Plants Affecting the Nervous System

Table of Contents

Part I: Locoweeds

Locoweed Poisoning
Astragalus Species Containing Nitro Compounds
Blue or Spotted Locoweed
Wooly or Purple Locoweed
White Locoweed, White Point Vetch, Crazy Weed
Purple Locoweed, Lambert’s Red Loco
Timber Milk Vetch
Crown Vetch

Part II : Other Plants Affecting the Nervous System

Sagebrush Poisoning
Sand Sage 
Fringed Sage, Sagewort, Estafiata
Big Sagebrush
Coyotillo, Tullidora
Bracken Fern, Brake Fern, Eagle Fern
Common Horsetail, Scouring Rush
Yellow Star Thistle and Russian Knapweed Poisoning
Yellow Star Thistle
Russian Knapweed
White Snakeroot Poisoning
White Snakeroot
Jimmy Weed, Rayless Goldenrod, Burrow Weed
Miscellaneous Neurotoxic Plants
Mescal Bean, Frijolito, Mountain or Texas Laurel
Buckeye, Horse Chestnut
Kentucky Coffee, Tree, American Coffee Berry, Kentucky Mahogany
Carolina Jessamine, False or Yellow Jessamine
Sweet Shrub, Carolina Allspice, Strawberry Bush
Golden Chain Tree, Bean Tree
Bleeding Heart, Dutchman's Breeches, Squirrel Corn, Stagger Weed
Lobelia
Western Horse Nettle, Potato Weed
Sudanand Johnson Grass Poisoning
Peas
Caltrop, Carpetweed
Hemp, Marijuana
Tobacco
Miscellaneous Plants Associated with Neurologic Signs

Alphabetic Plant List
Glossary

A variety of indigenous and exotic plants found in North American affect the nervous system of animals, some being associated with considerable economic losses to the livestock industry. Arguably the most important group of plants affecting the nervous system are those belonging to the genera Astragalus and Oxytropis, collectively known as locoweeds. These plants, found in vast areas of western North America and in many parts of the world, have long been recognized as a problem to livestock [1,2].

There are numerous other plants affecting the nervous system such as yellow star thistle (Centaurea solstitialis) and Russian knapweed (Acroptilon repens) that will be discussed in the second section of this chapter. These and a variety of other plants are significant not only because they are poisonous and cause neurological disease in animals, but they also aggressively displace indigenous plants and reduce the value of natural ranges for grazing. Others like white snakeroot (Eupatorium rugosum) have historical and contemporary significance because of their effects on the nervous system. For example, deaths of early settlers in eastern North America who drank the milk from cows with " milk sickness", a fatal disease characterized by severe muscle tremors, is attributed to the toxin in white snakeroot. Once the neurotoxic effects of the white snakeroot were recognized, preventive management measures have largely eliminated this form of plant poisoning in people. The plants listed in Table 6 - 1 cause poisoning when normal forages are scarce, or the plants are accidentally incorporated in hay and grain fed to animals.

Part I - Locoweeds

Locoweed Poisoning

More than 2000 species of the genera Astragalus and Oxytropis exist throughout the world, of which at least 370 occur in North America [3]. Collectively these plants are commonly called locoweeds, vetches, or milk vetches, and are similar in appearance. Only the experienced botanical taxonomist can readily differentiate the species. Livestock poisoning attributable to these genera has been recognized since the early part of this century, and the locoweeds continue to cause more economic losses to the livestock industry than all other plant-induced toxicities combined [1,4-7]. Although all species of Astragalus and Oxytropis in North America should be considered poisonous unless proven otherwise, some species of milk vetch such as A. cicer and A. tenellus are nontoxic, and serve as useful forages for range animals [8]. In one extensive survey of 1690 species of Astragalus, 221 (13%) tested positive for toxic nitro compounds [9]. This points out the necessity of testing exotic species of Astragalus to ensure they are not toxic before they are introduced as forages for livestock in arid areas, or as plants for erosion control.

The locoweeds or vetches have been associated with three general syndromes of livestock poisoning. The best known is that of locoism due to the effects of the alkaloid swainsonine [1,10-12]. In addition, the locoweeds/vetches cause respiratory problems and peripheral nerve degeneration due to nitroglycoside compounds in the plants [9,10,13]. A third syndrome is caused by chronic selenium toxicity due to the ingestion of locoweeds or vetches that accumulate selenium [10]. Selenium toxicity is discussed in Chapter 9. Some species of Astragalus may contain one or more of the toxins and consequently may cause a combination of clinical signs in animals that have eaten them [10,14].

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Principal Toxin

Early researchers suspected a toxic substance in locoweeds they called locoine, [1,15] an alkaloid that has now been named swainsonine because it was first isolated and characterized from the gray swainson pea (Swainsona canescens) [16,17]. The Swainsonaspp. are leguminous herbs mostly confined to Australia and are closely related to plants in the genus Astragalus found in other parts of the world [18]. Swainsonine is one of a group of indolizidine alkaloids found in locoweeds that appears to play a major role in the pathogenesis of locoweed poisoning [16,17]. There is a growing body of evidence that swainsonine is produced by an endophytic fungus growing in the locoweed plants. (Fungal Endophyte Infection and Swainsonine Toxicity in locoweed. Thesis by Karen Braun, 1998, New Mexico State University, Las Cruces, New Mexico) In North America, swainsonine has been found in variety of Astragalus and Oxytropisspp. listed in Table 6 - 2 [19-21]. Horses, cattle, sheep, goats, elk, and domestic cats are both naturally and experimentally susceptible to the toxic effects of swainsonine [22-25]. All animals, however, should be considered susceptible to the toxic effects of the alkaloid.

Signs of poisoning do not become evident until animals have consumed significant quantities of locoweeds over many weeks and the toxic threshold is reached. Although horses, cattle, and sheep were thought to develop an addiction for locoweeds, it is more correctly termed habituation because there is no dependence on the plants as there would be in the case of addiction [26,27]. Locoweeds are palatable and of similar nutrient value to alfalfa, which may explain why animals eat locoweed even when normal forages are present [28].

The quantity of swainsonine in locoweeds varies according to the species, stage of growth, and the growing conditions. The succulent preseed-stage plants appear to be the most palatable, although cattle appear to relish the flowers and immature seed pods [28]. The palatability of locoweed does not have any relationship to the quantity of swainsonine in the plant [28].

Swainsonine inhibits the action of two lysosomal enzymes (α-D-mannosidase and Golgi mannosidase II) that aid in the metabolism of saccharides [29,30]. The inhibition of α-mannosidase therefore causes cells to accumulate complex sugars or oligosaccharides [31]. When Golgi mannosidase II is inhibited, the normal structure of oligosaccharide components of glycoproteins is affected, thus furthering their accumulation [30]. As a result, oligosaccharides accumulate in the cells of the brain and many other organs and interfere with normal cellular function [11,12,32]. In effect swainsonine causes a generalized lysosomal storage disease similar to the genetically transmitted disease mannosidosis [33-35]. The indolizidine alkloid castanospermine isolated from the seeds of the Australian Morton Bay chestnut tree (Castanospermum australe) is similar to swainsone in its inhibitory effects on glucosidases [31]. In Brazil and Mozambique, lysosomal storage disease in goats, similar to that caused by swainsonine, has also been attributed to (Sida carpinifolia), and a morning glory species (Ipomoea carnea) [36,37]. Young animals are most severely affected by swainsonine because maturing neurons are more vulnerable to the effects of the toxin. In addition, swainsonine is passed through the milk, thereby increasing the dose of alkaloid a suckling animal may acquire to that which it ingests through the plants it eats [24,38].

The concentration of swainsonine in locoweed (0.09 - 0.23 percent dry weight) varies with the stage of growth. The highest concentrations of swainsonine are found in the flowers and seeds (0.28 and 0.36 percent, respectively) and consequently the quantity of plant that an animal has to eat to receive a toxic dose will vary [31,39]. However, the potency of swainsonine is such that it is not necessary for high doses to be ingested to induce poisoning. Experimentally, locoism can be produced by feeding 0.75 to 1.0 lb/day of dried locoweed to horses and cattle for 75 to 85 days [39]. In general, the greater the quantity of locoweed consumed, the more rapid the onset of poisoning.

Clinical Syndromes Attributable to Locoweed Poisoning

Locoism

Locoism, the term originally given to locoweed poisoning, is derived from the Spanish word "loco" meaning crazy [1,2]. This aptly describes the abnormal neurologic behavior shown by horses and other animals intoxicated by locoweeds. Horses show the nervous signs of locoweed poisoning more commonly than do cattle or sheep. Affected animals may exhibit a variety of signs including depression, circling, incoordination, staggering gait, and unpredictable behavior especially if the animal is stressed or excited [1,2,7,22,24,39]. Some horses become totally unpredictable in their response to handling and may fall down when being haltered or ridden. Poor vision, incoordination, and sudden changes in behavior such as rearing and falling over backward, make these horses dangerous and unsafe to ride. Cattle may become aggressive when handled, and are more difficult to manage and work with when intoxicated. Weight loss, despite ample forage and grain being available, is typical [40]. In young animals, weight loss and poor growth rates may be a result of nervous system depression and apparent inability to eat normally [27]. If removed from the source of the locoweeds and fed a nutritious diet, animals will improve and appear relatively normal after several months. However, regeneration of affected neurons in the brain and spinal cord may not occur completely making horses a potential liability to human safety if ridden [39]. The prognosis for locoed horses should therefore always be guarded.

Locoweed-Induced Infertility and Reproduction Failure

In cattle, locoweed poisoning is more commonly associated with abortions, infertility, subcutaneous edema in the fetus, and fetal deformities [41-45]. Cows consuming locoweed may exhibit abnormal and lengthened estrus cycles and fail to conceive [45]. The reproductive problems and congenital defects commonly associated with locoweeds most probably result from the effects of swainsonine acting directly on the uterus, placenta and fetus [11,43]. Cytoplasmic vacuolation identical to that seen in many other organs is also evident in the placental tissues [11]. The placenta appears to be most susceptible to the effects of locoweed during the first 90 days of pregnancy, but it is vulnerable at any stage [42]. Normal placentation may be interrupted causing fetal resorption, abortion, or hydrops allantois [45]. The latter condition has been observed in sheep and cattle and is commonly referred to as water belly because the uterus becomes greatly distended with fluid [4,46,47]. Cows with hydrops may carry the pregnancy to term, but more frequently abort or become recumbent and unable to rise owing to the massive weight of the fluid in the uterus. The severely distended uterus also compresses the abdominal organs and interferes with normal digestion. Retention of fetal membranes and subsequent infertility are common sequels to hydrops.

Lambs and calves born to locoweed-poisoned dams may be born alive but weak and often die after a few days. Others may be smaller than normal or have deformities of the limbs or head [39,48]. Pregnant mares that consume quantities of woolly loco (A. mollisimus) in early gestation may produce foals with crooked legs especially involving the bones of the fetlocks [49]. The formation of congenital abnormalities such as crooked legs is probably due to fetal immobilization induced by the locoweed [50]. These teratogenic effects of locoweeds and other plants are discussed further in Chapter 8.

Rams having consumed locoweed (A. lentiginosus) for prolonged periods have been observed to undergo testicular atrophy with decreases in spermatogenesis [51]. Similar changes in bulls grazing locoweeds can be anticipated. The formation of abnormal sperm and decreased motility of sperm are attributable to the cytoplasmic vacuolation of the cells of the seminiferous tubules, epididymis, and vas deferens [52]. The vacuoles result from the accumulation of oligosaccharides that impair normal sperm maturation and function [53]. The vacuolation, however, is transitory and disappears after 70 days of a locoweed-free diet [54].

Locoweed-Induced Heart Failure

There is correlation between the incidence of "high mountain disease" or congestive right heart failure in cattle and the consumption of locoweed (O. sericea) [55-58]. Cytoplasmic vacuolation characteristic of swainsonine toxicity, observed in the lungs of cattle with "high mountain disease", possibly compounds the effects of high-altitude hypoxia on the pulmonary vasculature, causing pulmonary hypertension and eventual right heart failure. Experimentally, the fetuses of ewes fed locoweed for 2 to 3 months developed heart irregularities and right ventricular hypertrophy, suggesting there may also be a direct effect of swainsonine on the heart [47,48].

Weight Loss and Ill-Thrift

The continuous consumption of locoweeds by young animals over the course of the growing season, and even when the plants are dry or dormant during the winter, can result in stunted, poorly growing animals. This affect on the growth of animals is probably due to the effects of swainsonine on the pituitary and thyroid glands affecting production of growth hormone and thyroxine, and decreased nutrient absorption from the intestinal cells affected by the alkaloid. Many calves with locoism exhibit symptoms identical to those produced by bovine virus diarrhea; poor body condition, rough hair coat, lower than normal weaning weights. Locoweed poisoned calves have significantly lower weaning weights and gain poorly when placed on a concentrate ration under feedlot conditions. However, once the effects of swainsonine have diminished after calves have been off all sources of locoweed for about 60 days, compensatory weight gains can be expected [59].

Animals poisoned by locoweed often appear to have a greater incidence of common diseases such as foot rot, pneumonia, warts, and other infections. This suggests that affected animals may have a compromised immune system [60]. Evidence for this is detectable in sheep, which when repeatedly fed locoweed had lymphocytes with decreased responsiveness to mitogens [60]. Peripheral lymphocytes in the affected sheep contained cytoplasmic vacuoles characteristic of swainsonine toxicity. Similarly calves chronically eating locoweed and concurrently vaccinated with a modified live virus vaccine develop a poor titer to the vaccine. It is therefore important to remove calves from locoweed for at least a month to allow recovery of their immune system with normal lymphocytes capable of response to vaccines [59].

Diagnosis of Locoism

Locoweed poisoning may be confirmed in animals by demonstrating the presence of swainsonine in the serum, coupled with decreased serum "α-mannosidase activity [61]. The half-life of swainsonine in the serum is 16 to 20 hours [62]. This means that an animal suspected of locoweed poisoning must have a blood sample taken within 2 days of eating locoweed for swainsonine to be detected. Similarly serum α-mannosidase activity will return to normal within 6 days of locoweed being eliminated from the diet [62]. Elevated levels of the serum enzymes alkaline phosphatase, aspartate amino- transferase, and lactate dehydrogenase are likely in locoweed poisoned animals [60,61,63]. Serum protein and thyroid levels (T4 and T3) are usually decreased in animals poisoned by locoweed [62]. The presence of vacuoles in the cytoplasm of peripheral lymphocytes is a characteristic finding in locoweed poisoning in some animals [39,60]. Vacuolated lymphocytes may persist in the circulation for several weeks after an animal has ceased eating locoweed.

At postmortem examination there no specific gross lesions characteristic of locoweed poisoning. Emaciation, occasional stomach ulcers, thyroid hypertrophy, and pale coloration to the liver and kidneys may be seen [11,64]. Animals exhibiting neurologic signs, often have cytoplasmic vacuolation of neurons in the brain. Similar vacuolation is often present in the pituitary gland, thyroid, pancreas, kidneys, liver, lymphnodes, retina and other structures of the eye [11,39,65].

In animals chronically affected with locoism, and which have not eaten locoweed for more than a month, the vacuolation is restricted to hepatocytes and neurons of the brain [39]. Purkinje cells of the cerebellum retain vacuoles for over a year. The noticeable loss of these cells over time helps to explain the residual neurologic abnormalities typical of locoweed poisoning [39]. Experimentally, vacuoles can be first demonstrated in the kidney tubules 4 days after initiating locoweed feeding. Vacuoles in the neurons are detectable by day 8, and placental lesions develop 8 to 16 days after the start of locoweed consumption [65,66]. The vacuoles present in cells that are characteristic of swainsonine toxicity are similar to those found with other lysosomal storage diseases in animals such as "α- andβ-D-mannosidosis reported in cattle and goats [34,67,68].

Treatment of Locoism

An effective treatment for locoweed poisoning has yet to be developed. Fowler's solution and reserpine, once recommended for treating locoism, are unwarranted in light of current knowledge regarding the cause of locoweed poisoning [69]. Animals will recover from locoism provided they are removed from the locoweed before extensive cellular degeneration has occurred in the brain. Animals that have aborted generally will conceive in subsequent seasons provided they do not develop severe secondary infections of the reproductive system. Compensatory weight gains can also be anticipated in animals once they are removed from locoweed and are fed a balanced nutritious diet. Further consumption of locoweed should be prevented immediately, and every year thereafter because animals may retain a preference for the plants from year to year.

Prevention and Management of Locoweed Poisoning

To manage livestock on rangeland or pasture containing locoweeds, it is important to recognize the growth characteristics of locoweeds and the conditions under which livestock eat the plants. Cattle and probably other herbivores eat locoweed particularly when grazing pressure is high and other forages are depleted [70-72]. However, cattle will voluntarily eat locoweed when it is in the flower and early seed pod stage [73]. Although this corresponds to when swainsonine levels are highest in the plant, it is not the swainsonine level in the plant that appears to attract the animals to eat the plant at this stage of growth. The early seed pod stage coincides with the highest levels of protein and carbohydrate in the plant, which may increase palatability [74]. As other forages green up in the spring and summer, cattle will usually stop eating locoweed until grasses are depleted as a result of the season or overgrazing [73]. If temperature and moisture conditions are ideal as occurs in mild winters, locoweeds may retain green leaves in winter that make the plant attractive to livestock. It is important to pay attention to the rainfall pattern because a wet summer can mean more growth of locoweed, which in turn can mean that more plants are available both in the summer and winter [75]. Locoweeds retain some of their toxicity even when dried.

It has long been observed that once a cow starts eating locoweed, she will teach others in the herd to eat it. Experimentally it has been shown that cattle naive to locoweed will greatly increase their consumption of locoweed when placed with locoweed eaters [76]. This phenomenon is referred to as social facilitation, and it is an important influence in a herd of cattle. Social facilitation is probably the reason that over a period of seasons the percentage of cattle grazing locoweed in the herd grows to the point that all animals will eat it. Cattle and sheep do not become addicted to locoweed as was once thought because they will voluntarily stop eating the plant when other, more palatable forages are available [77]. Animals develop a preference for locoweed, apparently because the plants taste good to them!

Because locoweed poisoning is dependent upon the dose of locoweed an animal eats, and it usually takes several weeks of grazing the plants to become intoxicated, grazing management strategies can be developed to take advantage of this. Through close observation of the cattle, it is possible to determine when the consumption of locoweed is becoming excessive and poisoning is likely. At this point the cattle should be moved to a "safe area" for several weeks, an area with little or no locoweed. By rotating the cattle from pastures with locoweed to those without, effective use of the rangeland can be accomplished without severely poisoning the cattle or sheep.

Locoweeds can be controlled by the use of herbicides, but it is important to recognize that the seeds of many locoweeds can persist for at least 50 years [78]. Repeated application of appropriate herbicides will generally be needed to control locoweed reemergence. A variety of herbicides are effective in controlling Astragalus and Oxytropis spp., including the approved chemicals clopyralid, dicamba, picloram, and triclopyr [79]. The phenoxy herbicides 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophe- noxyacetic acid (2,4,5-T) do control locoweeds as long as they are applied when the plants are actively growing. In all cases, it is most important to ensure the herbicide being used is approved for application in the area and that the manufacturer's recommendations are followed.

Using the principle of conditioned food aversion, it is possible to train cattle to avoid eating locoweed [80]. Locoweed eaters can be averted from eating locoweed by associating the eating of locoweed with a distasteful experience. This is accomplished by feeding the cows locoweed and at the same time dosing them with a bolus of lithium chloride, a chemically irritating compound. The cattle develop "colic" from the lithium chloride and associate this unpleasant experience with eating locoweed. This aversion to eating the locoweed persists even into subsequent growing seasons provided the averted animals are not mingled with locoweed eaters. Through social facilitation averted cows relearn to eat locoweed from the locoweed eaters. Food aversion methods have the potential for preventing locoweed poisoning under some controlled management systems, and provide an alternative means of grazing cattle on rangeland heavily infested with locoweed.

Although various mineral and protein supplements have been recommended for the prevention of locoweed poisoning in livestock, there is no proven preventative value of feeding them [81,82]. Animals, however, that are deficient in protein and minerals will potentially benefit nutritionally from such supplements.

Astragalus Species Containing Nitro Compounds

As early as 1932, milk vetches were recognized as plants poisonous to cattle and sheep in the Rocky Mountain states [83]. Some 263 species of Astragalus (milk vetches) located principally in western North America from Canada to northern Mexico contain toxic nitroglycoside compounds capable of causing livestock poisoning [3]. Most Astragalus spp. containing nitro compounds do not contain the alkaloid swainsonine responsible for locoism nor do they accumulate toxic levels of selenium. The only known species to accumulate selenium and nitro compounds is A. toanus (Toano milk vetch), a relatively uncommon plant of eastern Utah, Nevada, and Idaho [84]. The more common milk vetches that contain nitro compounds associated with livestock poisoning are listed in Table 6 - 3 [2,14,85,86].

Principal Toxins

The toxicity of the milk vetches is primarily attributed to the nitro compound called miserotoxin, so called because it was first recognized in timber milk vetch (A. miser) [87-90]. Miserotoxin, a glycoside 3- nitro-1-propanol, is hydrolyzed in the rumen to the toxic 3-nitro-1-propanol (3-NPOH) [91]. Other species of milk vetch contain 3-nitropropionic acid (3-NPA) and not 3-NPOH. Misertoxin (3-NPOH) is rapidly absorbed into the blood of cattle and sheep where it is converted to 3-NPA [92]. Although the mechanism is not fully understood, poisoning by these nitro compounds appears to occur in two ways. Nitrite (NO2) from 3- NPA oxidizes hemoglobin to methemoglobin (up to 33 percent), which causes severe respiratory distress [93-96]. Secondly, 3-NPA or other unidentified metabolite also affects the brain and spinal cord causing muscular weakness and collapse [94-96]. Cattle and sheep are most frequently poisoned but horses are also susceptible. Other legumes, Indigofera spicata (creeping indigo) [97] and Coronilla varia (crown vetch), [98,99] contain 3-NPA and have been associated with poisoning in horses [100,101]. Dogs that have eaten the meat from affected horses may also become intoxicated [102]. Crown vetch is toxic to nonruminants, and if diets contain more than 5 percent of the plant, growth and development retardation in the young can be expected [103].

The nitro compound content of milk vetches varies with the species and the stage of growth, being highest during the flower and seed pod stage [86]. Years with high rainfall not only produce a flush of milk vetch growth, but the level of misertoxin is also increased in the plants [87]. The nitro compound content of Emory milk vetch (measured as nitrite) is in the range of 6 to 9 mg NO2/g plant during the bud to flowering stage [96]. Nitro compounds are stable in the dried green plant but are lost rapidly from the dried, bleached-out plant [96]. The nature and severity of poisoning depends on the quantity and rate of absorption of 3-NPOH from the rumen. Cattle fed 2.2 g dry weight of Emory milk vetch per kilogram body weight daily develop signs of poisoning in 3 to 4 days [93]. Sheep appear to be much more tolerant of nitro compounds in milk vetch than are cattle [94].

Clinical Signs

The nitro-containing Astragalus spp. produce both acute and chronic syndromes of poisoning in cattle, sheep, and occasionally horses. The quantity and rate at which the plants are eaten determines the clinical course of the poisoning. Signs of acute poisoning include general weakness, depression, knuckling of the fetlock joints, ataxia, respiratory difficulty, cyanosis, and sudden collapse before death [93-96]. The cyanosis and respiratory distress result from the rapid oxidation of hemoglobin to form methemaglobin by nitrite derived from 3-NPA. Severe respiratory distress occurs when 20 percent or more of the animal's total hemoglobin is converted to methemoglobin. Any form of stress or forced movement often causes the animal to collapse. Death of the animal is, however, not solely due to the formation of methemoglobin, because serum levels of 30 percent methemoglobin are not fatal in animals with acute nitrate poisoning. Fatalities occurred when methemoglobin levels approached 80 percent [104]. That death is not solely due to methemoglobin formation is born out by the fact that treatment with methylene blue, the treatment for nitrate poisoning, did not prevent death of animals fed nitroglycoside containing Astragalus spp. [94,105].

Chronic milk vetch poisoning in cattle is referred to as "cracker heels" because affected animals click their hooves together while walking as a result of weakness in the hind legs and knuckling-over at the fetlocks. As the condition progresses, the animal may show posterior paralysis and be unable to stand. Milk vetch poisoning has also been referred to as "roaring disease" because of the noisy respiratory sounds associated with difficulty in breathing [93]. In chronic poisoning the first noticeable signs are those of rapid and labored breathing [95,96]. Sheep with chronic poisoning develop emphysema and pulmonary edema with marked respiratory difficulty with less muscular weakness and uncoordination [95,96]. All animals with chronic milk vetch poisoning show marked weight loss, and eventually become recumbent before dying. Recovery rarely occurs in the severely affected animal.

A diagnosis of milk vetch poisoning is generally based on the clinical signs of respiratory difficulty coupled with the characteristic hind leg weakness and evidence that the animals had been eating one of the nitroglycoside-containing milk vetches.

Treatment

There is no known specific treatment for milk vetch poisoning. Affected animals should be removed from the source of the toxic plants. New methylene blue may be given intravenously to help convert methemaglobin back to hemoglobin and reduce the respiratory problems [96]. This will not, however, alter the effects of the nitro compounds on the nervous system. If the animals have not consumed lethal quantities of the milk vetch, they may slowly recover but usually do not grow well, and many times these animals are an overall economic loss to the producer.

Postmortem Findings

At autopsy there are no definitive lesions of milk vetch poisoning. Pulmonary edema and emphysema may be present in animals showing respiratory signs. Congestion and swelling of the liver are common. Most affected animals have excessive amounts of cerebrospinal fluid [96]. Microscopically, the principal lesions include degeneration of the spinal cord and peripheral nerves, brain hemorrhages, edema, and emphysema of the lungs [96].

Prevention and Control

As with the locoweeds, the milk vetches are difficult to control and eradicate because they cover vast geographic areas and have seeds that exist in the soil for many years before germinating when optimum conditions of moisture and temperature exist. Careful monitoring of rangeland conditions to determine when milk vetches are abundant and moving animals to areas where there is minimal risk from the plants can be helpful in reducing losses yet enable the range to be used. In the fall and winter, when the plant has dried and lost its green color, levels of nitroglycosides in the milk vetches are negligible [96].

Appropriate use of herbicides such as 2,4-D, triclopyr, and picloram eventually kill milk vetches. Herbicides significantly lower the quantity of the nitroglycosides in the plants once dried and bleached out, thereby reducing the risk of poisoning to livestock [106].

Plants:

Blue or Spotted Locoweed

Astragalus lentiginosus -  Fabaceae (Legume family)

Habitat

Blue locoweed is found typically in the plains, dunes, and slopes at lower elevations from western Colorado, central New Mexico, westward to Arizona, California, Nevada, northern Idaho, Montana, and Utah.

Habitat of Blue or Spotted Locoweed. Astragalus lentiginosus - Fabaceae (Legume family).

Description

These are leafy-stemmed perennial plants with pinnately compound, alternate leaves. The leaflets number 13 to 21. The pealike purple flowers are in clusters on stalks that arise in the leaf axils (Fig. 6-1A). The pods are inflated two-celled pods with variable red-brown spotting (Fig. 6-1B).

Figure 6-1A. Blue or spotted locoweed (Astragalus lentiginosus).

Figure 6-1B. Blue or spotted locoweed showing flowers and spotted seed pods (A. lentiginosus).

Principal Toxin

The indolizidine alkaloid swainsonine is present in all parts of the plant, and the plant remains toxic when dried.

Woolly or Purple Locoweed

Astragalus mollissimus - Fabacea (Legume family)

Habitat

Woolly locoweed is found in the dry plains and foothills at lower elevations 2000- 4000 feet (610 to 1,219 meters) from southwestern South Dakota, western Nebraska, and southeastern Wyoming, western Kansas, southward to northwest Texas and eastern New Mexico.

Habitat of Woolly or Purple Locoweed. Astragalus mollissimus - Fabacea (Legume family).

Description

Woolly locoweed is a leafy perennial plant, with relatively short stems, usually less than 10 cm tall (Fig. 6-2A). The leaves are pinnately compound with 21 to 31 leaflets and are densely haired. The flowers are rose-purple, in dense spike-like racemes (Fig. 6-2B). The fruit is a pod, oblong in shape and not hairy.

Figure 6-2A. Wooly locoweed (Astragalus mollissimus).

Figure 6-2B. Wooly locoweed showing hairy leaves and purple flowers (A. mollissimus).

Principal Toxin

The indolizidine alkaloid swainsonine is present in all parts of the plant.

White Locoweed, White Point Vetch, Crazy Weed

Oxytropis sericea - Fabaceae (Legume family)

Habitat

White locoweed is typically found in open gravelly or well-drained slopes and hills at lower to middle elevations from western Canada, Montana, North Dakota, and western Minnesota, south to Arizona, New Mexico, and Texas.

Habitat of White Locoweed, White Point Vetch, Crazy Weed. Oxytropis sericea - Fabaceae (Legume family).

Description

White locoweed is a perennial, herbaceous plant growing in a tuft with a stout tap root. The leaves are usually alternate and basal, odd-pinnately compound, covered with silvery hairs. The flowers are borne on leafless stems above the leaves in a raceme (Fig. 6-3). The flowers are white with a distinctive purple-tipped point to the fused front petals or keel. The pealike pods are stalkless and have a short curved beak.

Figure 6-3. White locoweed (Oxytropis sericea).

Principal Toxin

The indolizidine alkaloid swainsonine is present all parts of the plant, even when it is dried. White locoweed seems to be most palatable when it is in bloom, although it is readily consumed at all times if other forage is absent. Overgrazing will therefore increase the probability that livestock will eat locoweed.

Purple Locoweed, Lambert's Red Loco

Oxytropis lambertii - Fabaceae (Legume family)

Habitat

Purple locoweed is commonly found on the prairies and mountains usually in drier situations, at lower to middle elevations from Minnesota to Saskatchewan and southward to Arizona, New Mexico, Texas, and Oklahoma.

Habitat of Purple Locoweed, Lambert's Red Loco. Oxytropis lambertii - Fabaceae (Legume family).

Description

This is a perennial herbaceous plant that grows in clumps with a tap root. The leaves are produced basally, odd-pinnately compound, and sparsely haired. The flowers are produced on a leafless stalk in a raceme above the leaves (Fig. 6-4). The corolla is purple to rose in color and has a pointed keel. The pealike seed pods are 1.5 to 2.5 cm (15 to 25 mm) long, tapering to a point or divergent beak. Purple locoweed often grows in the same area as white locoweed (O. sericea), but tends to bloom just as the white locoweed goes out of bloom and starts producing seed pods.

Figure 6-4. Purple or Lambert's locoweed (Oxytropis lambertii).

Principal Toxin

Indolizidine alkaloids are believed to be the primary cause of poisoning. Swainsonine, an indolizidine alkaloid, is not consistently present in O. lambertii. The plants are consumed readily by livestock especially if there is little else for them to eat. Overgrazing will increase the probability of locoweed consumption.

Note

Swainson pea (Sphaerophysa salsula), introduced from Asia, has become established in waste ground, along roadways, and in cultivated fields of the western United States, where its seeds have contaminated alfalfa seed and other grains.

It is an erect perennial plant reproducing from lateral roots and seeds, and forming dense stands. Leaves are pinnately compound, with numerous alternate, hairy leaflets. Orange-red showy pealike flowers are produced terminally on the branches. Many green-colored seeds are produced in translucent bladder-like pods. It should not be confused with the swainson pea (Swainsona spp.) found in Australia and that has the same toxin (swainsonine) as found in the locoweeds. A toxin in S. salsula has not been determined. It does not, however, contain the alkaloid swainsonine.

Timber Milk Vetch

Astragalus miser - Fabaceae (Legume family)

Habitat

Timber milk vetch is found growing in a variety of soil types, often under aspen trees, or in areas where sage brush has been cleared. Varieties of timber milk vetch range from southern Canada, Washington, Idaho, Wyoming, Utah, Colorado, and northern Arizona.

Habitat of Timber Milk Vetch. Astragalus miser - Fabaceae (Legume family).

Description

These perennial, multistemmed plants arise from a slender taproot, the crown of which is at or just below the soil surface. The alternate, odd-pinnate leaves are composed of 7 to 21 leaflets. The flowers are produced on leafless stems from leaf axils and range in color from creamy white with purple veins to purple. The pealike pods 0.75 to 1 inch (2 to 3 cm long) lack stalks, hang downward, and open from the apex along the lines joining the halves (Fig. 6-5).

Figure 6-5. Timber milk vetch leaves and pods (Astragalus miser). (Courtesy Dr. Michael H. Ralphs, USDA Poisonous Plants Research Laboratory, Logan, Utah).

The three varieties of timber milk vetch are difficult to differentiate and have been named according to their geographic location.Astragalus miser var. oblongifolius (Wasatch milk vetch), A. miser var. hylophilus (Yellowstone milk vetch), A. miser var. serotinus(Columbia milk vetch) [85].

Principal Toxin

Miserotoxin (3-NPOH), a nitroglycoside, is found in timber milk vetch and some 263 other members of the genus.

Crown Vetch

Coronilla varia - Fabaceae (Legume family)

Habitat

Crown vetch is frequently used as a drought-tolerant ornamental ground cover to help control erosion in the United States especially in the Midwest and Northeast.

Description

Crown vetch is a perennial herb with trailing or ascending, branching stems arising from a taproot. Leaves are alternate and pinnate with a terminal leaflet. The pealike flowers are produced from the leaf axils on a stalk 3 to 5 inches (7.5 to 12.5 cm) in length (Fig. 6-6A)(Figure 6-6A). Flower color varies from white to dark pink. Many brown, cylindrical seeds are produced in pods 1 to 2 inches (2.5 to 5 cm) in length.

Figure 6-6A. Crown vetch (Coronilla varia).

Principal Toxin

Crown vetch contains nitroglycosides, the most toxic of which, coronarian is poisonous to horses and other nonruminants [99]. Ruminants are not affected because they are able to convert the coronarian to 3-NPA that is readily detoxified in the rumen [98]. Toxicity may be due to the development of methemoglobinemia and the inhibition of succinate dehydrogenase, an important enzyme necessary for energy metabolism [101]. Crown vetch does not cause bloat in ruminants because it contains tannins that precipitate soluble proteins, which contribute to the rapid formation of a frothy foam in the rumen. Creeping indigo (Indigofera spicata), (Fig. 6-6B) a legume introduced into southern Florida and Hawaii, also contains nitroglycosides that have caused poisoning in horses [97-100].

Figure 6-6B. Creeping Indigo (Courtesy of Gerald D. Carr, University of Hawaii).

Clinical Signs

Nonruminants may show weight loss, poor growth rates, depression, ataxia, and posterior paralysis leading eventually to death of the animal [103].

Part II : Other Plants Affecting the Nervous System

In this section a wide variety of indigenous and introduced plants with different effects on the brain and nervous system will be discussed. All are important when considering the cause of nervous system disorders in animals that have access to the plants. Many of these neurotoxic plants also have effects on other organ systems that can cause a variety of clinical signs in addition to those involving the nervous system.

Sagebrush Poisoning

More than 200 species of sagebrush (Artemisi spp.) grow in North America, many of which are commonly eaten by both wild and domestic ruminants. Some of the more common sages have the potential to cause poisoning in horses especially if they eat large amounts of sagebrush when other forages are unavailable. From a clinical perspective, horses with sage poisoning exhibit very similar neurologic signs to those encountered with locoweed poisoning. Consequently it is important to consider sage poisoning along with locoweed poisoning when determining the cause of the neurologic disease in horses that are grazed on pasture or range containing both locoweeds and sage. In western North America both locoweeds and sages commonly grow in the same habitat.

Sand sage (A. filifolia), common in the sandy soils along the eastern side of the Rocky Mountains and south into Mexico, has been associated with a syndrome in horses called "sage-sickness" [107]. Budsage (A. spinescens) has caused similar problems in animals in California and Nevada [108,109]. Recently the author encountered a neurologic disease of horses that were wintered on overgrazed range in Colorado where fringed sage (A. frigida) was the predominant forage being eaten by the horses.

Although the actual toxin that causes sage sickness has not been defined, some monoterpenes present in sagebrush are known to be neurotoxins. Thujone, a terpene present in wormwood (A. absinthium), has been associated with a neurologic syndrome in humans that chronically consume absinthe, the alcoholic beverage produced from wormwood [111]. A similar toxicity is presumed to develop in horses that consume a sufficient quantity of sage. Wild and domestic ruminants are not affected by eating sagebrush.

Horses appear to develop neurologic signs after they are forced to eat sagebrush when other forage is depleted or unavailable either as a result of deep snow cover or pasture overgrazing. After eating sage for several days, horses suddenly exhibit abnormal behavior characterized by ataxia and a tendency to fall down or act abnormally to stimuli that would not normally elicit such responses [112]. Tying a horse to a fence, for example, will cause the animal to pull back violently, eventually throwing itself to the ground in panic. If left undisturbed, the animal will recover and will act relatively normal. Ataxia is particularly noticeable in the front forequarters with the hindquarters seemly normal. Some animals may circle incessantly, and others may become excitable and unpredictable. The characteristic smell of sage is often noticeable on the breath and in the feces. Horses poisoned by sagebrush maintain an appetite and have a normal temperature, pulse, and respiration. It is the author's observation that the clinical signs resemble those of a horse that has been poisoned by locoweeds [110].

However, unlike "locoed" horses that will not recover fully, "saged" horses tend to recover 1 to 2 months after they stop eating sage and are fed a nutritious diet. Some horses, after adapting to eating sage for a period of weeks, seem to be able to tolerate it without problem [112]. Supportive therapy, including protection from extreme climatic conditions, will aid in the recovery. A poisoned horse should not be ridden until it is fully recovered and evaluated for normal behavior and neurologic function.

The only lesion observable in severely "saged" horses is a nonspecific degenerative toxic encephalopathy, with intraneuronal pigment accumulation and degeneration, especially in the medulla, brain stem, and cerebellum [110].

Plants:

Sand Sage

Artemisia filifolia - Asteraceae (Sunflower family)

Habitat

Sand sage prefers sandy soils especially of the central plains from the Dakotas, south to north Texas, and west to Arizona and Nevada.

Habitat of Sand Sage. Artemisia filifolia - Asteraceae (Sunflower family).

Description

A perennial woody plant growing to a height of 4 feet (1 meter) (Fig.6-7). The multiple stems and leaves are covered with gray hairs, giving the plant a silvery green appearance. The leaves are up to 4 inches (10 cm) in length and are divided linearly into fine segments. The inconspicuous flower clusters are produced at the ends of the stems in the leaf axils.

Figure 6-7. Sand sage (Artemisia filifolia).

Principal Toxin

Sagebrush species contain both sesquiterpene lactones and essential oils or monoterpenes that are potentially toxic to horses, but not to cattle, sheep, goats, and wild ruminants [112]. The principal toxins in sagebrush vary considerably in quantity depending on growing conditions and season, being greatest in the fall and winter months [113-116].

Fringed Sage, Sagewort, Estafiata

Artemisia frigida - Asteraceae (Sunflower family)

Habitat

Fringed sagebrush is found in a vast area extending from Alaska, south through the western United States, into Mexico. Its range also extends into Siberia, Asia, and Europe. Fringed sage is common in the Rocky Mountain states, and ranges from low semidesert areas to altitudes of 11,000 feet (3,352 meters). Fringed sage can become invasive to the point of becoming a monoculture and as such its presence over large areas is indicative of overgrazing. In Colorado it is considered a noxious weed in may counties. In the southwestern States, fringed sage forms a palatable forage for cattle and sheep when other forages are depleted.

Habitat of Fringed Sage, Sagewort, Estafiata. Artemisia frigida - Asteraceae (Sunflower family).

Description

Fringed sage is a low-growing, perennial, with a woody base and deep taproot. Roots also form where the spreading stems touch the ground. Leaves are small up to 0.5 inch (1 cm), divided, and silvery haired. Numerous erect, densely haired, flowering stems up to 2 feet (0.2 meters) in height are produced annually. The stems contain many leaves and numerous drooping, globe-shaped structures with many small yellow flowers (Fig. 6-8). Crushing the leaves and stems yields a distinctive sage smell.

Figure 6-8. Fringed sage or sagewort (Artemisia frigida).

Principal Toxin

Sagebrushes contain both sesquiterpene lactones and essential oils or monoterpenes that are potentially toxic to horses, but not ruminants.

Big Sagebrush

Artemisia tridentata - Asteraceae (Sunflower family)

Habitat

Big sagebrush is found in large areas throughout the intermountain region of the western United States, from California to the Dakotas and south to Mexico. It prefers dry plains and hillsides and does not tolerate irrigation. It is commonly used as a food source for both domestic and wild ruminants, but it has occasionally been associated with poisoning in sheep [108].

Habitat of Big Sagebrush. Artemisia tridentata - Asteraceae (Sunflower family).

Description

Big sage is an erect, branching, woody, perennial shrub growing 4 to 12 feet (1.2 to 3.5 meters) in height. The leaves are narrow at the base and have three distinctive lobes at the apex (Fig. 6-9). The leaves are covered with fine gray hairs, and when crushed, have a strong sage smell. The flowers are numerous, in a loose terminal panicles, each flower head having up to eight inconspicuous flowers surrounded by numerous bracts.

Figure 6-9. Big sage showing 3-toothed leaves (Artemisia tridentata).

Principal Toxin

Sagebrushes contain both sesquiterpene lactones and essential oils or monoterpenes that are potentially toxic to animals. Big sagebrush has been suspected of being toxic to sheep. An experimental dosage of 3/4 lb of A. tridentata for 1 to 3 days was lethal to sheep [108]. It has also been associated with abortions in sheep [116]. However, most of the many species of Artemisia are useful forage plants for range livestock.

Coyotillo, Tullidora

Karwinskia humboldtiana - Rhamnaceae (Buckthorn family)

Habitat

Coyotillo grows in the dry, gravelly soils of hillsides and canyons of southwestern North America and is found in the dry plains of Texas, New Mexico, and Mexico.

Habitat of Coyotillo, Tullidora. Karwinskia humboldtiana - Rhamnaceae (Buckthorn family).

Description

Coyotillo is a large shrub or small tree of the buckthorn family, growing up to 24 feet (7 meters) in height. The leaves are opposite, ovate or elliptic, and are dark green above and pale green beneath. The leaf veins and young twigs have black spots. The flowers are in axillary cymes, are perfect and actinomorphic. The petals, sepals and stamens are all five in number and are inserted on a disk. The flowers are sparsely pubescent. The fruits are ovoid and berry-like, turning brown-black when ripe with one seed.

Principal Toxin

The principal toxin responsible for causing the neurologic signs is unknown. The plant leaves and especially the brownish black fruits are toxic to cattle, sheep, goats, horses, pigs, chickens, and humans [117-120]. Poisoning can develop following a single feeding on the fruits (0.05 - 0.3 percent body weight of the dried fruit), with cattle being the most susceptible and chickens the least [121]. The leaves are also toxic. Clinical signs of poisoning may take from several days to several weeks to develop. The toxins cause nervous symptoms characterized by progressive impaired function of the cerebellum and peripheral nerves.

Clinical Signs

Initially goats poisoned with coyotillo show increased alertness, hypersensitivity to stimuli, muscle tremors, abnormal gait, and a hunched back [119,120]. Rapid breathing and a high stepping gait with exaggerated flexing of the legs develops in some goats. A progressive polyneuropathy causes a progressive decrease in neuromuscular reflexes, with paralysis developing especially in the rear quarters. Recumbency precedes death in poisoned animals. Appetite, defecation, and urination are unaffected until shortly before death. Pulmonary edema, which is usually fatal, develops in some animals. Segmental demyelination, degeneration of axons in peripheral nerves, and myodegeneration are characteristic of Karwinskia toxicity [119-122].

There is no specific treatment for coyotillo poisoning other than to prevent the animal from eating any more of the plant and providing a nutritious diet. Mildly affected animals will recover with time, but those showing severe muscle weakness and recumbency seldom survive.

Bracken Fern, Brake Fern, Eagle Fern

Pterdium aquilinum - Polypodiacae (Fern family)

Habitat

Bracken fern is found throughout the United States and has been associated with poisoning in cattle, sheep, pigs, horses, and humans [122,123]. In North America bracken fern is commonly found in the eastern, intermountain, and western states, from Canada to Mexico. Its growth in the midwestern states is sparse. Bracken fern prefers to grow in moist open woodlands with sandy soils, often forming dense stands following clear-cutting or burning of forests. It will grow in relatively dry soils and because of its prolific root system spreads rapidly to form dense monocultures to the exclusion of any other plants.

Bracken fern is also found in most parts of the world with most cases of animal poisoning occurring in England and Europe [123,124].

Description

Bracken fern is a perennial fern with a black horizontal branching root system often extending for several meters. Leaves arise directly from the rhizome, are broadly triangular, up to 6.5 feet (2 meters) in height, bipinnately compound, and heavily haired on the underside (see Fig. 5-5A). Characteristic brown reproductive spores are produced under the rolled edge of the leaflets in late summer (see Fig. 5-5B).

Bracken Fern Poisoning

Bracken fern has been associated with a variety of different syndromes in animals, the best recognized of which include:

• Thiamin deficiency
• Retinal degeneration and blindness
• Hemorrhaging and bone marrow destruction (thrombocytopenia)
• Urinary bladder cancer (enzootic hematuria)
• Digestive tract cancers

In the interest of continuity, all the syndromes of bracken fern poisoning will be discussed in Chapter 8, and only the neurologic signs of bracken fern poisoning are briefly mentioned here.

Principal Toxins

Bracken fern contains an enzyme thiaminase, which splits the essential vitamin thiamin (B1) into its two inactive components pyrimidine and thiazole [125]. Thiamin is essential in energy metabolism, especially in the conversion of pyruvate to acetylcoenzyme A (CoA), and the oxidation of α-ketoglutarate to succinyl-CoA in the citric acid cycle [125]. Horses and pigs are most susceptible to the effects of thiaminase. Ruminants are rarely affected because they produce ample thiamin in the rumen [126-129]. Horses have to consume a diet containing 3 to 5 percent bracken fern for at least 30 days before clinical signs appear [130]. Sheep can be experimentally poisoned if they are fed large quantities of bracken fern for prolonged periods [131]. Affected animals develop a thiamin deficiency that is characterized by central nervous system depression and polioencephalomalacia. A similar thiaminase enzyme is also found in other plants including horsetail (Equisetum arvense), the Australian nardoo fern (Marsilea drummondii), and the rock fern (Cheilanthes sieberi) [132,133].

Bracken Fern Poisoning in Horses

Bracken fern poisoning in horses is uncommon. When encountered it is characterized by a nervous system disease resulting from depletion of thiamin [123]. Affected horses refuse to eat and consequently lose weight. Depression, muscle tremors, uncoordinated gait, especially of the hindlegs and paralysis are typical of bracken fern poisoning. Horses may show colic, constipation, hemoglobinuria, severe anemia, elevated temperature, and rapid heart rate [123].

Diagnosis of bracken fern poisoning should be based on evidence that horses have eaten the fern, the clinical signs, and the animal's response to thiamin therapy. Elevated serum pyruvic acid levels (normal 2 - 3 :g/dL) and decreased thiamin levels (normal 8 - 10 :g/dL) are helpful in confirming the diagnosis. Bracken fern poisoning in horses should be differentiated from viral encephalitis and hepatic encephalopathy, which have similar clinical signs.

Treatment

Horses with thiamine deficiency should be treated with intravenous thiamine in a dose of 5 mg/kg body weight. This dose should be repeated intramuscularly for several days. Horses should be provided with a balanced diet that is free of bracken fern.

Common Horsetail, Scouring Rush

Equisetum spp. - Equisetaceae (Adder's tongue family)

Habitat

The common horsetail is a weed of moist, sandy soils in fields, roadsides, and along banks of rivers and lakes throughout most of North America. Six species (or varieties) of Equisetum occur throughout the United States.

Habitat of Common Horsetail, Scouring Rush. Equisetum spp. - Equisetaceae (Adder's tongue family).

Description

Horsetails are perennial rushlike plants with characteristic jointed, hollow stems that readily separate at the nodes (Fig. 6-10A). The leaves have been reduced over time to black- tipped papery scales surrounding the stems at each node. The stems are cylindrical, ridged, and coarse to touch owing to their high silicate content. Multiple whorled branching occurs at the nodes in some species (Fig. 6-10B). The plant reproduces from a deeply buried rhizome and from terminal spore-bearing cones.

Figure 6-10A. Horsetail or scouring rush fertile stems with terminal spore caps (Equisetum arvense).

Figure 6-10B. E. arvense with sterile branching stems.

Principal Toxin

Although a variety of substances have been identified, including silica, various alkaloids, and organic acids, the primary toxicity of bracken fern appears to be related to its antithiamine effect [134-136]. Successful treatment of the affected horses with thiamine hydrochloride (vitamin B1) indicated that the primary toxin in horsetail is a thiaminase enzyme [135,136]. Thiamin is essential in energy metabolism, particularly in the conversion of pyruvate to acetyl-CoA, and the oxidation of α-ketoglutarate to succinyl-CoA in the citric acid cycle [137]. Horses are most frequently poisoned by horsetail, but cattle and sheep are occasionally affected especially by E. palustre[134]. The plants are toxic at all stages and remain toxic in hay. Hay containing 20 percent horsetail fed to horses for over 2 weeks has caused clinical signs [135].

Clinical Signs

Young horses are most susceptible to Equisetum poisoning; clinical signs develop after the horse has eaten the plants for several days. Initially weight loss is most evident followed several weeks later by incoordination of the hind legs. Diarrhea may precede the onset of weight loss and incoordination. Affected animals become progressively weaker and eventually recumbent, but continue to eat relatively well throughout. Serum pyruvate levels increase, while thiamin levels are depleted. Once horses are down and cannot get up, they usually die in 1 to 2 weeks. Cattle poisoned with horsetail show weight loss, decreased milk production, diarrhea, and hyperexcitability [134].

Treatment

Horses suspected of being poisoned by Equisetum should be taken off of hay or pasture containing the plant and fed a nutritious diet that includes cereal grains that are rich in thiamine. Treatment with a large dose of thiamine hydrochloride (3 - 5 mg/kg body weight) intravenously followed by several days of thiamine intramuscularly (1 - 2 mg/kg body weight) provides rapid recovery and restores thiamine levels to normal [137,138].

Yellow Star Thistle and Russian Knapweed Poisoning

Both yellow star thistle and Russian knapweed produce a unique poisoning of horses that is generally fatal. The plants occur in areas of the western United States, Australia, and Argentina [139,140]. Both plants were introduced to the United States when their seeds contaminated imported grains, and since have become well established as noxious weeds [139,140]. Unfortunately the range of these noxious weeds continues to spread.

Plants:

Yellow Star Thistle

Centaurea solstitialis - Asteraceae (Sunflower family)

Habitat

Yellow star thistle is a weed that was introduced from the Mediterranean area and has become well established in California, Oregon, Idaho, Washington, and in some areas throughout the southwestern, and southeastern states. It is an invasive noxious weed of cultivated areas and spreads along roadsides and waste areas. Malta star-thistle or tocalote (C. melitensis) is a similarly introduced plant that has become a noxious weed in some areas of the southwest. It has not been reported as toxic.

Habitat of Yellow Star Thistle. Centaurea solstitialis - Asteraceae (Sunflower family).

Description

The plant is an annual herbaceous weed, branching from the base up to 12 inches (30 cm) tall (Fig. 6-11A). The branches are winged and ascending. Leaves are covered with cottony hair, the basal leaves being deeply lobed; the stem leaves are linear and entire (Fig. 6-11B). The disc flowers are yellow and fertile. The bracts are tipped with characteristic stiff yellow spines 0.5 to 1 inch (1 to 2 cm) long (Fig. 6-11C).

Figure 6-11A. Yellow star thistle immature plant (Centaurea solstitialis).

Figure 6-11B. Yellow star thistle mature blooming plant (C. solstitialis).

Figure 6-11C. Yellow star thistle with yellow ray flowers and long spiny bracts (C. solstitialis).

Malta star-thistle or tocalote (C. melitensis) is a similar plant but is smaller and the spines on the bracts are small and dark tipped (Fig. 6-11D). It is not reported to be poisonous.

Figure 6-11D. Malta star thistle (C. meletensis).

Principal Toxin

Several neurotoxic components of yellow star thistle have been identified including aspartic and glutamic acids and two sesquiterpene lactones, solstitialin A 13- acetate and cynaropicrin [142-144]. A dopaminergic neurotoxin, 2,3 dihydro-3, 5 dihydroxy-6-methyl-4 (H) pyran-4-1, very similar to the compound that induces Parkinson's disease in people, has been isolated from yellow star thistle [145]. This compound specifically destroys the dopaminergic nigrostriatal pathway that has coordinating and inhibiting effects on the cerebral cortex pathways that control prehension and chewing of food (cranial nerves V, VII, IX) [146-148]. The plant is poisonous only to horses and is toxic in both its green and dried states. Horses will eat yellow star thistle in all its stages of growth and will acquire a preferential liking for the plant. Cattle and sheep graze the plants without problem and have been used as a means of controlling the weed. Signs of toxicity in horses do not occur until the plant has been eaten in large quantities for 30 to 60 days. Experimentally it takes approximately the animal's body weight in green plant over 33 days to produce clinical signs [143]. It has been calculated that horses have to consume an amount of green yellow star thistle equal to 86 to 200 percent of their body weight before clinical signs develop [147,148]. Although this is a relatively large amount of plant, horses apparently develop a preference for the plants and will eat them even in the mature spiny state. In California there are two periods of the year, June/July and October/November, when yellow star thistle poisoning is most prevalent, suggesting some seasonal variation in palatability or toxin content of the plants.

Russian Knapweed

Acroptilon repens (Centaurea repens) - Asteraceae (Sunflower family)

Habitat

Introduced from Russia in alfalfa seed, the plant has established itself in cultivated fields, pastures, and roadsides [138,140]. It is considered a noxious weed in many areas of Colorado and other Rocky Mountain states where it has become a highly invasive weed. Russian knapweed grows in all soil types and spreads by an extensive root system. It is also allelopathic, meaning it is capable of producing an inhibitory substance from its roots that retards other plant growth in its vicinity.

Habitat of Russian Knapweed. Acroptilon repens, (Centaurea repens) - Asteraceae (Sunflower family).

Description

Russian knapweed is a creeping perennial plant with black horizontal roots. It is erect, rather stiff, and branched, usually ranging from 1 to 3 feet (1 meter) high. The young stems are covered with soft gray hair or nap. The lower leaves are alternate with toothed margins, which become entire margined at the top of the plant and are covered with short stiff hairs. The flowers are in heads like some thistles, one-third to one-half inch in diameter and are lavender to whitish in color (Fig. 6-12). The bracts are papery and have no spines. The seeds are chalky white or grayish in color and about one-eighth inch long with bristles at one end. The seeds are rarely shed from the seed head itself that may aid in their dispersal. Rodents readily carry off the seed heads and hide them in their burrows, and by so doing inadvertently plant the seeds and spread the weed.

Figure 6-12. Russian knapweed in bloom (Acroptilon repens).

Principal Toxin

Russian knapweed contains a sesquiterpene lactone, repin, that has shown neurotoxic properties [149,151]. However, a dopaminergic neurotoxin isolated from yellow star thistle that interferes with the dopamine pathway may also be identified in Russian knapweed in due course [145]. Russian knapweed is toxic only to horses and causes lesions and clinical signs identical to those produced by yellow star thistle (C. solstitialis) [147,150]. Russian knapweed appears to be more toxic than yellow star thistle requiring less plant mass (1.8 - 2.6 kg/100 kg body weight) and a shorter feeding period (28 to 35 days) to produce disease in horses [147]. It has been calculated that horses have to consume an amount of green Russian knapweed or yellow star thistle equal to 59 to 71 percent and 86 to 200 percent of their body weight, respectively, before clinical signs develop [147,148].

Clinical Signs

Prolonged consumption of yellow star thistle and Russian knapweed results in a disease of horses called "chewing disease," characterized by increased tonicity and incoordination of the muscles that enable prehension and chewing of food [145-148,152-154]. The hypertonicity of the facial muscles produces a "wooden" expression to the face. Food is often held in the mouth because it cannot be chewed normally. The continual chewing movements cause frothing of the saliva, which can resemble that seen in rabies. Some horses may wander about with their lips brushing through the grass, which to the unobservant, could be mistaken for normal grazing.

Even though prehension and mastication are severely affected, swallowing is unaffected. Some horses may learn to submerge their heads far enough into a deep trough of water to allow water to reach the pharyngeal area where it can be swallowed. The tongue has increased tone and the horse will often curl the tongue from side to side. Some horses may show more involvement of one side so that the lips, tongue, and head movements are to one side. Circling to the same side may also occur. Other abnormal behavior may include violent head tossing and excessive yawning. Clinical signs are most severe initially and after a few days the horse may show some improvement. Weight loss and depression are common. Pneumonia resulting from inhalation of feed is a serious sequel to the disease.

Although the clinical signs of yellow star thistle poisoning are unlike any other, they should be differentiated from viral encephalitis (sleeping sickness), rabies, glossopharyngeal and hypoglossal nerve injuries, pyrrolizidine alkaloid poisoning, and foreign bodies lodged in the mouth or esophagus [154].

There is no effective treatment for either yellow star thistle or Russian knapweed poisoning because the affected areas in the brain undergo liquefactive necrosis and do not regenerate. Affected horses may be kept alive by administering water, electrolytes, and a high-energy liquid diet through a nasogastric tube or an esophagotomy. Euthanasia of affected horses is eventually necessary because of the debilitating and irreversible effects of the brain lesions and complicating inhalation pneumonia.

Postmortem Findings

The lesions of yellow star thistle and Russian knapweed poisoning are unlike any other plant-induced poisoning and consist of bilaterally symmetrical foci of liquefactive necrosis in the globus pallidus and the substantia nigra [145,147,148,153]. Occasionally the lesions are unilateral. The lesion of nigropallidal encephalomalacia are microscopically discernable within 2 days of the appearance of clinical signs and are grossly visible after 2 days as yellowish necrotic lesions.

White Snakeroot Poisoning

White snakeroot is the plant that was responsible for the syndromes of "milk sickness" in humans and "trembles" in animals that early settlers encountered in the eastern and central United States [155-157]. As early as 1777, there were reports of an unknown poisoning of humans and cattle in the Carolinas and Tennessee, now known to be due to white snakeroot or richweed (Eupatorium rugosum) [158]. Abraham Lincoln's mother reportedly died of milk sickness in 1818 after drinking milk from a cow that had access to white snakeroot growing at the Lincoln cabin site [159]. Many human and animal deaths were attributed to white snakeroot poisoning. Human poisoning virtually ceased once the plant was identified as the source of the problem and farmers learned to keep their animals away from the plant. Animals continue to be poisoned by snakeroot sporadically if they gain access to the plant [160-162]. The incidence of white snakeroot poisoning has the potential to increase in the future as many new small acreage farms are being established in areas of white snakeroot. These new farmers may well be unaware of the lethal potential of the plant.

White Snakeroot

Eupatorium rugosum - Asteraceae (Sunflower family)

Habitat

White snakeroot is found in low, moist areas or bordering streams, often on rich or basic soils of open woodlands, from eastern Canada, west to the Dakotas, south to Georgia, and west to Texas [163-165]. Synonyms for white snakeroot include Eupatorium urticaefolium and Ageratina altissima [166].

Habitat of White Snakeroot. Eupatorium rugosum - Asteraceae (Sunflower family).

Description

This showy, herbaceous perennial forms erect, stiff stems as much as 39 to 55 inches (100 to 140 cm) tall, developing from a shallow mat of fibrous roots. Leaves are opposite, long petioled, ovate to cordate, and range from 3 to 6 inches (7.5 to 15 cm) in length. The leaf margins are coarsely and sharply serrate; the tip sharply pointed, and the leaves with three distinct veins. The tubular flowers are showy, snow white, and small in composite heads of 10 to 30 flowers (Fig. 6-13). The heads are grouped in open corymbs.

Figure 6-13. White snakeroot (Eupatorium rugosum).

Principal Toxin

The toxic component of white snakeroot has been named tremetone (tremetol) and requires microsomal activation before it becomes toxic to mammalian cells [163,164]. All animals including man are susceptible to poisoning [166-169]. The toxin has its highest content in the green plant and remains toxic when dried in hay. The tremetone is cumulative in animals and is secreted in milk from cows that have eaten snakeroot. Humans drinking the milk develop a severe nervous syndrome known as "milk sickness" [160]. In animals the toxicity is known as "trembles" because of the muscle tremors induced by the toxin. Poisoning develops after an animal has eaten from 0.5 to 1.5 percent of an its body weight in green plant [163]. Feeding horses 1 to 2 percent of their body weight of the plant induced poisoning in 1 to 2 weeks [170]. Approximately 20 lb of green plant consumed over several days induces poisoning in horses [170]. The toxin of white snakeroot is readily secreted through the milk and is therefore a hazard to humans or animals that drink it [171]. Foals may develop white snakeroot poisoning when they drink the milk from their dam that has been eating the plant [160]. E. wrightii of Texas, Arizona, and Mexico has been reported to cause sudden death in cattle. Other species of Eupatorium including E. adenophorum (crofton weed) and E. riparium from Australia are toxic to horses [172-175]. In addition to white snakeroot, tremorgenic toxins are also found in rayless goldenrod (Haplopappus heterophylus), Jimmy fern (Notholaena sinuata), western mountain laurel (Sophora secundiflora), and silky sophora (Sophora sericea) [176].

Various fungi growing on plants produce tremorgenic toxins that cause muscle tremors in livestock that can resemble those encountered in white snakeroot poisoning. Fungal tremorgens include those produced by the fungus Claviceps paspalli in Dallis grass (Paspalum dilitatum) and Bahia grass (Paspalum notatum) [176,177]. Perennial ryegrass (Lolium perene) staggers is caused by the endophytic fungus Acremonium loliae, whereas annual ryegrass (Lolium rigidum) staggers is caused by a toxin produced by a bacterium Corynebacterium rathayi growing on the grass. Bermuda grass (Cynodon dactylon) and Phalaris or canary grass (Phalaris spp.) staggers are similar to other tremorgenic syndromes [179].

Clinical Signs

Horses, cattle, sheep, and goats poisoned with white snakeroot are initially listless, depressed, lethargic, and disinclined to move much [157,158,168,178,179]. Cattle, in particular, develop muscle tremors, especially after exercise, and may show signs of colic, constipation, blood in the feces, and a peculiar acetone-like odor to the breath [166,176,177]. Once muscle tremors begin, animals are reluctant to move, showing marked stiffness and eventual recumbency.

Horses may show signs of choking due to the paralysis of the pharyngeal muscles. Nursing animals may have milk run out the nostrils [162,167,168]. Patchy sweating may be evident. The urine may become dark brown due to myoglobinurea [170]. A rapid and irregular heart rate and signs of congestive right heart failure may precede death [167]. Electrocardiograms taken from horses with white snakeroot poisoning may reveal complete atrioventricular block, ventricular premature beats, and marked ST-segment depression indicative of myocardial ischemia [170].

Poisoning in humans who have consumed milk containing tremetol is characterized by weakness, muscle tremors, depression, garlicky odor to the breath, abdominal pain and vomiting, constipation, delirium, and death. People who survive experience prolonged signs of weakness [158,159].

Postmortem Findings

Mortality is usually high in livestock showing "trembles." Death appears due to severe skeletal and myocardial degeneration [168-170]. Fatty degeneration of the liver and kidney is a prominent necropsy finding. In Australia, horses poisoned by crofton weed (E. adenophorum) develop a respiratory syndrome characterized by severe pulmonary fibrosis and infarction [172-174].

Diagnosis

There is no specific diagnostic test for tremetone that does not give false- positive results due to normally occurring miscellaneous ketones secreted in milk [168]. Diagnosis therefore is based on the clinical signs and the presence of white snakeroot in the hay or pasture where the animal has been eating.

Treatment

There is no specific antidote for white snakeroot poisoning. Further consumption of the plant or affected milk should be stopped immediately. Excitement and exercise should be prevented. Where possible lactating animals should be repeatedly milked to help remove the toxin from the animal's system. The milk should be carefully discarded to ensure no animal drinks it. Laxatives and activated charcoal improve chances of recovery if administered early. Horses that exhibit difficulty in swallowing should be given water, electrolytes, and appropriate nutrition via nasogastric tube. Recumbent animals should be placed in well bedded stalls to prevent the development of pressure sores.

Poisoning in humans today is infrequent due to the practice of pooling milk from many cows, which dilutes any tremetone that may have been present. The individual family in rural areas that drinks raw milk from their cow have a greater potential for poisoning if there is white snakeroot in the animal's pasture. Pasteurization does not detoxify tremetone in milk.

Jimmy Weed, Rayless Goldenrod, Burrow Weed

Isocoma pluraflora (Isocoma wrightii, Haplopappus heterophyllus) - Asteraceae (Sunflower family)

Habitat

Jimmy weed is commonly found in the alkaline soils of drier rangeland, river valleys, drainage areas, and irrigation canals in Texas, Arizona, and New Mexico.

Habitat of Jimmy Weed, Rayless Goldenrod, Burrow Weed. Isocoma pluraflora (Isocoma wrightii), (Haplopappus heterophyllus) - Asteraceae (Sunflower family).

Description

Jimmy weed is an erect, sparsely branched, woody perennial growing to 2 to 4 feet (0.5 to 1 meter). Leaves are sticky, linear, and alternate. Flowers are yellow, borne in numerous, small, terminal flat topped heads composed of 7 to 15 flowers each (Fig. 6-14).

Figure 6-14. Burrow weed (Isocoma pluraflora). (Courtesy of Dr. Robert Glock, Veterinary Diagnostic Laboratory, Tucson, Arizona).

Principal Toxin

A compound tremetone (tremetol), similar to that found in white snakeroot (E. rugosum), appears to be responsible for causing poisoning in livestock [174]. Tremetone is secreted in milk and is therefore potentially hazardous to people or animals drinking affected milk. Poisoning of livestock most often occurs in the fall and winter when other forages are scarce and livestock are forced to eat the jimmy weed. The toxic dose of the plant that needs to be eaten to induce poisoning is approximately 1.5 percent of the animal's body weight of green plant over a period of a week [180]. The dried plant appears to be less toxic.

Clinical Signs

The symptoms of Haplopappus and Eupatorium spp. poisoning are similar. Initially animals exhibit marked depression and are reluctant to move. Forced exercise often precipitates muscle tremors and collapse [180-182]. As the disease progresses the animals become weak and unable to walk. Death frequently occurs at this stage. Urinary incontinence and an acetone-like smell to the breath may be noted in severe cases.

Treatment

Further consumption of the plants or milk from affected animals should be prevented. Treatment with laxatives may help in preventing further absorption of the toxin. Food, water, and other supportive treatment should be given as necessary.

Miscellaneous Neurotoxic Plants

Mescal Bean, Frijolito, Mountain or Texas Laurel

Sophora secundiflora - Fabaceae (Legume family)

Habitat

Mountain laurel or mescal bean is commonly found growing in the limestone rangelands, dry hills, and canyons of western Texas, Arizona, and Mexico.

Habitat of Sophora secundiflora - Fabaceae (Legume family).

Description

Mescal bean is a woody perennial evergreen shrub or small tree up to 33 feet (10 meters) in height. Leathery leaves are alternate, pinnate, opposite, once compound with terminal leaflet. Leguminous blue to purple, showy, fragrant, flowers appear in a one-sided terminal raceme. The fruit is a multiple seeded woody pod up to 6 inches (15 cm) long (Fig. 6-15A). Seeds are bright red to orange in color and have a very hard seed coat (Fig. 6-15B).

Figure 6-15A. Mescal bean or Texas laurel (Sophora secundiflora).

Figure 6-15B. Mescal beans (S. secundiflora).

Principal Toxins

The toxicity of S. secundiflora has been recognized for both humans and animals for some time [183]. The red seeds have been used as hallucinogens by Indian tribes, and the leaves and seeds have been recognized as a cause of poisoning in cattle, sheep, and goats [183]. A suspected case of mescal bean poisoning has been reported in a dog that had been chewing the beans [184]. The quinolizidine alkaloid cytisine (sophorine), along with other alkaloids and amino acids in combination, are responsible for the toxicity [185-187]. The mature leaves and fruit are toxic. The seeds are poisonous if crushed but otherwise pass through the animal's digestive system intact and without effect. Livestock only eat the plant if other forage is unavailable in the late summer and winter months. Silky sophora (S. sericea) is similarly toxic. Other plants containing similar alkaloids include wild indigo (Baptisia spp.), scotch broom (Cytisus scoparia), golden banner (Thermopsis spp.), and white loco (Sophora nuttalliana). This last plant is not related to white locoweed (Oxytropis sericea).

Clinical Signs

Poisoned animals show minimal clinical signs until they are stressed or forced to exercise, in which case muscle tremors, incoordination, and a stiff gait are characteristic [187]. If left alone, affected animals appear to recover, but clinical signs can be induced when the animals are stressed. Severely poisoned animals become recumbent and comatose and eventually die. No known specific treatment for mescal bean poisoning is known, and therapy should be directed at providing supportive care and a nutritious diet.

Buckeye, Horse Chestnut

Aesculus spp. - Hippocastanaceae (Buckeye family)

Habitat

There are at least 25 species of horse chestnut, some of which have been introduced to North America from Europe. Seven species of Aesculus are indigenous to various areas of North America and have become widely cultivated as desirable shade trees. They generally prefer rich, moist soils of woodlands, although some species have adapted to drier conditions. The buckeye or horse chestnut is not related to the edible chestnut (Castanea spp.)

Habitat of Aesculus spp.  - Hippocastanaceae (Buckeye family).

Description

These trees or shrubs have opposite, palmately compound leaves, with five to seven serrated leaflets (Fig. 6-16A). The inflorescence is a panicle of large, erect flowers which are usually yellow, whitish yellow, or red in color depending on the species (Fig. 6-16B). The fruit is a one- to three-seeded leathery capsule with or without sharp spines (Fig. 6-16C). The seeds are large, 1 inch (2.5 cm) in diameter, glossy brown when newly exposed with a conspicuous lighter scar (Fig. 6-16D).

Figure 6-16A. Swamp buckeye flower and typical leaves (Aesculus octandra).

Figure 6-16B. California buckeye blooms (A. california).

Figure 6-16C. Horse chestnut fruits (A. hippocastanum).

Figure 6-16D. Horse chestnut seeds (A. hippocastanum).

• A. californica (California buckeye)
• A. glabra (Ohio buckeye)
• A. hippocastanum (horse chestnut)
• A. octandra (yellow buckeye)
• A. pavia (red buckeye)

Principal Toxin

The glycosides aesculin and fraxin, and possibly a narcotic alkaloid, present in the young growing sprouts, leaves, and seeds are thought to be responsible for toxicity in animals [188,189]. Five bioactive triterpene oligoglycosides named escins have been isolated from the seeds of the horse chestnut, the toxic significance of which has yet to be determined [190]. Cattle, sheep, horses, swine, chickens, and humans have been poisoned naturally and experimentally by various species of buckeye [188,189,191].

The nectar and sap of A. californicum is known to kill honey bees that feed on it, so much so that bee keepers recommend moving hives during the flowering period of the California buckeye [192]. Poisoning of livestock generally occurs when animals eat the leaves and sprouts of the buckeye because it generally leafs out before other plants in the spring. The green husk of the immature fruit is especially toxic [193].

Clinical Signs

In simple-stomached animals, vomiting and gastroenteritis are the predominant effects of the toxic glycoside. In ruminants, the glycoside is converted in the rumen to the soluble aglycone, which following absorption, produces neurologic and not gastrointestinal signs [194]. Animals develop signs of poisoning about 16 hours after consuming toxic quantities of the plant, and as little as 0.5 percent body weight of ground nuts fed to calves produced severe poisoning [195]. Affected animals initially show muscle twitching, weakness, and a peculiar "hopping" gait, especially involving the hind legs [191,194,196,197]. In severe cases of buckeye poisoning, muscle tremors rapidly progress to muscle spasms and recumbency. These spasms may occur every 30 seconds and can be induced by handling or stressing the animal. A dorsal-medial strabismus occurs in severe cases. Hyperglycemia, glucosurea, and proteinurea appear to be consistent features of severe toxicity. Vomiting and abdominal pain may also occur. Once animals become recumbent and progress into a coma they rarely recover.

Treatment

There is no specific therapy for buckeye poisoning. Laxatives may be given to help remove the ingested plant as rapidly as possible from the intestines. Supportive intravenous fluid therapy with calcium gluconate and dextrose may be beneficial.

Kentucky Coffee Tree, American Coffee Berry, Kentucky Mahogany

Gymnocladus dioica - Fabaceae (Legume family)

Habitat

The Kentucky coffee tree is indigenous to eastern North America, from Ontario south to Florida and west to Nebraska. It is grown as a large, semihardy shade tree in other areas.

Habitat of Gymnocladus dioica. - Fabaceae (Legume family).

Description

This is a deciduous, multibranched, large tree to 90 feet (27 meters) in height. Leaves are large, twice pinnate; each leaflet is oval (Fig. 6-17A). Trees may have both male and female flowers that are small, greenish white, and fragrant. The characteristic fruits are hard, brown, leguminous pods 4 to 6 inches (10 to 15 cm) long, containing five to seven hard, dark brown seeds (Fig. 6-17B).

Figure 6-17A. Kentucky coffee tree branch with leaves (Gymnocladus dioica).

Figure 6-17B. Kentucky coffee tree seed pods (G. dioica).

Principal Toxin

Little is known about the toxin other than it is thought to be the quinolizidine alkaloid cytisine, which acts on the nervous system like nicotine [198,199]. New sprouts, leaves, and the fruits are toxic to animals and humans [198]. The dried seeds when roasted appear to be nontoxic and have been used as a coffee substitute [198]).

Clinical Signs

Cases of poisoning have infrequently been reported in cattle, sheep, horses, and humans [198]. Signs of intense gastrointestinal irritation (vomiting, colic, and diarrhea) begin within an hour of eating the shoots, leaves, or chewed seeds [193]. Hypotension, decreased heart and respiratory rates, muscle paralysis, and convulsions may precede death depending on the quantity of plant consumed. No specific lesions are visible at necropsy other than those of gastroenteritis.

Treatment

No specific treatment is available, and therapy where possible should be directed at preventing further absorption of the toxin from the gastrointestinal tract. The use of oral activated charcoal and saline cathartics is helpful in this respect. Intravenous fluid therapy to counteract hypotension, atropine to reverse the bradycardia, and phenobarbital or diazepam to control convulsions should be administered as necessary.

Carolina Jessamine, False or Yellow Jessamine

Gelsemium sempervirens - Loganiaceae (Logania family)

Habitat

Carolina jessamine is a common indigenous plant of the southeastern states, where it is found growing in open woods, fence rows, and stream banks. It has been widely cultivated as an ornamental plant in other areas.

Habitat of Gelsemium sempervirens. - Loganiaceae (Logania family).

Description

The plant is a twining or trailing, evergreen perennial vine up to 20 feet (6 meters) in length, with opposite, simple, ovate, glossy leaves, and reddish brown stems. The flowers are fragrant, showy, and yellow and produced in clusters from the leaf axils (Fig. 6-18). Many winged seeds are produced in two-celled, elliptical capsules.

Figure 6-18. Carolina jessamine (Gelsemium sempervirens).

Principal Toxin

Gelsemine, and several other indole alkaloids with properties similar to strychnine, are found in all parts of the plant including the flowers and nectar. All animals, birds, and humans are susceptible to the toxin. The honey made from the nectar of Carolina jessamine is reportedly toxic, and children have been poisoned after sucking the flowers [200,201]. Poultry have been poisoned in large numbers after eating the roots of Gelsemium [201].

Clinical Signs

The usual presenting sign of Gelsemium poisoning in livestock is the finding of a prostrate animal. Other signs of poisoning, including hypothermia, dilated pupils, weakness or rigidity of the legs, incoordination, and respiratory failure, precede death. Most animals die within 2 days of developing signs of poisoning.

Treatment

No known specific treatment is known, and animals are best given supportive therapy including activated charcoal and saline cathartics orally, intravenous fluids, and anticonvulsants as needed.

Sweet Shrub, Carolina Allspice, Strawberry Bush

Calycanthus fertilis, C. floridus - Calycanthaceae

Habitat

Found mostly in the southern tier of States, species of Calycanthus grow either wild or are cultivated as ornamentals. Most cases of sweet shrub poisoning have been reported in Tennessee and surrounding area.

Habitat of Calycanthus fertilis, C. floridus.  - Calycanthaceae.

Description

This perennial, large shrub to small tree attains a height of 10 feet (3 meters). Leaves are alternate, 2 to 3 inches (5 to 7.5 cm) ovate with blunt or pointed tips, dark green in the summer, and yellow in the fall. Flowers have dark brown or maroon petals and sepals fused at their base into a cup, and sweet fragrance suggestive of strawberries (Fig. 6-19). The seed pods are urn-shaped, turning brown when ripe, and containing several one-seeded achenes.

Figure 6-19. Sweet shrub (Calycanthus floridus).

Principal Toxin

Little is known about the toxin in Calycanthus spp. , but the indole alkaloid calycanthine, with strychnine-like properties is believed to be responsible for the clinical signs [202,203]. A dog experimentally poisoned with an aqueous extract of the seeds exhibited strychnine-like symptoms [203].

Clinical Signs

There are very few confirmed reports of Calycanthus spp. poisoning [202-204]. Clinical signs that have been associated with Calycanthuspoisoning include hyperexcitability, recumbency, tetanic muscle spasms resulting in rigid extension of the extremities, opisthotonus, coma, and death [203]. Death occurs shortly after onset of tetanic signs. Diagnosis is based on confirming that the animal had access to the plant and evidence that the plant has been eaten. The detection of the seeds in the rumen is helpful in diagnosis.

Treatment

There is no known specific antidote, and symptomatic treatment should be administered. Activated charcoal via stomach tube and sedation to manage the animal's convulsions are appropriate.

Golden Chain Tree, Bean Tree

Laburnum anagyroides - Fabaceae (Legume family)

Habitat

The golden chain tree grows in most areas except where winters are severe. It is frequently cultivated for its showy yellow flowers that hang in long chains.

Habitat of Laburnum anagyroides. - Fabaceae (Legume family).

Description

This large deciduous shrub or tree grows to 30 feet (9 meters) in height. The leaves are produced on long stalks, each with three leaflets, the undersides of which are covered with soft hairs. The pendulous racemes are up to 30 inches (76 cm) in length, with numerous bright yellow pealike flowers (Fig. 6-20). Numerous legume pods have up to eight flat seeds. The root has a licorice taste.

Figure 6-20. Golden chain tree (Laburnum anagyroides).

Principal Toxin

The quinolizidine alkaloid cytisine with nicotine-like properties is thought to be the principal toxin. Horses, cattle, dogs, and humans have been poisoned by eating the seeds [205-207]. The oral toxic dose of seeds for a horse is 0.05 percent of the animal's body weight. The immature seed pods and seeds are highly toxic. Cytisine is secreted in milk [205].

Clinical Signs

Affected animals may show loss of appetite, excitement, muscle tremors, irregular gait, convulsions, coma, and death. Vomiting, diarrhea, and dilated pupils may be observed before death. Degeneration of the muscles is observable microscopically [205].

Treatment

There is no specific treatment, and therapy should be supportive. Activated charcoal orally may help to reduce further toxin absorption.

Bleeding Heart, Dutchman's Breeches, Squirrel Corn, Stagger Weed

Dicentra spp. - Fumariaceae (Fumatory family)

Habitat

About a dozen species of Dicentra are found in North America, occurring in the eastern, southeastern states, and northwestern states. Bleeding hearts usually grow in rich, well-drained soils of forests and woodlands. Cultivated varieties (D. spectabilis) are widely grown for their showy flowers and fernlike foliage.

Habitat of Dicentra spp. - Fumariaceae (Fumatory family).

• D. cucullaria (Dutchman's breeches)
• D. canadensis (squirrel corn)
• D. formosa (western bleeding heart)
• D. eximia (wild bleeding heart)

Dutchman's breeches is the name also given to plants of the western and southwestern United States belonging to the genus Thamnosma that are unrelated to the Dicentra spp. , and cause photosenitization [208].

Description

Arising from a perennial tuberous root, delicate fernlike leaves are produced in early spring. The leaves are hairless, broadly triangular, finely divided, giving a lacy appearance. The characteristic flowers are pendant, symmetrical, pink to white in color, and produced in racemes extending above the leaves (Fig. 6-21).

Figure 6-21. Bleeding heart plant in flower (Dicentra spp.).

Principal Toxin

A variety of isoquinolone alkaloids (protoberberines) have been demonstrated in Dicentra and Corydalis spp. that are poisonous to cattle and horses but apparently not to sheep. Most poisoning occurs in the early spring because Dicentra and Corydalis spp. emerge before most other plants. Fitweed (C. aurea) and the similar Dicentraspp. contain similar alkaloids and have produced poisoning in cattle and sheep [209-212].

Clinical Signs

Cattle may first exhibit muscle tremors, running back and forth, and incoordination that has been referred to as "spring staggers" [210,213]. Depending on the amount of plant eaten, projectile vomiting, convulsions, and lateral recumbency with the head thrown back and legs rigidly extended may develop. Animals usually recover from the convulsive seizures [210,213].

Treatment

There is no specific treatment, and animals tend to recover if removed from the area where the plant is present. Mineral oil or other saline cathartic may be given orally to prevent further absorption of the toxins.

Lobelia

Lobelia spp. - Campanulaceae (Bellflower family)

Habitat

Lobelias grow in moist, fertile soils, along water courses, and in open woods from North Dakota, south into Texas and Mexico, and in much of the southeast. Hybrids of lobelia are grown as ornamentals in most of North America. Species that have been associated with poisoning include:

• L. berlandieri - Berlandier lobelia
• L. siphilitica - Great blue lobelia
• L. inflata - Indian tobacco
• L. cardinalis - Cardinal flower

Habitat of Lobelia spp. - Campanulaceae (Bellflower family).

Description

Lobelia are perennial, erect plants that may reach 3 to 4 feet (1 meter) in height. Leaves are throughout the stem, being larger at the base of the stem, alternate, hairless, and irregularly serrate. The inflorescence is a raceme of tubular flowers, the lower lip having three lobes and the upper two lobes. The color ranges from scarlet (L. cardinalis) to pale blue (L. siphilitica) (Fig. 6-22A), and various colored hybrids (Fig. 6-22B). Fruits are ellipsoid capsules with many small brown seeds.

Figure 6-22A. Cardinal flower (Lobelia cardinalis). Inset: Great blue lobelia (L. siphilitica).

Figure 6-22B. Lobelia hybrid (Lobelia spp.).

Principal Toxin

Lobelias contain many nicotine-like alkaloids, lobeline being common to most species.

Cattle, sheep, and goats are most frequently poisoned by L. berlandieri, especially in Mexico and Texas [214-216]. Humans are also susceptible to poisoning from the alkaloids.

Clinical Signs

Clinical signs include excessive salivation, vomiting, diarrhea, dilated pupils, coma and death [214-216]. Ulcers may be found on the cornea and in the mouth. A diagnosis of lobelia poisoning may be made on the basis of the clinical signs, evidence that the plants have been eaten, and the finding of identifiable plant parts in the animal's stomach.

Treatment

There is no specific treatment for lobelia poisoning, although atropine is helpful in relieving some of the signs. Administration of mineral oil and saline laxatives soon after an animal has eaten the plants may help in reducing the absorption of the toxic alkaloids.

Western Horse Nettle, Potato Weed

Solanum dimidiatum - Solanaceae (Nightshade family)

Habitat

Western horse nettle grows in prairies, fields, along roadsides and waste areas.

Description

These erect, perennial herbs grow to 1 to 2 feet (0.3 to 0.5 meters) tall, with a deep branching root system. Leaves are alternate, ovate to elliptical, 3 to 7 inches (7.5 to 17.5 cm) long and 2 to 4 inches (5 to 10 cm) wide, with stiff hairs along the stripes on both sides of the leaves.The stems have sparse, yellow spines. The flowers are produced terminally and consist of panicles of star-shaped, bluish purple to white flowers. The fruits are yellow round berries approximately 1 inch (2.5 cm) in diameter. S. dimidiatum closely resembles S. carolinense.

Principal Toxin

The toxin responsible for causing the neurologic signs associated with S. dimidiatum toxicity is not known. Calystegins, which are glycosidase inhibitors, have been identified in S. dimidiatum and S. kwebense, a plant from South Africa that produces similar cerebellar degeneration in cattle [217-220]. In Brazil, S. fastigiatum and S. bonariensis produce similar neurologic signs in cattle [220]; goats in Australia have been reported to develop cerebellar degeneration after eating S. cinerum [221]. Calystegins are similar to the indolizidine alkaloid swainsonine found in some of the locoweeds (Astragalus spp. ), and it has been hypothesized that these various Solanum spp. induce a lysosomal storage disease similar to that of locoism [219,221]. The neurologic signs are primarily associated with cerebellar degeneration.

Clinical Signs

"Crazy cow syndrome," the name given to the disease in Texas, aptly describes the behavior of animals poisoned by western horse nettle. Cattle appear normal until they are stressed or excited, whereupon they fall over and struggle futilely to stand. If left alone the affected animal regains its normal neuromuscular control. Animals infrequently die directly from the disease, although many are prone to drowning after falling into waterholes or creeks [223].

The most distinctive lesion found at postmortem examination of chronic cases is cerebellar atrophy [220,221]. Microscopically, there is severe depletion of the Purkinje neurons in the cerebellum, and those that are present contain vacuolated cytoplasm [218,220,223].

Sudan and Johnson Grass Poisoning

In addition to the acute toxic effects of cyanide poisoning discussed in Chapter 1, it is well known that low levels of cyanogenic glycosides found in some plants are associated with a chronic neurologic disease in man and animals [224-228]. A chronic poisoning has also been recognized in people in Africa who consume cassava (Manihot esculentum) containing cyanogens. The result is a degenerative disease of the nervous system referred to as tropical ataxic neuropathy, and that is characterized by degeneration of the peripheral, optic, and auditory nerves [229]. Enlargement of the thyroid gland (goiter) is common and is due to increased levels of thiocyanate that inhibits the uptake of iodine by the thyroid gland. The precise cause of the degenerative process in the nervous system is not known and is assumed to be related to the chronic elevation of thiocyanate levels that result following the consumption of cyanogens [230].

A similar syndrome of chronic cyanide poisoning occurs in horses, cattle, and sheep that are fed on pasture or hay containing sorghums such as Sudan and Johnson grass [224-228]. Animals consuming these grasses for prolonged periods develop a syndrome of posterior ataxia, urinary incontinence, cystitis, and weight loss. The disease results from lower spinal cord degeneration induced by low levels of cyanogenic glycosides in the plants that cause demyelinization of the peripheral nerves. It has been hypothesized that some cyanide may be converted to T-glutamyl-β-cyanoalanine, a known lathyrogen that interferes with the neurotransmitter activity of glutamate [231]. Lathyrogens affect normal development of nervous tissue causing signs of ataxia, urinary incontinence, and musculoskeletal deformities similar to those seen in foals and calves born to mares and cows grazing Sudan grass in early pregnancy [226,227,231-233]. In addition to limb deformities (arthrogryposis), calves also develop severe degeneration of the spinal cord and brain [226].

Clinical Signs

Ataxia is most noticeable in affected horses when they are backed or turned, causing the horse to sit on its hindquarters or fall over. Paralysis of the urinary bladder results in the continual dribbling of urine, which causes scald and hair loss of the lower hind legs in the male and perineum area in mares. Paralysis of the perineum may cause the lips of the vulva to stay open resulting in vaginitis. Loss of tone to the rectum may occur causing fecal impaction and constipation. Flaccid paralysis of the tail develops in some cases. Affected animals generally retain a good appetite and physical parameters remain normal until cystitis and an ascending nephritis develop secondary to incontinence. As this occurs, the urine becomes thick and opaque and contains large amounts of amorphous sediment. On rectal palpation, the bladder is characteristically enlarged and flaccid and contains concretions adherent to the dependent portion of the bladder [225,231].

The clinical signs of chronic cyanide poisoning should be differentiated from those of equine herpes virus-1 myeloencephalitis, equine protozoal encephalomyelitis, and equine viral encephalitis. The history of feeding sorghum grasses and the presence of cystitis, which is not usually a feature of the previously mentioned diseases, should help confirm the diagnosis of chronic Sudan grass poisoning.

Postmortem examination generally reveals a severe ulcerative necrotizing urethritis and cystitis extending to a pyelonephritis. Degeneration and demyelination of axons throughout the length of the spinal cord are evident histologically [231]. The predominant finding in sheep dying after grazing Sorghum pastures was the presence of focal axonal enlargement (spheroids) in the medulla, cerebellum, midbrain, and spinal cord [228].

Animals slowly recover from the syndrome if they are removed from the toxic sorghum grasses before the cystitis and ataxia become complicated by serious secondary problems, such as the ascending infection of the kidneys and pylonephritis. Complete recovery seldom occurs once horses have developed severe signs of ataxia and cystitis. Some improvement in the animal's condition can be expected if it is removed from the source of the toxic sorghum grasses and the urinary system infections are treated with appropriate antibiotics.

Plants:

Peas

Lathyrus sativus - Chickling pea
L. odoratus - Sweet pea
L. latifolius - Perennial sweet pea
L. sylvestris -  Flat pea
L. hirsutus - Rough pea
Fabaceae (Legume family)

Description

The perennial or everlasting pea (L. latifolius) has multiple climbing or trailing stems 3 to 6 feet (1 to 2 meters) in length developing from rhizomes. The stems are hairless, slightly glaucous, with two obvious wings. Leaves are alternate, pinnate, with the rachis ending in a branched tendril. The flowers, white, pink or purple, sometimes striped, are produced from leaf axils on a long peduncle that extends beyond the leaves (Fig. 6-23). The pods are 2 to 3 inches (5 to 7.5 cm) long and contain up to seven seeds.

Habitat of Peas - Fabaceae (Legume family).

Figure 6-23. Perennial sweet pea pink and white varieties (Lathyrus latifolius).

Lathyrism

Lathyrism is a disease of people in some eastern Asian and African countries where the seeds of certain peas (Lathyrus spp.) are eaten when other foods are scarce [234-238]. Lathyrism is an irreversible, nonprogressive, spastic, paraparesis associated with degeneration of the spinal cord caused by an as yet poorly defined neurotoxin. In humans there are two recognized forms of lathyrism: neurolathyrism and osteolathyrism. Neurolathyrism is the most common and is due to spinal cord degeneration caused by a neurotoxin in L. sativus. The disease affects mostly men who eat the uncooked or poorly fermented pea seeds for several months and are stressed through arduous work. Symptoms include muscular rigidity, weakness, and paralysis of the legs that results in people eventually only being able to crawl around on their knees [238]. Death eventually results unless the eating of the peas is stopped and effective nursing care is provided [229].

Osteolathyrism is the most common form of lathyrism affecting animals. The perennial sweet pea (L. latifolius) and the annual sweet pea (L. odoratus) seeds contain lathyrogens capable of producing osteolathyrism in animals, especially horses [229]. This disease in horses is characterized by skeletal deformities and aortic rupture due to defective synthesis of cartilage and connective tissue [229]. A similar syndrome of musculoskeletal deformities in foals and calves has been associated with pregnant mares and cows having eaten Sudan grass (Sorghum sudanense) or sorghum hybrids over a period of months [239,240]. In addition to limb deformities (arthrogryposis), calves also develop severe degeneration of the spinal cord and brain [240]. Adult animals may develop posterior ataxia, urinary incontinence, and cystitis resulting from lower spinal cord degeneration [245].

Principal Toxins

The primary neurolathyrogen in the chickling pea is β-N-oxalyl-L-α-diamino propionic acid. It apparently interferes with glutamate receptors in the brain, causing an influx of calcium into the cells with resulting cell death [241]. Additionally, the neurolathyrogen may cause free radical damage to the brain [242]. This is supported by finding that the antioxidant ascorbic acid when given to guinea pigs prevented the neurotoxic effects of the peas [242]. The toxin can be destroyed by boiling the peas or by allowing them to ferment thoroughly [243,244]. The primary lathyrogen in the annual sweet pea is the amino acid, β-amino proprionitrile, that causes defective cross-linking of collagen and elastin molecules [229].

Sorghums, especially those containing low levels of cyanogenic glycosides, appear to contain lathyrogens similar in effect to those found in pea seeds. The lathyrogens may either affect the developing fetus causing skeletal and brain degeneration or may cause loss of the myelin sheath surrounding peripheral nerves with resulting loss of nerve function. The neuronal degeneration and demyelinization of the peripheral nerves is thought to result from the conversion of the cyanide to β-cyanoalanine and then to T-glutamyl β-cyanoalanine, a known lathyrogen that interferes with neuro- transmitter activity [231]. The neuronal degeneration in the brain may also result when cyanogens cause the depletion of hydroxycobalamin [240]. Animals may slowly recover if they are removed from the Sudan grass before neuronal degeneration is severe and if cystitis is not complicated by an ascending infection of the kidneys.

Caltrop, Carpetweed

Kallstroemia hirsutissima - Hairy caltrop

K. parviflora - Warty caltrop

Zygophyllaceae (Caltrop family)

Habitat

Caltrop or carpetweeds are common in the southwestern states, especially in Texas and Arizona, preferring sandy soils in overgrazed or waste areas. As the name implies the plants can form dense carpets if allowed to proliferate.

Description

These multibranched prostrate annuals have up to 3 feet (1 meter) long stems arising radially from a central root. The leaves are opposite, evenly pinnate with four to six pairs of leaflets and conspicuously hairy. Single, orange to yellow, five-petalled flowers are produced from the leaf axil on peduncles longer than the leaf (Fig. 6-24). The fruits contain 8 to 12 one-seeded segments.

Figure 6-24. Hairy caltrop (Kallstroemia spp.). (Courtesy of Mark Dimmit, Tuscon AZ).

Kallstroemia spp. are similar in appearance to puncture vine or goathead (Tribulus terrestris) and are both members of the caltrop family. They differ in that T. terrestris has flower stalks shorter than the leaves, and the fruits separate into five, three to five-seeded, hard, spiny segments that look like the head of a horned goat (see Figure 4-14). The toxicity of this plant is discussed in Plants affecting skin and liver.

Principal Toxin

The toxin in Kallstroemia spp. is not known. Cattle, sheep, goats, and rabbits are reportedly susceptible to poisoning when they eat large quantities of the caltrop [245]. Animals generally will not eat the plant unless hungry and little else is available for them to eat.

Clinical Signs

Initially affected cattle develop weakness of the hind legs and knuckling of the fet- lock joints. Paralysis of the hind legs and convulsions occur before death [246]. Sheep may show similar signs but are reported to walk on their front knees. Removing animals from the caltrop before the animals are severely affected often results in their recovery. Those that die exhibit hemorrhages and congestion of the thoracic and abdominal organs [245].

Hemp, Marijuana

Cannabis sativa - Cannabaceae (Hemp family)

Habitat

Introduced originally from Asia, Cannabis is now found in most areas of the United States, and especially where it was originally grown for its fiber. It will grow in most soils except in desert areas and is often found growing along fence rows, weedy areas, and disturbed soils.

Habitat of Cannabis sativa.  - Cannabaceae (Hemp family).

Description

Hemp is an annual that grows to 6 feet (2 meters) in height, with a central, multibranched stem (Fig. 6-25A). The leaves, opposite near the base, becoming alternate near the top of the plant, are palmate, with three to seven lanceolate, serrated leaflets (Fig. 6-25B). Male and female greenish white flowers are produced on separate plants. Male flowers are produced as loose, leafy panicles in the leaf axils, whereas the female flowers are dense panicles. The fruit consists of papery bracts surrounding a single smooth brown seed.

Figure 6-25A. Marijuana (Cannabis sativa) plant (Courtesy of Carol Salman, Fort Collins, Colorado).

Figure 6-25B. Marijuana showing typical leaf structure (C. sativa).

Principal Toxin

More than 60 cannabinoid compounds have been isolated from C. sativa, the most toxic of which on the nervous system is tetrahydrocannibinol [247]. The content of the alkaloids is highest in plants grown in warm climates. Poisoning in animals is rarely encountered because the plant is not very palatable. Cattle, horse, pigs, and dogs have been intoxicated after eating marijuana [249]. Dogs are most likely to be poisoned when fed human food containing Cannabis [250]. Pollen from the flowers is a cause of allergy in humans and dogs [251].

Clinical Signs

Although a wide variety of signs of marijuana poisoning have been reported in humans, the most prevalent sign of poisoning in the dog is central nervous system depression [251]. Other animals may show hyperexcitability, vomiting, salivation, muscle tremors, and ataxia. Coma and death may result in severe cases.

Tobacco

Nicotiana tabacum - Cultivated tobacco

N. trigonophylla - Wild or desert tobacco

N. attenuata - Wild or coyote tobacco

N. glauca - Tree tobacco

Solanaceae (Nightshade family)

Habitat

With the exception of cultivated tobacco, which is grown predominantly in the southeastern United States, most wild tobaccos are found in drier areas of the southwest.

Habitat of Tobacco. - Solanaceae (Nightshade family).

Description

Tobacco is an erect, herbaceous, branching annual that grows 1 to 4 feet (0.3 to 1.2 meters) in height. The stems and leaves are hairy and sticky. Leaves are alternate, petioled, lanceolate and vary in size depending on the species. Flowers have five parts and are white, fragrant, and tubular. N. trigonophylla flowers open at night (Fig. 6-26A); N. attenuata is a day bloomer.

Figure 6-26A. Desert tobacco (Nicotiana trigonophylla).

Tree tobacco (N. glauca) is an evergreen, shrub, or small tree growing 6 to 20 feet (2 to 6 meters) in height. It is has slender, loosely branching stems, with alternate, bluish green, hairless leaves. The leaves and stems have a covering of whitish powder that rubs off easily. The tubular, yellow flowers, about 2 inches (5 cm) long, are produced on leafless branches at the end of the stems (Fig. 6-26B). The plant reproduces via the large number of kidney-shaped seeds produced in the egg-shaped, pendulous, brown seed pods.

Figure 6-26B. Tree tobacco (N. glauca).

Principal Toxins

Nicotine, a potent pyridine alkaloid, is probably present in all species of Nicotiana and in all parts of the plant. Animals usually find the plants unpalatable but will eat tobacco when other food is scarce. The minimum lethal dose of desert tobacco to cattle is 2 percent body weight of green plant [252]. Horses have been poisoned by eating dried tobacco leaves. Similarly dogs have been poisoned by eating tobacco [253,254]. Nicotine acts primarily on the autonomic nervous system, mimicking the action of acetylcholine at the autonomic ganglia and myoneural junction. The lethal dose of nicotine to animals is 100 to 300 mg total dose [255].

The alkaloid anabasine and not nicotine is responsible for the skeletal deformities that develop in the fetus of pregnant animals eating tobacco in the first trimester of pregnancy [256-258]. These teratogenic effects of the Nicotiana spp. and other plants are discussed in Chapter 8.

Clinical Signs

In small doses nicotine is a stimulant that causes excitement, rapid heart rate, salivation, vomiting, colic, and diarrhea. Ruminants may develop bloat. At higher doses nicotine causes blockade at the neuromuscular junction with resulting muscle weakness, staggering, collapse of the front legs, and a rapid, weak, and irregular heart rate. Difficulty in breathing due to respiratory paralysis, blindness, prostration, coma, and death develop rapidly when large quantities of tobacco are consumed. Some animals may be found dead without having been observed with neurologic signs [259].

Treatment

There is no specific treatment for nicotine poisoning other than to try and prevent further intestinal absorption by administering an oral adsorbent such as activated charcoal. Cathartics may help in the rapid removal of the toxic plant material from the intestinal tract. Additional supportive therapy in the form of intravenous fluids is necessary in severely poisoned animals.

Miscellaneous Plants Associated with Neurologic Signs

The plants listed in Table 6-4 have been suspected of causing poisoning characterized by neurologic signs. They are not discussed in detail because either poisoning from them rarely occurs in animals in North America or there is minimal current corroborating documentation of their toxicity to animals.

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