Important mycotoxic (fungal poisoning) diseases are seen in domestic animals worldwide ( see Table: Fungal Poisoning in Domestic Animals Fungal Poisoning in Domestic Animals ). Mycotoxicoses are diseases caused by toxins of fungi. Poisoning can result from exposure to feed or bedding contaminated with toxins that can be produced when various fungi or molds grow on cereals, hay, straw, pastures, or any other fodder.
Sometimes 2 or more mycotoxins may be present in feedstuffs, making the signs more difficult to evaluate. Feed intake is often reduced, and animals may have reproductive difficulties. Some mycotoxins suppress the immune system, which can result in secondary disease caused by viruses, bacteria, or parasites. Other diagnoses must be excluded by evaluation of the history and signs and by diagnostic testing.
There are no specific antidotes for mycotoxins. Removing the source of the toxin (such as the moldy feedstuff) is necessary to prevent further exposure. If financial circumstances do not allow for disposal of the moldy feed, it can be blended with unspoiled feed just before feeding to reduce the toxin concentration, or fed to less susceptible species. When contaminated feed is blended with good feed, care must be taken to prevent further mold growth by thorough drying or by adding organic acids (for example, propionic acid) to the feed. Aluminosilicate can prevent the absorption of some mycotoxins (for example, aflatoxin).
Aflatoxins are produced by certain Aspergillus fungi on peanuts, soybeans, corn (maize), and other cereals either in the field or during storage when moisture content and temperatures are high enough for mold growth. Usually, this means day and night temperatures are consistently higher than 70°F (21°C). Signs in mammals vary depending on species, sex, age, nutritional status, amount of aflatoxins in the diet, and the length of time the diet has been fed. Aflatoxicosis is seen in many parts of the world. Dogs can be affected.
High doses of aflatoxins result in severe liver damage, while prolonged low dosages result in reduced growth rate and liver enlargement. In short-term outbreaks, deaths occur after a short period of a lack of appetite. Blood vessels rupture, causing internal bleeding, and jaundice often develops. Less severe outbreaks are more usual, and poor condition, weakness, loss of appetite, and sudden deaths can be seen. Breathing difficulties often develop, and response to treatment is usually poor.
History and examination of body tissues after death can point to the type of toxin. Feed should be analyzed for the presence and levels of aflatoxins. Aflatoxin can sometimes be detected in urine or the kidneys, or in milk of milk-producing animals if toxin intakes are high.
Batches of feed should be monitored for contamination with aflatoxin. Young, newly weaned, pregnant, and milk-producing animals require special protection from feeds suspected of being toxic. Contaminated feed can be diluted with non-contaminated feedstuff.
Ergotism is a worldwide disease that results from ingestion of the parasitic fungus Claviceps purpurea that replaces the grain or seed of rye and other small grains and forage plants. The fungus contains variable amounts of poisonous alkaloids. Cattle, pigs, sheep, and poultry are involved in sporadic outbreaks, and most other species are susceptible. Poisoning can occur from grazing seed heads or from infected grains in concentrated rations.
The first sign of poisoning is lameness, which may appear 4–6 weeks after initial ingestion. Lameness is variable and dose related. Hindlimbs are more often affected. Body temperature and respiratory rate may also be increased. Lameness progresses to dry gangrene, which appears as an indented line at the junction between normal skin and affected skin. Once gangrene is present, recovery is not likely, and affected parts of the limbs may slough off. Tips of ears and tail may also be affected.
Diagnosis is based on finding the fungus in grains, hay, or pastures.
Control is based on pasture management to minimize grazing when fungus-infected seed heads are present, typically in late summer. Concentrations of the toxins in feed can be tested. Immediate change to an ergot-free diet may avoid adverse consequences.
Estrogenism and Vulvovaginitis
Estrogenism and vulvovaginitis is a condition is caused by Fusarium species molds that are extremely common and often contaminate growing plants and stored feeds. Corn, wheat, and barley are commonly affected in moderate climates under humid weather conditions. The mold (fungus) produces a potent, nonsteroidal estrogen that mimics the action of the hormone estrogen in the body. Chickens and turkeys are affected, along with cattle and sheep.
Clinical effects cannot be distinguished from excessive estrogen administration (estrogenism). The physical and behavioral signs of estrus are induced and include enlargement of the vulva (vulvovaginitis), mammary glands, and uterus. Abdominal straining may be seen, with prolapse of the uterus in severe cases. Breeding behavior may be seen in both sexes.
Diagnosis is based on observing attempted breeding in the herd or flock, clinical signs, history of diet-related exposure, and excluding other known causes of infertility.
Changing the feed should lead to recovery of normal reproduction over several weeks.
Also known as pithomycotoxicosis, facial eczema is a disease of grazing animals that causes liver damage and results in what is called photodynamic dermatitis. Pithomyces chartarum, a fungus that feeds on decaying organic material and the source of the toxin, is most common during hot summer and autumn periods after a warm rain. It mostly affects cattle and sheep, but does occur occasionally in horses.
Skin exposed to ultraviolet light is affected. In sheep, this is only the face, thus the name facial eczema. Animals of all ages can be affected, but the condition is most severe in young animals. The signs of photosensitive skin and jaundice appear approximately 10–14 days after ingestion. Even short exposure to the sun rapidly produces redness and swelling in nonpigmented skin. The condition is painful, and animals frantically seek shade.
To lower the risk, grazing on short pasture should be limited and weather conditions that support mold growth should be monitored. Offering alternative feed during danger periods and encouraging clover growth in pastures helps to offset potential exposures.
Fescue lameness is a condition that appears similar to ergot poisoning Ergotism Important mycotoxic (fungal poisoning) diseases are seen in domestic animals worldwide ( see Table: Fungal Poisoning in Domestic Animals). Mycotoxicoses are diseases caused by toxins of fungi... read more , beginning with lameness in one or both hindfeet and progressing to gangrene of the extremities. A fungus that grows within tall fescue grass, Neotyphodium coenophialum, produces toxic compounds. Tall fescue is a cool-season perennial grass that is prevalent in Australia, New Zealand, and the US.
Fescue lameness is most common in late fall and winter. Horses are more sensitive to poisoning than cattle, and cattle are more sensitive than sheep. Cattle display responses that vary among individuals. The amount of toxin present can vary with fescue strain, environmental conditions, and pasture management practices (for instance, high nitrogen applications can increase toxicity).
Signs include progressive lameness, anorexia, depression, and later, dry gangrene of the limbs (feet affected first). Signs usually develop within 10-21 days after exposure, and cold temperatures may exacerbate the lesions.
To control exposure, all infected forage should be removed, and animals should be moved off the affected pastures.
Summer Fescue Poisoning
Summer fescue poisoning is a warm-season condition characterized by loss of appetite, weight loss, or lowered milk production. Horses are affected during the summer when they are grazing or being fed tall fescue forage or seed contaminated with the fungus Neotyphodium coenophialum. The severity of the condition varies from field to field and year to year.
Signs may appear within 1 to 2 weeks after fescue feeding is started and include reduced performance, fever, rapid breathing, rough coat, lower prolactin levels (a hormone), and excessive drooling. The animals seek wet spots or shade. Decreased reproductive performance, including birth of weak foals and lack of milk production, can be seen in horses. The severity increases when environmental temperatures are higher than 75 to 80°F (24 to 27°C) and if high nitrogen fertilizer has been applied to the grass.
For control, toxic tall fescue pastures must be destroyed and reseeded with seed that does not contain the fungus, because the fungus transfers from plant to plant primarily through infected seed. Other measures to reduce severity of the disease include not using pastures during hot weather, diluting tall fescue pastures with interseeded legumes, clipping pastures to reduce seed formation, and offering other feedstuffs.
Equine leukoencephalomalacia is a mycotoxic disease of the central nervous system that affects horses, mules, and donkeys. It is seen in North and South America, South Africa, Europe, and China. It is associated with the feeding of moldy corn (maize), usually over a period of several weeks. Fumonisins are produced worldwide primarily by certain Fusarium fungi. Conditions favoring fumonisin production include a period of drought during the growing season, followed by cool, moist conditions during pollination and kernel formation.
Signs include mild depression, drowsiness, paralysis of the throat, blindness, circling, staggering, and a reluctance to stand. The signs may last several hours or several weeks, but are usually present 1 to 2 days. Brain damage is characteristic. Liver damage can be seen and lead to jaundice. Horses may develop leukoencephalomalacia from prolonged exposure to very small amounts of fumonisins in the diet.
No treatment is available. Avoiding moldy corn is the only prevention, although this is difficult because the corn may not look moldy or it may be part of a mixed feed. However, because most of the toxin is present in broken or small, poorly formed kernels, fumonisin concentration can be markedly reduced by cleaning grain to remove the smaller particles. Corn suspected of containing fumonisins should not be fed to horses or pigs. Cattle, sheep, and poultry are considerably less susceptible to fumonisins.
Lupines cause 2 distinct forms of poisoning—lupine poisoning and lupinosis. Lupine poisoning is a nervous syndrome caused by bitter lupines. Lupinosis is a mycotoxic disease characterized by liver damage and jaundice, caused mainly by sweet lupines. Lupinosis is important in Australia and South Africa and also has been reported in New Zealand and Europe. Livestock and occasionally horses are affected.
The fungus that causes mycotoxic lupinosis is Phomopsis leptostromiformis. It produces sunken stem lesions that contain black masses, and it also affects the pods and seeds. The fungus also grows well on dead lupine material (stems, seed pods, stubble) under favorable conditions, especially after rain. Early signs are reduced appetite and depression. Complete loss of appetite and jaundice are the major signs. In severe outbreaks, deaths occur in 2 to 14 days. Feeding of moldy lupine material, together with signs and increased blood levels of liver enzymes, strongly indicate lupinosis.
Lupine fodder material should be monitored frequently for characteristic black spot fungal infestation, especially after rains.
This condition results from eating paspalum grasses infested by Claviceps paspali. The fungi mature in the seed heads in autumn. Ingestion causes nervous signs. Horses and guinea pigs are susceptible.
The time of onset of signs depends on the degree of the fungal infestation of the seed heads and the grazing habits of the animals. If large enough, a single dose can cause signs that last for several days. Large muscles tremble continuously, and movements are jerky and uncoordinated. Animals may be hostile and dangerous to approach or handle. If they try to run, the animals fall over in awkward positions. After prolonged exposure, complete paralysis can occur.
Recovery follows after animals are fed a diet free of fungus. Animals are less affected if left alone and provided readily available nutritious forages. Accidental access to ponds or rough terrain should be prevented to avoid the possibility of accidental drowning or trauma. Topping of the pasture to remove affected seed heads has been effective in control.
Red clover (Trifolium pratense) can become infected with the fungus Rhizoctonia leguminocola (black patch disease), especially in wet, cool years. Rarely, other legumes (white clover, alsike, alfalfa) are infected. Slaframine is the toxic substance, and it is stable in dried hay and probably in silage. Horses are highly sensitive to slaframine.
Excessive drooling develops within hours after the contaminated hay is eaten. Signs also include tearing of the eyes, diarrhea, mild bloat, and frequent urination. After the contaminated hay is removed, animals recover within 24 to 48 hours.
Diagnosis is tentatively based on the signs and the presence of “black patch” on the forages. Analysis of the forages can detect slaframine. There is no specific antidote for slaframine toxicosis, although atropine may control some of the salivary and gastrointestinal signs. The contaminated hay must be removed from the diet. Preventing infection of clovers is difficult, although some varieties of clover may be relatively resistant to black patch disease. Using less red clover for forages or diluting the clover with other feeds is helpful.
The trichothecene mycotoxins are a group of closely related toxins of several families of fungi including species of Fusarium, Trichothecium, Myrothecium, Cephalosporium, Stachybotrys, Trichodesma, Cylindrocarpon, and Verticimonosporium.
Animals typically refuse to eat the contaminated feedstuff, which limits intake of the toxin and development of other signs. If no other food is offered, animals may eat reluctantly. In some instances, excessive drooling and vomiting may occur. Irritation of the skin and mucous membranes, ulceration of the esophagus, and inflammation of the stomach and intestines are other typical signs. Blood vessels can rupture, and other serious blood disorders can develop. Weakness, seizures, and paralysis are seen in almost all species. Eventually, very low blood pressure may lead to death. Because trichothecenes suppress the immune system, secondary bacterial, viral, or parasitic infections may mask the primary illness.
In the former Soviet Union, Europe, and South Africa, a trichothecene-related disease known as stachybotryotoxicosis of horses has been diagnosed. Signs include tissue changes in skin and mucous membranes, disturbances of the nervous system, and abortions. Death may occur in 2 to 12 days. Myrotheciotoxicosis and dendrodochiotoxicosis have been seen in the former Soviet Union and New Zealand. The signs resemble those of stachybotryotoxicosis, but death may occur in 1 to 5 days.
Because the signs are nonspecific or masked by secondary infections, diagnosis is difficult. Analysis of feed is often costly and time consuming but ideally should be attempted. In the meantime, the feedstuff should be carefully examined for signs of mold growth or caking of feed particles. Changing the feed supply often results in immediate improvement and may provide another clue that the original feed was contaminated. Symptomatic treatment and feeding of uncontaminated feed are recommended.
For More Information
Also see professional health content regarding mycotoxicoses Overview of Mycotoxicoses in Animals For discussion of mycotoxicoses in poultry, see Mycotoxicoses in Poultry. Acute or chronic toxicoses in animals can result from exposure to feed or bedding contaminated with toxins produced... read more such as aflatoxicosis Aflatoxicosis in Animals Aflatoxicosis is a worldwide mycotoxicosis with production of potent hepatotoxins on animal feed both in the field and storage during hot temperatures (drought) and often occurs concurrent with... read more , ergotism Ergotism in Animals Ergotism in animals generally presents as lameness; necrosis of the tip of the tail, ears, and hoof tissue; and decay of the wattle, comb, beak, and feet in birds. Additional adverse effects... read more , estrogenism and vulvovaginitis Ergotism in Animals Ergotism in animals generally presents as lameness; necrosis of the tip of the tail, ears, and hoof tissue; and decay of the wattle, comb, beak, and feet in birds. Additional adverse effects... read more , facial eczema Facial Eczema in Animals Facial eczema, also known as sporidesmin toxicosis and pithomycotoxicosis, is a disorder of grazing livestock caused by the fungus Pithomyces chartarum growing on dead plant material... read more , fescue poisoning Fescue Poisoning in Animals Fescue lameness, which resembles ergot toxicosis, is believed to be caused by ergot alkaloids, especially ergovaline, produced by the endophyte fungus Neotyphodium coenophialum in tall... read more , fumonisin poisoning Fumonisin Toxicosis in Animals Fumonisins are responsible for two well-described diseases of livestock, equine leukoencephalomalacia and porcine pulmonary edema. Equine leukoencephalomalacia is a mycotoxic disease of the... read more , mycotoxic lupinosis Mycotoxic Lupinosis in Animals Lupinosis is a liver disease or hepatotoxicosis caused by ingestion of lupine plants infected with Diaporthe toxica (previously identified as Phomopsis leptostromiformis). Lupinosis... read more , paspalum staggers Paspalum Staggers in Animals The incoordination known as paspalum staggers results from eating paspalum grasses (Paspalum spp) infested by Claviceps paspali and C clavispora. The life cycle of this... read more , slaframine Slaframine Toxicosis in Animals Trifolium pratense (red clover) may become infected with the fungus Slafractonia leguminicola (formerly Rhizoctonia leguminicola) (black patch disease), especially in wet... read more , and trichothecene poisoning Trichothecene Toxicosis in Animals Trichothecene mycotoxins contain a large number of compounds classified as tetracyclic sesquiterpenoids with a 12,13-epoxytrichothec-9-ene core structure. The 12–13 epoxy ring structure is responsible... read more in animals.