoning occurs when large amounts are consumed in a short period of time.
Signs of chronic poisoning with arsanilic acid include goose-stepping, hind limb ataxia, limb paresis, and blindness. Blindness is not typical of poisoning with other organic arsenicals. Paralyzed pigs remain alert. If provided with feed and water, they will continue to eat and drink. There are few or no associated gross lesions. Signs of acute poisoning include cutaneous erythema, ataxia, vestibular disturbances, and terminal muscular weakness. An acute gastroenteritis will often be present in these cases. Although signs and lesions of roxarsone poisoning will often be similar, an additional syndrome has been described that includes repeated convulsive seizures following exercise without the blindness produced by arsanilic acid. Microscopic lesions associated with chronic poisoning by these compounds include neuronal degeneration of optic and peripheral nerve trunks, including the sciatic nerves. Neuronal lesions may not be present in acute cases.
A tentative diagnosis can often be based on a history of misuse of the compounds and the presence of characteristic clinical signs in chronically affected swine. Diagnosis may be assisted by toxicologic assays of kidney, liver, muscle, and feed.
Prevention of organic arsenical poisoning can be achieved simply by correct management of these legal compounds during feed preparation or medication. In particular, water treated with these compounds should not be given to thirsty pigs, as they are likely to consume a toxic dose. Directions provided with the compounds should be followed carefully. The neurotoxic effect of poisoning sometimes is reversible if the compound is removed within two or three days of the appearance of signs. Blindness and long standing peripheral nerve damage may be permanent.
Pigs allowed access to pastures or lots containing pigweed (Amaranthus retroflexus) may be poisoned.
Most poisonings occur in the late summer or fall. Signs appear within five to ten days after exposure and include trembling, weakness, incoordination, knuckling, and almost complete rear leg paralysis. Morbidity is variable; mortality can be high (75-80%) in pigs showing signs.
Lesions are those associated with acute nephrosis and heart failure. There is a marked perirenal edema. The kidneys are normal in size but may appear blanched. Other lesions include ascites, hydrothorax and edema of the ventral body wall; long-standing cases may have chronic fibrosing nephritis. Microscopic lesions in the kidneys of acutely affected pigs include necrosis of both proximal and distal convoluted tubules with numerous casts in tubules. Many glomeruli will be atrophic and have a distended Bowman’s capsule containing filtrate. Diagnosis can usually be made after identification of the plants, obtaining a history of sudden access to them, and observing the clinical signs and rather unique kidney lesions. The toxic principal is not known.
There is no widely accepted treatment. Pigs should be denied access to the plants immediately, but new cases may develop for as long as ten additional days.
Salt poisoning can occur in pigs either as a consequence of water deprivation or from sudden ingestion of too much salt.
Poisoning in water-deprived pigs can occur in pigs consuming a proper level of salt but it is more likely if the salt level in the feed is excessive. Signs often are precipitated, or worsened, by allowing the pigs sudden, unlimited access to water. Water deprivation can occur for many reasons but commonly may be the result of freezing of the water source, plugged water nipples, or inadvertently leaving a water valve closed. Operators may not always be forthright in admitting human errors related to water deprivation. Poisoning has occurred following prolonged shipping without access to water, followed by unlimited access.
Following sudden heavy rains, salt poisoning can occur in swine after ingestion of salty brine from overflowing, loose-salt boxes provided for other livestock and is also reported following ingestion of whey. This type of poisoning is more likely in water-deprived pigs.
Clinical signs of sodium ion toxicosis are caused by the acute cerebral edema that occurs as a result of multiple central nervous system (CNS) lesions. Because the condition most often occurs secondary to water deprivation (rather than a primary toxic intake of salt), salt poisoning is frequently apparent at a “pen” or “herd” level. Signs include aimless wandering, blindness, deafness and head pressing. Affected pigs sometimes “dog-sit”, slowly raise their nose upward and backward, and fall on their side in spasms that may be followed by paddling of the legs. They then may arise and continue their wandering.
Diagnosis associated with water deprivation may be suggested by history, signs, and elevated sodium levels in serum or cerebrospinal fluid. Gross lesions may be absent or limited to gastroenteritis. Gastroenteritis is more likely in pigs consuming salty brine and may be accompanied by diarrhea. A valuable but not infallible diagnostic aid is the microscopic observation of rather unique meningeal and cerebral perivascular cuffing by eosinophils in brain. Later and less reliably there may be laminar subcortical polioencephalomalacia or necrosis. Salt poisoning must be differentiated from all other encephalitic diseases. In an affected pen, a clue to the occurrence of water deprivation will be the absence of any urine or wet feces on the pen floor.
Water-deprived or affected pigs should be reintroduced to water slowly, given only small amounts of water at frequent intervals. This may suppress mortality. Pigs showing clinical signs usually die regardless of treatment.
Five gases (ammonia, carbon dioxide, carbon monoxide, hydrogen sulfide, and methane) are associated with swine environments, especially confinement rearing.
Ammonia (NH3) and hydrogen sulfide (H2S) are normally generated from the decomposition of swine excrement. Carbon dioxide (CO2) can cause deaths but is perhaps a lesser threat than carbon monoxide (CO) because it is heavier than air and usually only accumulates in slurry pits below pig housing and working areas. Methane (CH4) is an explosion hazard. All five gases represent potential threats to both swine and people but ammonia, carbon monoxide and hydrogen sulfide toxicities are by far most common and are discussed below.
Ammonia gas (NH3) is formed by the decomposition of animal waste and is present at some level in most animal facilities. The odor can be detected by most people at concentrations of around 10 ppm; a level which appears to have little detrimental effect on pig health. However, when the concentration reaches 50 ppm or more, NH3 may act as an irritant of the mucous membranes of the eyes, nasal passages, and lungs and cause ocular and nasal discharge. Concentrations of NH3 that are high enough to be irritating to mucous membranes of pig farm workers likely have a similar effect on animals continuously exposed.
Research on swine suggests that toxic concentrations of NH3 (over 50-100 ppm) reduce growth rate, reduce bacterial clearance from the lungs (interferes with mucociliary apparatus), exacerbate nasal turbinate lesions in pigs infected with Bordetella bronchiseptica and may influence the course of infectious diseases.
Carbon monoxide (CO) has a much greater affinity for hemoglobin than does oxygen, effectively displacing oxygen from the blood. It combines with hemoglobin to form carboxyhemoglobin, reduces oxygen exchange, and causes mortality. Carbon monoxide is produced by incomplete combustion of any carbonaceous fuel, but most poisonings occur because of improperly functioning (yellow versus blue flame) space heaters or furnaces. Carbon monoxide is a colorless, odorless, and tasteless gas.
Recognition of malfunctioning heaters should alert one to the possibility of poisoning.
In late pregnancy sows, a high level of stillbirths and neonatal mortality is associated with CO poisoning. The sows themselves may show no other signs. Affected piglets usually show no lesions other than a pink to bright red color imparted to their blood and tissues by carboxyhemoglobin. Blood from affected piglets and fetuses with CO poisoning is usually characterized as “cherry red.” The concentration of carboxyhemoglobin in fetal thoracic fluid or blood of an affected pig can be used to confirm CO poisoning.
Hydrogen sulfide gas (H2S) inhaled at toxic levels is dangerous and fatal to both pigs and people. The danger of high concentrations (greater than 100 ppm) of H2S should be recognized, respected, and avoided but the usual, low level of the gas in closed confinement facilities, (less than 0.2 ppm) is not toxic and of little consequence. A “sewer gas odor/rotten egg smell” detectable by humans from 0.1 to 5 ppm, is sometimes offensive but is not toxic. Levels from 10 ppm to 100 ppm can cause eye and respiratory irritation. Humans cannot detect the odor of H2S at levels greater than 150-200 ppm because of olfactory paralysis induced by the gas. Levels greater than 200 ppm affect the nervous system; immediate collapse and respiratory paralysis occurs at levels greater than 1000 ppm.
Hydrogen sulfide is heavier than air and accumulates in liquid manure holding pits below confinement buildings. The gas usually remains dissolved in the liquid component of swine effluent and remains below the toxic level in air unless the effluent is agitated. Effluent storage pits are often agitated just prior to and during the emptying process at which time high levels of H2S can be released. If inhaled in high concentration, H2S can cause instant fatal systemic intoxication of exposed swine or people by directly suppressing the respiratory center in the brain. High levels of the gas paralyze a worker’s sense of smell and may give a false sense of security. Workers trying to rescue affected swine or co-workers are at a very high risk of asphyxiation.
Exposure to toxic levels of H2S can be avoided by emptying and cleaning the pit when the building is empty or when pigs and people have been moved out of the building temporarily. Adequate ventilation should be provided (fans on, curtains down) whenever pits are agitated to keep H2S at a nontoxic level.