A diagnosis of mycotoxin poisoning, like any feed-related poisoning, can be made by either reproducing the disease by feeding the suspected feed to other healthy animals, or by identifying from the feed, animal tissues, or body fluids toxins in amounts sufficient to cause a problem. The liver and kidney are most likely to contain mycotoxins in affected animals. The urine of affected horses may also contain aflatoxins. Microscopic evaluation of affected tissue and alternations in blood and tissue constituents can suggest, but not confirm, mycotoxin poisoning. Confirmation requires identification of a mycotoxin at a concentration known to produce disease typical of the clinical signs that occurred in feed representative of that consumed. When feed is moldy, animals may refuse to eat it altogether, or they may eat less of it than normal. Even if the mold is absent, the mycotoxin alone can cause complete or partial feed refusal. In addition, simply determining that a feed representative of that consumed is moldy or contains a mold capable of producing mycotoxins, or finding that small nontoxic amounts of mycotoxins are present, is not sufficient to confirm that mycotoxicosis is responsible for the health problems of concern. However, the true concentration of a mycotoxin in a feed is difficult to estimate accurately by measuring the concentration in a sample taken from the feed because of wide variability of mycotoxins within a feed. In addition, it has been stated that no levels of mycotoxins have been demonstrated to be safe; i.e., any level of mycotoxin carries with it a risk. This may be surprising to those who assume that regulatory guidelines on maximum allowable levels of various mycotoxins in various feeds are based on safety data. Unfortunately, regulatory agencies are required, sometimes by law and by political necessities, to adopt positions not justified scientifically; further, these positions can change for many reasons. Based on such factors, allowable aflatoxin levels in corn have varied from 20 to 300 ppb, and currently are twofold higher for corn for intrastate use than for interstate use, implying that aflatoxin becomes twice as toxic when it crosses a state line. Often a lack of data on safe levels has been responsible for forcing regulatory personnel to adopt subjective positions.

Feed Sampling for Mycotoxin Poisoning Diagnosis

Because of the uneven distribution of mycotoxins in a feed, a number of samples should be taken from representative portions of each feed the animals are consuming. Increases in the size of the sample, number of samples taken, and number of sites sampled all increase the reliability of the results obtained. Most errors in detecting mycotoxins in feeds result from faulty sampling rather than from deficiencies in laboratory analysis.

A sample will be most representative if the feed has recently been mixed or, if not, if small samples are taken from many different locations within the feed, such as from a moving stream of grain being harvested, loaded, etc., or less ideally, probe samples from the perimeter and center of a grain bin at every 6 feet (3 m) of depth. Combine the small samples taken, mix them thoroughly, and analyze a sample of this mixture or submit a composite sample of at least 10 lbs (4.5 kg) for evaluation. In most cases, individual samples of feed from specific problem areas may be useful to detect mycotoxins. These areas might include grain from parts of a bin exposed to water leaks or caked in feeders. Although small amounts of highly contaminated feed may be responsible for an individual case, it is unlikely to be responsible for a herd problem.

Prior to sending a sample to a laboratory for analysis, if the sample is moist, it should be dried to reduce moisture to 12% or less. Drying, as well as chemicals and sunlight, may reduce mold growth and mycotoxin production, but it won’t destroy mycotoxins. However, if the feed is to be checked for mold as well as mycotoxins, the sample should not be dried at over 140°F (60°C) to preserve mold viability. A dry feed sample should be placed in a cloth or paper, but not a plastic bag, for transport, as moisture may accumulate if plastic is used. High-moisture feeds should be frozen if not dried, or treated with a mold inhibitor.

Field Mycotoxin Assays

The first and most commonly used means of detecting possible mycotoxins in feed is the “Woods Lamp” or black light. It doesn’t, however, detect the presence of mycotoxins. Instead, it detects kojic acid, which is produced by mold that may have but not necessarily has, produced aflatoxins. Thus, under black light or long-wave ultraviolet light (365 nm), a bright greenish-yellow fluorescence indicates only the presence of aflatoxin-producing mold (called “shiners” or “glowers”) and not the presence of aflatoxins themselves or the presence of any other mycotoxin. Fluorescence may also occur as a result of substances other than that produced by aflatoxin-producing molds. The use of the “Woods Lamp, “therefore, produces many false positives (i.e., suggests a feed contains aflatoxins when it does not). However, it produces few false negatives (i.e., suggests a feed does not contain aflatoxin when it does) and, therefore, serves as a rapid screening test for aflatoxins in finely ground corn and other grains. Feed showing fluorescence under the “Woods Lamp” should be evaluated by additional assay procedures. Feed not showing fluorescence, however, may still contain numerous other mycotoxins.

There are a number of rapid field tests for detecting mycotoxins more reliable than the “Woods Lamp” and that detect nearly all of the clinically relevant mycotoxins affecting horses and other domestic animals. These are shown in Tables 19–3 and 19–4. These tests use one of three types of assay: minicolumn, ELISA, and CSID (chemiselective immobilization and detection). All are rapid, economical, and relatively easy to use. Minicolumn assay, however, is applicable only for aflatoxins and is not as sensitive, repeatable, or selective as ELISA or CSID. But minicolumn and CSID test kits have a longer shelf life than do those for ELISA and can selectively detect a mycotoxin from a mixture of several mycotoxins. Concurrent use of these different assays together in a single test allows for highly reliable detection of various mycotoxins in a wide variety of agricultural commodities. It’s been reported that antioxidants, such as ethoxyquin, which are often added to commercially prepared feeds, may interfere with mycotoxin analysis. Therefore, in testing these feeds check with the mycotoxin assay manufacturer to determine if this is a problem with that test. If it is, a diagnostic laboratory test may be necessary. Thin-layer chromatography is currently the standard test used in most laboratories and may require as long as 2 to 4 weeks for the results.

TABLE 19–3 Aflatoxin Test Kits

Mycotoxin Destruction in Feeds

There are two approaches for reducing the effect of mold and mycotoxin contamination of feeds: (1) preventing mold growth and mycotoxin production with proper harvesting, storage, and use of mold inhibitors as described in Chapter 4; and (2) destruction or removal of mycotoxins from contaminated feed. Many approaches have been investigated for detoxification of contaminated crops and feeds. Procedures that have been successful include removal of contaminated material by hand and by electronic or pneumatic sorting, extraction with solvents, and various chemical treatments.

TABLE 19–4 Mycotoxin Test Kits

Heating and most acid or alkali treatments sufficient to destroy the majority of mycotoxin in a feed result in damage to the feed. However, heat treatments used in normal feed processing, such as steam flaking, cooking, roasting, micronizing, and popping, still provide a feasible mechanism for substantially reducing the mycotoxin concentration in feeds. Ammoniation has been shown to be an effective and economically feasible means for reducing the aflatoxin content of feeds without adverse effects. Its efficacy on other mycotoxins is less well known. Solar radiation may be effective but impractical to use in most situations. Adding some clays to mycotoxin-containing feeds has been shown to prevent their effect. Many mycotoxins are adsorbed by compounds such as clay, preventing their adsorption by the animal and enhancing their excretion in the feces. In one study, adding 0.5% sodium bentonite or hydrated sodium calcium aluminosilicate to a diet containing 500 ppb aflatoxin prevented the aflatoxin’s inducement of a 30% reduction in feed intake and growth rate of pigs, had a minimal effect on the adsorption of nutrients, and was more effective than five other types of clay tested.

FESCUE POISONING IN HORSES

Fescue poisoning is a commonly occurring problem in mares during the last months of pregnancy and in growing horses grazing mold infected fescue pastures. For other horses, even heavily infected fescue is a good and safe forage. However, during late pregnancy, its ingestion may result in the absence of signs of impending foaling, a prolonged pregnancy, a thickened placenta causing difficult foaling, the birth of weak or dead foals, decreased or no milk production, retained placenta, and death of the mare or decreased postfoaling conception. In young horses it may decrease their growth rate. Cattle and sheep, as well as horses, are affected by fescue poisoning.

Cause of Fescue Poisoning

Fescue poisoning is caused by the consumption of tall fescue (Festuca arundinaceae) infected with the mold Acremonium coenophialum (formerly referred to as Epichochloele typhina). Poisoning is due to a mycotoxin that. produces mold, that causes a decrease in the mares plasma concentrations of the hormones prolactin and progesterone. Tall fescue is usually referred to simply as fescue, although there are other types of fescue that are not infected by this mold. These include chewing fescue (F. rubra var. commutata) used for turf or lawn grass, sheep fescue (F. ovina), meadow fescue (F. elator), and F. pratensis. However, these species of fescue are not grown for forage production because of their lower productivity. Tall fescue is a cool-season, perennial grass that grows in deeply-rooted vigorous clumps. Because optimum growth occurs during cool ambient temperatures and adequate soil moisture, forage-growth surges occur most frequently in spring and fall. Its broad, dark green leaves are ribbed and rough on the upper surface, giving it a coarse texture which reduces its acceptability to horses when it is fully mature, whereas prior to maturity it is well accepted. At maturity it reaches a height of 3 to 4 feet (0.9 to 1.2 m) and seeds out. Two strains of tall fescue, Kentucky 31 and Alta, have been most widely used as a forage crop.

Tall fescue is the most widely grown forage grass, and is the major forage growing on about 35 million acres (14 million ha) in the continental United States, particularly in the transition zone between northern and southern regions in the eastern one-half of the United States. It has been estimated that nearly 700,000 horses are maintained on tall fescue pastures in the United States. Tall fescue is widely grown because of its high productivity, it can be grazed most of the year, and its ability to tolerate wide temperature and moisture extremes, heavy grazing and trampling, and soils varying in texture, moisture, salinity and alkalinity.

The mold causing fescue toxicosis grows inside the plant (i.e. is an endophyte) that moves up the stem and into the seed as the plant grows. The mold is then transmitted via the seed to the next generation of fescue plants. In contrast to most other molds it is not transmitted from plant to plant or from the ground to the plant, but instead is transmitted only in the seed. Because it grows inside, rather than on the outside of the plant its doesn’t affect the plant’s appearance. As a result, its presence can’t be detected by looking at the plant, but can be detected microscopically. Even in infected plants it is not present in their leaf blades or roots, but only in their stems and seeds.

It is estimated that 80% of fescue growing in the United States is infected to varying degrees, usually at levels of 70% or more of the fescue plants in a pasture. It is known that horses grazing fescue pastures are affected at infection levels as low as 25%, and levels below 7% are recommended for fescue toxicosis prevention.

Fescue infection, and as a result the occurrence of fescue poisoning, is greater in warmer humid climates, such as the southeastern and south central United States, particularly in fall pasture regrowth when autumn rains follow a dry summer. Thus, fescue poisoning occurs most commonly during late fall and winter. Although tall fescue is commonly grown and fed to horses in cooler or dryer areas, fescue poisoning is much less common in these areas. Fescue poisoning is most commonly caused by grazing infected fescue pastures, but may also be caused by infected fescue hay. However, the effects of infected hay are minimal if it is cut prior to maturity and, therefore, doesn’t contain seeds which contain the highest concentration of the mold and its mycotoxins. Grazing infected fescue pastures that are mature also results in greater effects than consuming either infected hay or grazing immature pastures because horses, like cattle, selectively graze the seedheads if they are present.

Effects of Fescue Poisoning

Gestation in mares consuming infected fescue forage during late pregnancy may be prolonged to more than 13 months, during which time signs of approaching foaling, such as udder development and others (as given in Table 14–1), may not occur and fetal size continues to increase. The placenta is generally edematous with increased collagen, making it thicker and harder for the foal to break through at birth. The thickened, tough placenta, poor relaxation of the pelvic ligaments and cervix, and large fetal size lead to difficult delivery, cervical tears, and soft tissue trauma to other components of the mare’s reproductive tract. Frequently the foal is in the wrong position for birth, with a 90°-rotation from normal. Premature separation of the placenta may occur resulting in fetal suffocation. Even without premature placental separation foals may be born dead, or weak and fail to breathe, although some may be normal. Affected mares tend to gain less weight during pregnancy, and as a result be in poorer body condition than those not consuming infected fescue. This may be because of reduced intake and digestibility of infected fescue. However, digestibility of infected fescue has been shown not to be reduced at least in growing horses.

In contrast to affected cows and ewes, affected mare’s rectal temperature doesn’t increase. Following foaling, if premature placental separation did not occur, the placenta is often retained, which in conjunction with dystocia and related trauma, may result in death. If the affected mare lives, she is generally more difficult to get rebred. However, the most consistent effect is decreased or absence of milk production, which in one survey was found to occur in 15% of mares grazing tall fescue pasture as compared to 1.8% in mares on other forages, and to occur in the majority of fescue toxicosis-affected mares. In one study, in 8 mares consuming 94% infected fescue pasture during the last 72 to 181 days of pregnancy, none aborted; of their foals, 4 were stillborn, 2 were weak, 2 were normal at birth, and 3 survived. An abscence of milk production occurred in 7 of the 8 mares, 5 had retained placentas, and only 3 of 7 that were rebred conceived. Identical symptoms occur as a result of ergot ingestion by mares or foals, but as described later in this chapter in the section on ergot, ergot is present in grains or other grasses seedheads but not fescue and rarely affects horses.

It’s been reported that 40% of mares grazing infected fescue pastures have decreased reproductive efficiency. Although there are numerous other causes for reproductive problems in mares, as discussed in Chapter 13, it’s reported that fescue toxicosis is responsible for the majority of reproductive-related problems in mares grazing heavily infected fescue pastures. Decreased reproduction and milk production has also been reported to occur in cows grazing infected fescue pastures.

Three syndromes may occur in cattle and sheep but haven’t been reported in horses grazing infected fescue pastures. These are the following:

The growth rate and efficiency of feed utilization of horses, like cattle and sheep, grazing infected fescue pasture forage or hay may be decreased. In one study growth rates of both yearling horses and steers were reduced in similar amounts when a high- as compared to a low-endophyte-infected (≥75% or ≤25%) fescue pasture with ample forage was grazed. The average daily weight gain was reduced from 1.2 to 0.5 lb/day (0.56 to 0.24 kg/d) for the horses and from 1.5 to 0.5 lb/day (0.69 to 0.23 kg/d) for the steers. Neither species rectal temperatures were increased. The effects of infected fescue forage consumption by growing horses can be prevented by feeding a grain-mix as one-half of the weight of their total diet. This would be the amounts given in Table 15–3.

Treatment of Fescue Poisoning

Removing mares from infected fescue pasture, or not feeding infected fescue hay, is effective in rapidly alleviating fescue toxicosis effects. Even when bromocriptine (which induces all of the effects of fescue toxicosis) is administered to mares up until 320 days of gestation, and until an average of 12 (7 to 17) days before foaling the mares are unaffected. Even mares that are past their expected foaling date because of fescue poisoning will be all right if they are removed from infected pasture and fed a noninfected hay. This was well demonstrated in one report in which 7 of 14 mares on infected fescue pasture had difficult delivery without any prior signs of impending foaling; all 7 foals died, 4 of the mares died, and none of the mares lactated. Within 48 hours of moving the remaining 7 mares to a noninfected pasture, their udder development began, and all delivered live foals within 7 days and lactated without trouble.

Mares not removed from infected fescue should be monitored closely so they can be assisted at foaling. Frequently the placenta must be broken, as it may be too thick and tough to be broken by the mare and foal during delivery. Assistance in delivering the foal is also frequently necessary because of decreased pelvic ligament and cervical relaxation, and because of the foal’s larger size due to the increase in the length of gestation. The foal may be dead, or weak at birth and require respiratory assistance. Since most affected mares don’t lactate, the newborn foal must be given adequate quantities of good colostrum and fed until the mare recovers sufficiently from the poisoning to produce adequate milk for the foal. This will generally take only about a week after she stops consuming infected fescue forage. If the placenta is retained, the mare must be cared for properly if she is to survive and conceive when rebred. Procedures for providing assistance in delivery and caring for the foaling mare and newborn foal, including providing respiratory assistance, colostrum, and feeding, are described in Chapter 14.

Prevention of Fescue Poisoning

Pastures containing a significant amount of fescue should not provide the major part of the diet for growing horses, or for mares during the last 60 days of their pregnancy, unless it is known not to be infected. If weanlings or yearlings are to be grazed on pastures or fed mature hay containing a significant amount of endophyte-infected fescue, or fescue whose infestation status isn’t known, they should be fed a grain-mix as 50% of their total diet (Table 15 – 3). This will be approximately 1 lb of grain-mix/ 100 lbs (1 kg/100 kg) body weight daily. Pregnant mares consuming fescue not known to be infestation-free should be closely monitored beginning 6 weeks before their expected foaling date.

If a mare has no udder development by 2 weeks before her due date, she and all other pregnant mares on that pasture should be removed from that pasture and either put on a pasture or fed a hay known to be either noninfected or not fescue. If all the mares can’t be fed a nonproblem-causing forage, or removed from a problem-causing pasture, they should be fed alfalfa hay as a substantial portion of their diet (over 10 lbs or 4.5 kg/mare daily) and continue to be monitored closely for fescue-poisoning-induced problems.

Whether a fescue pasture or hay has the potential to cause problems can be determined. To do so collect an equal number of fescue seeds or, (ideally in the fall but anytime from fall to spring) stems from several sites throughout the hay or entire pasture. Collect from at least 5 sample sites/acre or 30 sample sites/pasture. Combine the samples into one composite sample of at least 2 oz per 10 acres or less (60 g/4 ha). The samples should be seedhead, or from the bottom 2 inches (5 cm) of the plant stem above the ground, and be devoid of roots and leaves since the mold is not in them. Put the composite sample into a jar or test tube and fill the container half full of water. Send it to a laboratory able to determine if the Acremonium coenophialum endophyte mold is present. Since the mold is on the inside, not on the outside of the plant, it can’t be detected by visual observation. At the laboratory each seed or stem should be stained (e.g., with lactic acid and aniline blue) and examined microscopically to determine the percent of infected fescue plants in the pasture or hay. Infected plants can also be detected by enzyme-linked immunosorbent assay (ELISA) and by tissue-print immunoblot (TPIB). These two methods are comparable in accuracy, and both are more specific than the staining method, but aren’t currently available commercially.

If more than 7% of the fescue is infected, to ensure that fescue poisoning doesn’t occur, mares must be removed from that pasture or hay during the last 2 weeks, and preferably 2 months, of pregnancy. Feeding grain in amounts up to even one-half of the pregnant mare’s energy needs will not decrease the incidence or severity of fescue poisoning if she remains on infected pasture, but may, if the infected forage is hay rather than pasture, since on pasture more seeds which are higher in the mold and its toxins are consumed. Feeding a grain-mix as one-half of the growing horse’s diet will prevent any effect of consuming an infected fescue hay, but may not if they are on a heavily infected fescue pasture.

All mature horses, including pregnant mares until the latter stages of pregnancy, may be safely kept on infected fescue pasture, as they are not known to be affected by fescue poisoning. In contrast to previous suggestions, neither increasing nor decreasing nitrogen fertilization or giving pregnant mares selenium have any effect on altering the incidence or effects of fescue poisoning.

Overseeding pastures that have 25% or less infected fescue with legumes, such as red or white clover or alfalfa, so as to maintain at least 20% legumes in the pasture may decrease fescue poisoning, presumably by decreasing the concentration of the mold in the total pasture forage. Overseeding grass pastures with legumes is often also beneficial in increasing both the amount of pasture forage produced and the nutritional value of forage obtained from that pasture, as described in Chapter 5.

Fescue toxicosis can be prevented by killing the fescue in an infected pasture with tillage or a herbicide (e.g., Roundup-Monsanto, or Gramoxone Super) and replanting as described in Chapter 5 with either fescue seed certified to be endophyte-free, or with a different forage. Since the fescue-toxicosis-inducing mold is transmitted only through the seed and, in contrast to most molds, is not in the soil and does not spread from plant to plant, whether a plant is infected depends entirely on whether or not the seed from which it grows contains the live mold. The mold is reported to die in seed stored for more than a year, although 2 years storage has been recommended. Because it is spread only in the seed, its spread is slow and can be prevented by grazing or cutting fescue before it matures and produces seeds. Also, since the seeds contain the highest concentration of the mold, cutting fescue before seeds form decreases the amount present in the hay and thus its detrimental effect; it also results in a more palatable, higher nutritional value hay.

If a mold-free fescue seed is to be planted, ensure that all of the old infected fescue is dead. This can be difficult, particularly in old established sod. It is best to not plant noninfected fescue seed immediately after killing an old infected fescue pasture. If possible, it is best to plant an annual forage or a row crop for at least one growing season prior to planting the noninfected fescue. This reduces the likelihood of the old fescue sod damaging the fescue seedlings; it allows infected seeds that might be present in the soil to age making them less likely to germinate and produce infected plants; and it allows a thorough assessment of the extent to which old plants were destroyed before replanting noninfected seed.

Fescue seed free of infection, which may be referred to as fungus-, mold-, or endophyte-free seed, is available in most areas. There are no known varieties of fescue that are resistant to the mold. However, all of the commercially available seed of some varieties is mold free. For other varieties, seed bought commercially can be either mold free or mold infected, depending on the source of the seed. Most certified fescue seed now contains a statement on the seed tag as to whether or not it is infected. Only seed that has 5% or less, and preferably zero percent, mold infection should be used to plant an infection-free pasture.

It may be better in some areas, however, not to plant noninfected fescue. Noninfected fescue is less productive and less resistant to insects, flooding, drought, and variations in fertilizer application than is infected fescue. Infected fescue is hardier and will tend to take over noninfected fields. Because noninfected fescue has less vigor, particularly as seedlings, care must be taken to provide favorable conditions during its establishment, including planting at the optimum time, fertilizing and liming according to soil tests, using an adequate seeding rate, and avoiding overgrazing, especially during the first year of growth.

Besides keeping the mare off infected fescue pasture during the last 60 days of pregnancy, or replanting infected fescue pastures, a third alternative that may be beneficial is to feed compounds that counteract infected fescue’s effect. The oral administration of domperidone to mares during the last 30 days of pregnancy has been reported to be effective in preventing the effects of fescue poisoning with no negative side effects. Perphenazine, a phenothiazine derivative, fed twice daily at 0.3 to 0.5 mg/kg body wt beginning 1 week before foaling is due has been shown to increase non-pregnant mare’s plasma prolactin concentration, back toward normal, induce mammary growth and to initiate milk production. Care must be taken to use a pure perphenazine preparation, because this drug marketed for people, is often combined with the antidepressant drug, amitriptyline. Twice the recommended dosage of perphenazine causes sweating, colic and excessive sensitiveness to activity. Feeding phenothiazine and thiabendazole has been shown to have a preventive effect in cattle, but not horses, grazing infected fescue pastures.

EQUINE ERGOTISM

Ergot is the common name for the mycotoxin-containing hardened covering of the mold Claviceps purpurea and C. paspali. It is unique in that the mycotoxin is produced only during flowering and seed maturation, and not in the mature plant or seed and, therefore, not during their storage. Ergot formation and, therefore, epidemics and cases of ergotism are most likely to occur during damp weather around plant flowering time. Conversely, ergot formation and spread are inhibited by periods of drought.

Ergots are black- to brown-colored, hard, banana-shaped masses from ¼ to ¾ inch long (0.6 to 2 cm) that project from the plant seedheads. Those produced by C. purpurea are present most often in rye, but also triticale (the cross between rye and wheat) and ryegrass seedheads, but may be present in any of the cereal grains and seedheads of other grasses. Ergots produced by C. paspali are present primarily in Paspalum grass seedheads, such as Dallis and Bahia grasses. C. paspali, in addition to ergot, also produces tremor producing mycotoxins which are probably responsible for causing “Grass or Paspalum staggers” in horses, and not ergotism as described in the following section on this condition.

Ergot produced by C. purpurea is toxic to all animals, including people, and was responsible for the death of thousands of people in the Middle Ages who ate contaminated rye bread, causing what was referred to as St. Anthony’s Fire. Although ergot contains many compounds, its alkaloids are its toxic principle. These include the hallucinatory drug LSD, (lysergic acid diamine) which may be responsible for the behavioral effects ergot causes. Ergot alkaloids also cause blood vessel constriction causing dry gangrene of the extremities, and inhibit the reproductive hormone prolactin, which may be responsible for the reproductive effects of ergot poisoning. Thus, in livestock, ergot alkaloids may cause:

Cattle and sheep, which appear to be the most sensitive to ergot, may demonstrate any of these clinical effects, whereas swine show primarily the last two effects, but not abortion. Horses are rarely affected by ergotism. Horses fed over 1 lb (500g) of ergot showed only transient symptoms. But horses may show any of these clinical effects, with behavioral changes being most common. Dry gangrene of the legs, difficulty in swallowing, slow respiration, weak pulse, and death of horses ingesting large quantities of ergot-infected ryegrass may occur. No udder development, thickened fetal membranes that required manual rupturing, difficult delivery, poor cervical dilation, and uterine contractions, retained placenta, and uterine rupture has been reported in mares consuming oats containing ryegrass seeds contaminated with Claviceps purpurea and ergot. Their absence of milk production usually did not resolve, although several mares began lactating 10 to 15 days after foaling. Abortions and prolonged gestation also occurred. Embryonic death and anestrus occurred in rebred mares. Affected foals were unable to stand, were icteric, and had no sucking reflex. These effects are similar to those occurring as a result of fescue poisoning. Despite tube-feeding and blood or plasma transfusions, 21 of 33 ergot affected foals died within the first 5 days of life.

GRASS STAGGERS IN HORSES

Staggers, or incoordination, may occur in horses as a result of: (1) moldy corn disease, as discussed in the following section; (2) ergotism, as discussed in the previous section; and as a result of two types of grass staggers: (3) paspalum staggers and (4) perennial ryegrass staggers. Both moldy corn disease and ergotism occur primarily in horses consuming mycotoxin-contaminated grains, generally result in additional clinical signs, and are often fatal. In contrast, grass staggers usually occur when these grasses are grazed, but may occur when they are consumed as hay, straw, or seed cleanings, and are rarely fatal, with affected horses recovering when a noncontaminated diet is consumed.

With both types of grass staggers, behavioral changes usually occur suddenly in horses within 1 to 4 weeks of the continual consumption of a contaminated forage. From 5 to 75% of horses consuming the contaminated feed are generally affected. Clinical signs vary in severity from mild excitability and muscle tremors to spastic incoordination and tetany. Even horses severely affected often appear normal at rest but have a fine tremor of the head or neck, or weave when standing still. When incited to move, affected horses may have a stiff, spastic uncoordinated gait that affects either the forelegs or all legs, exaggerated leg action, muscular spasms, and occasionally tetanic seizures. Those with tetany, when left undisturbed, will recover, generally in less than 20 minutes, stand, and walk off stiffly. Development of abdominal muscle spasms leading to straining may occur. Loss of body weight does not occur.

Clinical signs are predominantly attributable to reversible biochemical, not pathological, changes. As a result, all effects are reversible, and no visible or microscopic lesions occur even in severely affected animals. Treatment is not generally necessary, as the diseases are self-curing when the animals are removed from infected paspalum grasses or perennial ryegrasses. Marked improvement occurs within 2 to 14 days, and complete recovery occurs within a few months or less if a noncontaminated diet is fed.

Paspalum staggers is caused by tremor producing mycotoxins produced by Claviceps paspali primarily in the seedheads of Paspalums spp. grasses—especially Dallis or Bahia grasses. Although this mold may also produce ergot, it is its tremor producing mycotoxins that are thought to cause paspalum staggers in horses. Dallis grass (Paspalum dilatatum) is the most common of the two paspalum grasses responsible for the condition in the United States and, therefore, it is sometimes referred to as Dallis grass staggers instead of paspalum staggers.

Dallis grass is a common pasture grass of the more humid regions of the United States, ranging from southern California to the southeastern states. Under humid conditions it may become infected with C. paspali. This mold invades only the flowering part of the plant and produces a sticky substance referred to as honeydew that is attractive to insects, which aid in the dissemination of the mold. In time, the honeydew dries to form a brown mycotoxin-containing mass that resembles the grass seeds.

Perennial ryegrass staggers is caused by the tremor producing neurotoxins lolitrems, which are produced by, or their production stimulated by, Acremonium lolii. This endophytic mold grows, and the toxin is produced, in the lower outer leaf sheaths, seeds, and seed cleanings of perennial ryegrass (Lolium perenne). Since the toxin is produced in the lower leaf sheaths, the lower to the ground animals graze perennial ryegrass, the more likely they are to be affected. Thus, the disease most frequently occurs in herbivores, including horses, on intensively or overgrazed perennial ryegrass pastures during late summer or fall.

Confirming perennial ryegrass as a cause of the staggering symptoms described is usually based on finding (most commonly in the lower portions of the plant) and identifying the causative mold Acremonium lolii. Diagnosis is also confirmed by the occurrence of clinical signs in mice injected with plant extracts or by assaying for the toxin. Lolitrem concentrations of 5.3 mg/kg for horses and 2 mg/kg for sheep have been found to result in perennial ryegrass staggers.

Paspalum staggers can be prevented by mowing the pasture at or prior to the flowering stage to prevent formation of the toxic mycotoxin-containing mass, which is formed only in the flowering part of the plant. Procedures for preventing perennial ryegrass staggers include: (1) replacement of the pasture with perennial ryegrass free of the causative mold, (2) not overgrazing, (3) removing animals from affected pastures for a few weeks until new growth appears, and (4) supplementing with noncontaminated feed during hazardous periods (late summer to fall in most areas). Replacement of pasture with mold-free perennial ryegrass may be undesirable, as the mold or mycotoxin increases the grass’s resistance to insects, and mold-free perennial ryegrass is less productive.

Facial eczema, characterized by lesions on light-colored or exposed areas of the skin around the face, resulting in edema, exudation, blistering, and tissue death sloughing, may occur instead of staggers in sheep, but not horses, grazing ryegrass pastures. Staggers resembling perennial ryegrass staggers may occur in sheep and cattle, but are not reported in horses, grazing annual ryegrass (Lolium rigidum). Annual ryegrass staggers, however, is not due to a mycotoxin poisoning but instead to the neurotoxin corynetoxin. It is produced in annual ryegrass infected with the nematode parasite Anguina agrostris and the bacterium Corynebacterium spp.

Ruminants, but not horses, may also be affected by both “Phalaris Staggers” and “Bermudagrass Staggers” or tremors. Both result in clinical signs similar to those occurring with either type of ryegrass staggers and with paspalum staggers. The cause for Bermudagrass (Cynodon dactylon) staggers or tremors is unknown. Phalaris staggers is caused by hordenine (p-hydroxyphenylathyl-dimethylamine) produced by Phalaris grasses, primarily reed canarygrass (Phalaris arundinacea). It is sometimes referred to as reed canarygrass staggers instead of phalaris staggers.

Hordenine is also produced by sprouting barley, millet, milo and wheat, and is thought to be the hallucination producing compound in peyote cactus. Hordenine has actions similar to epinephrine or adrenalin. It stimulates the heart, constricts blood vessels, and relaxes constricted lung airways. However, there appears to be no evidence that the amount of hordenine in reed canarygrass or sprouted grains has any significant effect on horses. But some racing commissions (e.g., New Jersey and West Virginia) disqualify horses if hordenine is found in their urine, which it may be if they are consuming these feeds.

Hordenine has been associated with decreased feed palatability and poor growth and/or condition in ponies and ruminants grazing reed canarygrass. But chronic phalaris toxicosis or staggers, which may occur in ruminants, is not known to occur in horses. Clinical signs in ruminants may be acute or chronic. Acute poisoning results in a sudden onset of neurologic signs or collapse, abnormal heart rythms, and respiratory distress followed by death or recovery. Chronic poisoning effects, in addition to poor growth and/or condition, include decreased feed intake, loss of control of the tongue or the ability to swallow, excess excitability, incoordination, stiff gait, head nodding, muscle twitching, tetanic seizures, and death. Clinical signs may be delayed for as long as 4 months after ruminants are removed from phalaris pastures. Pretreatment with cobalt pellets apparently prevents clinical signs. Brown pigment may occur in nerve cells in the brain stem and spinal cord of affected ruminants.

MOLDY CORN DISEASE IN HORSES

Moldy corn poisoning in horses and other equine species results in a degenerative softening of the white matter of the brain, i.e. results in leukoencephalomalacia, another name for the disease. It is also referred to as blind staggers (as are locoweed and excess selenium poisonings) which it causes, as well as other neurologic signs. These generally occur for only 4 to 72 hours, but occasionally 1 to 2 weeks, duration, before death. Liver damage may also occur. In addition to moldy corn disease, blind staggers, and equine leukoencephalomalacia, it has also been referred to as leucoencephalitis, encephalomyelitis, cerebrospinal meningitis, fumonisin poisoning, foraging disease, corn stalk disease, epizootic cerebritis and mycotoxic equine encephalomalacia. It affects only horses and other equine species.

It is one of the most common poisonings of domestic horses. Nearly 200 cases were confirmed by veterinary diagnostic laboratories in 11 states in a 2-year period, and outbreaks with many horses affected can occur. The disease occurs worldwide, most often in areas with temperate humid climates following a dry summer and wet fall, such as throughout eastern and midwestern United States. Fusarium, the causative mold appears to increase when hot, dry conditions are present during pollination, and continues to increase when warm temperatures occur during the last 30 days of maturity. Outbreaks of the disease are usually seasonal, occurring from fall through early spring, but cases can occur any time of the year from stored corn containing the mycotoxin. In contrast to most mycotoxicoses, older horses are reportedly more susceptible to moldy corn disease than younger horses.

Cause of Moldy Corn Disease

Moldy corn disease is caused by a fumonisin mycotoxin that injures the lining of blood vessles. The toxin is produced by the molds Fusarium moniliforme, and by F. proliferatum. The presence of fumonisin mycotoxin in a feed, and the occurrence of the disease from the ingestion of that feed, is generally due to the feed becoming contaminated with the causative mold prior to harvesting and not during storage. Although Fusarium molds may grow in a wide range of different feeds and occasionally are isolated from hay and small cereal grains, moldy corn disease has been reported only in horses consuming corn grain or any portion of the corn plant, or feed containing them. The mold can grow at a wide temperature range when the feed moisture content is above 13 to 15%. Infected corn kernels may be recognized by a pink to reddish brown color. Although affected horses are usually associated with shelled or ear corn, the mold may grow in, its mycotoxin be present in, and the disease be due to consumption of, cornstalks and leaves and in commercially prepared mixes and pellets containing any portion of the corn plant. However, corn containing the Fusarium mold may or may not contain the fumonisin mycotoxin and, therefore, be harmful. Fusarium ear rot was found to be present in 50 to 96% of corn fields sampled in Indiana from 1989 through 1992. But fumonisin was present in only 13 to 84% of the samples that contained Fusarium, and there was no relationship between the amount of mold and the amount of the mycotoxin present. Conversely, although non-Fusarium containing corn generally does not contain fumonisins, it may; that is, nonmoldy-appearing corn-product-based feed may cause moldy corn disease. Determining feed that may or has caused moldy corn disease, therefore requires that the fumonisin mycotoxin be found in the feed. In suspected cases all feeds being consumed, not just moldy-appearing corn, should be analyzed as described in the previous section on “Diagnosis of Mycotoxin Poisoning.”

Fusarium molds produce a wide variety of fumonisin mycotoxins which have various effects on different species of animals. In horses the mycotoxin appears to damage the lining of the blood vessles in the brain, and in some cases to cause liver damage. Some have suggested that neurologic signs are caused by a low dose of toxin over time, whereas liver damage is a result of a higher dose. However, this has not been found to be the case in some outbreaks. Others have postulated that different toxins cause the liver and the neurologic forms of the disease, with fumonisin B₁ likely responsible for the neurologic form, which is by far the most common form of the disease. Forty-five horses that died from moldy corn disease in one outbreak had been associated with feeds containing over 5 ppm fumonisin with fumonisin B₁ present at levels of 0.6 to 96 ppm and B₂ at 0 to 38 ppm.

Moldy corn responsible for outbreaks of the disease in horses has been fed to numerous nonequine species, including goats, pigs, monkeys, hamsters, rats, mice, guinea pigs, rabbits, and chickens without causing illness or death. However, feeding other horses contaminated feed responsible for outbreaks in horses doesn’t always produce the disease either, even after extended exposure.

Clinical Effects of Moldy Corn Disease

The course of the disease depends on the amount and rate of mycotoxin consumption and the individual horse’s tolerance to the toxin, which is variable. In most outbreaks, 15 to 25% of horses consuming the contaminated feed are affected, although 100% may be affected and die. The onset of clinical signs is usually 2 to 9 weeks, but may be from less than 1 to 21 weeks, after the onset of continuous consumption of fumonisin-contaminated feed.

Neurologic signs usually appear abruptly and end in death within 4 to 72 hours of their onset, but occasionally the duration may be as long as 4 weeks. However, more subtle signs, such as decreased feed intake and depression, often precede severe neurologic signs by days or weeks.

The clinical signs are characterized by rapidly progressive neurologic alterations. These include intermittent to complete absence of food intake, and mild to profound depression with little response to stimuli, but when affected horses respond they may be quite excitable. Affected horses have a progressive incoordination, may press their heads against something, have delirium, blindness, sweating, circling, or leaning against a wall, but remain standing until shortly before death. Muscle tremors and incoordination lead to an inability to stand. Once down, convulsions may occur prior to coma and death. Outbreaks may individually be characterized by unique predominant clinical signs such as colic, a high incidence of blindness, or although able to eat and drink a refusal to do so resulting in rapid weight loss and dehydration. The temperature of affected horses is generally normal, in contrast to those with sleeping sickness viral encephalopathies. Some horses with moldy corn disease show many, some only a few, and some no clinical signs prior to death. Horses that show neurologic signs generally die, regardless of treatment, although there are instances of horses recovering, but some retain brain damage. In several outbreaks 64 to 100% of horses showing clinical signs died.

Clinical signs associated with the less common moldy corn induced liver disease form, which may occur alone but more often in conjunction with neurologic alterations, include icterus, which is generally severe; swelling of the lips and nose; bloody spots in the mucous membranes; lowered head; reluctance to move; abdominal breathing; cyanosis; and a bloody urine. As with the neurologic form, clinical signs appear acutely and death usually occurs within a few hours to days.

Moldy corn disease should be considered as a cause of an acute onset of rapidly progressive neurologic signs (e.g., incoordination, blindness, absence of feed intake, little response to stimuli, or severe depression to agitation) and death occurring in two or more horses in a group that has been consuming a corn-containing feed for more than 1 week, even if the feed isn’t visibly moldy, but particularly if it is, and if the problem occurs from late fall to early spring in areas with a dry summer, wet fall, and humid climate, such as the eastern and midwestern United States. The presence of Fusarium moniliforme or F. proliferatum in affected horses’ feed is quite indicative that the problem is due to moldy corn disease but confirmation requires the identification of fumonisins in feed being consumed. Test kits for detecting fumonisins are available (Table 19–4). It has been hypothesized that the fumonisins in contaminated feed may degrade after a variable period, but deaths have occurred in horses consuming fumonisin containing feed stored for over 1 year.

An acute onset of similar neurologic signs with a rapid progression and high mortality affecting more than one horse on a farm may occur as a result of the diseases given in Table 19–5. Other equine neurologic diseases may have similar clinical signs as moldy corn disease but usually occur in a single horse on a farm and generally aren’t as rapidly progressive or severe.

TABLE 19–5 Causes of Neurologic Diseases Characterized by an Acute Onset and Rapid Progression Generally in More Than One Horse in a Group^a

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