TABLE 18–1 Mechanically Injurious Plants^a

^a Most commonly cause oral lesions resulting in excess salivation or slobbering, difficulty in eating, and decreased feed intake. Occasionally, some may cause skin trauma; bristles of burdock may cause eye injury.

Profuse salivation as the only major clinical sign occurs in horses and other livestock eating clover or alfalfa pasture or hay that is infected with the fungus Rhizoctonia leguminicola. The factor responsible has been identified as slaframine, a mycotoxin produced most commonly by this mold on red clover (Trifolium pratense), but may also occur on other common legumes, including alfalfa, white clover, alsike clover, lupines, cow pea, and kudzu. Slaframine is chemically similar to the toxin swainsonine produced by locoweeds (Astragalus and Oxytropis spp.). Under wet or humid conditions, the slaframine producing mold grows on the leaves, producing black or brown spotting. After eating infected legumes for several days, horses begin to salivate excessively, lose weight, and may have excessive tearing or lacrimation, diarrhea, and frequent urination. Pregnant mares may abort if they continue to consume the infected clover. Recovery occurs rapidly once horses are removed from the infected forage. Problem pastures can be grazed if they are mowed, the affected hay is removed, and the regrowth has no brown or black spotting on the leaves.

COLIC- AND DIARRHEA-INDUCING PLANTS

Poisonous plants are but one of many causes of colic and diarrhea in horses. The action of various plant toxins may either have a direct irritant effect on the intestine, causing increased motility, colic, and diarrhea, or they cause the same effects by acting on the nervous system. Yet other plants may cause severe colic through obstruction or impaction of the small or large intestine, respectively. Fruits of plants such as Cockspur hawthorn (Crataegus crusgalli), mesquite (Prosopis glandulosa), and persimmon (Diospyros virginiana) when eaten by horses can cause obstruction of the small or large intestine. Plants such as halogeton (Halogeton glomeratus), greasewood (Sarcobatus vermiculatus), and shamrock, soursob, or sorrel (Oxalis spp.) contain high amounts of oxalate, which have the potential to cause stomach and intestinal inflammation and diarrhea. Prolonged consumption of low amounts of oxalate from these plants, or other plants containing low amounts of oxalate, may cause a calcium-deficiency as described in Chapter 2.

Plants most frequently associated with either or both colic and diarrhea in horses are listed, along with their toxin and additional effects on the horse, in Table 18–2. Horses eating the fruit, seeds, or leaves of avocado (Persea americana) trees usually die within a few days or less, depending on the amount consumed, as described later in this chapter in the section on “Sudden Death-Inducing Plants.” Prior to death, however, colic, diarrhea, and signs of acute congestive heart failure occur. A variety of other common plants also may be incriminated as a cause of colic and diarrhea if horses are deprived of normal forages. Invasive pasture plants such as leafy spurge (Euphorbia esula), wild iris (Iris missouriensis), horsetail or scouring rush (Equisetum arvense), bitter weeds (Helenium spp.), and a variety of mustard plants (Brassica spp.) should be considered as a cause of colic and diarrhea when other causes are not found.

Determining that colic or diarrhea are due to a plant is difficult because generally there are no specific lesions of plant poisoning detectable in the gastrointestinal tract at postmortem examination, and it is difficult to identify plants in the gastrointestinal tract once they have been chewed and acted upon by digestive enzymes. When plants are suspected of causing colic and diarrhea, a careful history and a thorough examination of the horse’s pasture and food should be made in an attempt to identify plants given in Table 18–2.

Horse Chestnut and Buckeye

Horse chestnut and buckeye (Aesculus spp.) are common small- to medium-sized shrubs or trees with large palmate leaves, white to red flower spikes born terminally on the branches, and characteristic spiny or smooth fruit capsules containing one to three shiny brown nuts when ripe (Fig. 18–2). A variety of horse chestnut species grow throughout most states but are concentrated in the eastern and southern states. Those reportedly toxic to animals are: Ohio, California, red and yellow buckeyes (A. glabra, californica, pavia and octandra, respectively), and the introduced species horse chestnut (A. hippocastanum). These toxic chestnuts are not related to the edible chestnut (Castanea spp.).

The toxin in buckeyes and chestnuts is aesculin, a glycoside present in the new growth, the leaves, and the nuts. Its principal action appears to be on the gastrointestinal tract and nervous system. Colic has been the main problem reported in horses, although muscle tremors, incoordination, and paralysis are possible. There is no specific treatment, but mineral oil given by stomach tube as a laxative, and supportive fluid therapy may be beneficial.

TABLE 18–2 Colic-^a or Diarrhea-Inducing Plants

Field Bindweed (Morning Glory)

Field bindweed (Convolvulus arvensis), found throughout North America, is an extremely persistent, invasive, perennial, twining or creeping weed with alternate leaves and white or pink funnel-shaped flowers (Fig. 18–3). The plant reproduces readily from seed and from its extensive root system.

The toxins in bindweed, are present in all parts of the plant. Colic as the result of intestinal paralysis, decreased heart rate, and dilated pupils may result if toxic levels of bindweed are consumed. No specific treatment is known.

Oak

Horses are susceptible to oak poisoning caused by the tannic acid that accumulates in new leaves and acorns that horses will eat when normal forages are scarce. Although all 60 species of oak that grow in North America are potentially toxic, most livestock poisoning is attributed to Gambels oak (Quercus gambelii), Shinnery oak (Q. havardii), and Q. breviloba. Oaks range from shrubs to large trees. All have alternate, simple, toothed or lobed, dark green glossy leaves that become red in the fall (Fig. 18–4). The plants are monoecious, with the staminate flowers occurring in long catkins and the pistillate flowers occurring singly or in small clusters. The fruit, an acorn, is a nut partially enveloped by an involucre of scales (Fig. 18–4).

Fig.18–2. Fruits of horse chestnut or buckeye (Aesculus spp.)

Tannins found in the leaves, bark, and acorns of most oak species are presumed to be the toxin causing poisoning in animals. Tannins are potent precipitators of cellular protein (astringents), which when ingested cause severe damage to the intestinal tract and kidney. Oaks at any stage of growth are poisonous, but are particularly toxic when the leaf and flower buds are just opening in the spring. As the leaves mature, they become less toxic. Ripe acorns are also less toxic than green acorns. Cattle, sheep, horses, and pigs are susceptible to oak poisoning. Ruminants frequently browse on oak without apparent problems, provided they have ample access to normal forages.

Clinical signs of oak poisoning vary according to the quantity of oak leaves, bark, or acorns consumed. Initially animals stop eating, become depressed, and develop colic. The feces are hard and dark, but a bloody diarrhea often occurs later in the course of poisoning. Some horses may appear to have choked with ingested food, and saliva passes out the nose. Mouth ulcers may also be present. Severe gastrointestinal, liver and kidney damage and a low blood calcium and phosphorus concentrations are usually present. Horses may die within a 24-hour period after eating large quantities of acorns, or may live for 5 to 7 days after the onset of clinical signs.

Fig. 18–3. Field bindweed (Convolvulus arvensis)

Fig. 18–4. Gambels oak (Quercus gambelii) showing typical leaves and acorn

Affected animals should be removed from oak pasture and given supportive care in the form of fresh water and hay. Mineral oil, intravenous fluids and drugs to control pain are particularly indicated for colicky horses.

Mountain Laurel

Laurels (Kalmia latifolia) are common branching shrubs or small trees with glossy, green, alternate lanceolate leaves. The characteristic white to pink flowers are produced in showy clusters (Fig. 18–5). Laurels are common to the eastern and southern United States.

The principal toxins in laurels are present in all parts of the plant. Similar toxins are also present in azaleas (Rhododendron spp.) (Fig. 18–6), fetterbush (Leucothoe spp.) (Fig. 18–7), mountain pieris (Pieris spp.) (Fig. 18–8), and maleberry (Lyonia spp.) (Fig. 18–9). The principal effects of the toxin when these plants are ingested are gastrointestinal irritation and disruption of the heart’s normal electrical activity.

Although all animals are susceptible to laurel and rhododendron poisoning, horses and donkeys are only occasionally poisoned. Affected animals may show excessive, green frothy salivation, colic, frequent defecation, depression, weakness, and incoordination. If a sufficient quantity of laurel has been eaten, an inability to stand, coma, and death occur. There is no specific treatment. Mineral oil and intravenous fluids may be helpful.

Pokeweed

Pokeweed (Phytolacca americana) is a perennial branching herb 3 to 10 ft (1 to 3 m) tall, with a large taproot, green or purple stems, and large, alternate, petioled and ovate leaves. The flowers are small, white in color, and petalless. The distinctive fruits are shiny purple berries (Fig. 18–10). Pokeweed grows mostly in the eastern and southern United States. All parts of the plant, especially the roots, contain saponins and oxalates. Pokeweed mitogens may also cause mild to severe colic and diarrhea depending on the amount consumed. Fatalities are rare.

Fig. 18–5. Mountain laurel (Kalmia latifolia)

Fig. 18–6. Azaleas (Rhododendron catawbiense)

Fig. 18–7. Fetterbush (Leucothoe spp.)

Fig. 18–8. Mountain pieris (Pieris spp.) (Courtesy of Drs. John and Emily Smith, Baldwin, GA)

Fig. 18–9. Maleberry (Lyonia spp.)

Fig. 18–10. Pokeweed berries (Phytolacca americana) (Courtesy of Drs. John and Emily Smith, Baldwin, GA)

Buttercups

Buttercups (Ranunculus spp.) are perennial herbaceous plants with fibrous roots, erect hairless stems, and leaves deeply divided into three lobes. The upper leaves are smaller. The flowers vary from few to many, and have five bright yellow petals and five green sepals (Fig. 18–11). Buttercups are commonly found in wet areas throughout North America.

Some, but not all, species of buttercups contain ranunculin which forms the toxic blistering agent protoanemonin when the plant is chewed or crushed. When dried, buttercups lose their toxicity. Other plants that contain protoanemonins include hellebore (Helleborus spp.), marsh marigold (Caltha palustris), clematis (Clematis spp.) and anemone (Ranunculus spp.)

Fig. 18–11. Buttercup (Ranunculus spp.)

Ingestion of plants containing protoanemonins results in excessive salivation, mild colic, and diarrhea varying in severity depending on the amount the horse has eaten.

Castor Oil Plant

Castor oil plants (Ricinus communis) are common perennial plants of tropical areas, growing 6 to 13 ft (2 to 4 m) high, with a single, hollow branching stem. The stem is often purplish in color with a waxy coating. Leaves are large, alternate, usually 8 lobed, each with a main vein that radiates from the off-centered attachment of the petiole (Fig. 18–12). Yellowish flowers are produced in racemes at the end of the main stem and form fruits covered with soft spines that dry into sharp spines surrounding three characteristic seeds. Poisoning occurs from eating either the plants or grain contaminated with castor beans (Fig. 18–13).

Fig. 18–12. Castor oil plant (Ricinus communis) leaves and spiny fruit capsules

Fig. 18–13. Castor beans (Ricinus communis)

All parts of the plant and especially the seeds contain ricin, a highly toxic lectin that inhibits protein synthesis. Similar toxic lectins are found in rosary peas (Abrus precatorius) (Fig. 18–14) and black locust (Robinia pseudoacacia) (Fig. 18–15). Lectins are proteins that have the capability of binding to cells; they can cause agglutination of cells and acute hypersensitivity reactions. Horses are poisoned by eating seeds (castor beans) in an amount as small as that equal to 0.01% of their body weight. This amount could be provided by only 1 to 2% castor beans in the horse’s grain. However, castor oil extracted from the seeds is not toxic, as the ricin is insoluble in the oil. The oil is, however, a potent intestinal purgative or cathartic.

Early signs of castor bean poisoning in horses include trembling, sweating, and incoordination which appear several days after the animal has eaten grain contaminated with castor beans. Colic, diarrhea, and a rapid weak pulse develop as the poisoning progresses. Horses that develop clinical signs seldom survive.

Fig. 18–14. Rosary peas (Abrus precatorius) with characteristic black patch on the scarlet seeds

Fig. 18–15. Black locust (Robinia pseudoacacia) flowers, compound leaves, and thorns on branches

Jimson Weed, Potato, and Tomato

In the large family of nightshade (Solanaceae) plants, horses have been poisoned by various genera that include nightshades (Solanum spp.), jimson weed or thorn apple (Datura stramonium) (Fig. 18–16), tomato (Lycopersicon spp.), potato (Solanum tuberosum), and jessamine (Cestrum spp.).

A variety of toxins are found in Solanaceae plants, especially in the green parts of the plant and the unripe fruits. These toxins inhibit the animal’s parasympathetic nervous system. They also have a direct irritant effect on the digestive system. Horses are most often poisoned by the feeding of grain contaminated with jimson weed seeds (Fig. 18–17) green or rotting potatoes, or potato or tomato plants. Compared to other livestock, horses may be more susceptible to of solanine toxins.

Initially there may be excitement, but depression follows with decreased heart and respiratory rate, muscle weakness, dilated pupils, colic, and watery diarrhea that may be bloody. When large amounts of solanine are ingested, death results from cardiac arrest. Therapy is symptomatic as no specific treatment exists.

Fig. 18–16. Jimson weed or thorn apple (Datura stramonium) showing characteristic trumpet-shaped flower and spiny fruit (thorn apple)

Fig. 18–17. Jimson weed or thorn apple seeds (Datura stramonium)

PRIMARY PHOTODERMATITIS-INDUCING PLANTS

The common cause of plant-induced dermatitis or skin inflammation is photosensitization, which can be induced by the consumption of plants given in Table 18–3. These plants induce photodermatitis as a result of the accumulation of photodynamic compounds in the skin, which when exposed to ultraviolet rays from sunlight fluoresce, releasing radiant energy that causes cellular damage. The less pigmented the skin, the more ultraviolet rays are able to reach photosensitive compounds in the skin, and the more susceptible that skin consequently is to photosensitization (Fig. 18–18). Horses with completely pigmented skin are often fully protected even though the photodynamic pigments are present in the skin. In such animals, excess tearing or lacrimation and an abnormal intolerance to light may be the only manifestations of photosensitivity.

TABLE18–3 Photodermatitis-Inducing Plants

Fig. 18–18. Photosensitization in a horse showing severe dermatitis affecting the nonpigmented skin only

Photodermatitis may be primary or secondary. Primary photosensitization develops when horses eat plants containing photosensitive pigments, which are absorbed and accumulate in the skin. Two plants associated with primary photosensitization in horses are buckwheat (Fagopyrum esculentum) and St. John’s wort (Hypericum perforatum). Horses are also potentially at risk from plants such as spring parsley (Cymopterus watsonii) and bishop’s weed (Ammi majus), which contain photoreactive substances that induce primary photosensitization in other livestock and poultry and, therefore, may in horses.

Secondary, or hepatogenous, photosensitization occurs more commonly in animals than primary photosensitization. Unlike primary photosensitization, liver disease is the underlying cause for secondary photosensitivity. The plant toxins themselves are not photoreactive, but they cause liver damage. Once 80% or more of the liver is affected, it is unable to eliminate phylloerythrin, a normal breakdown by-product of plant chlorophyll, which then accumulates in the blood. Phylloerythrin fluoresces when exposed to ultraviolet light, causing the cellular damage resulting in photosensitization. The prognosis for animals with secondary photosensitization is always far poorer than that for primary photosensitization because the underlying liver disease is frequently irreversible and eventually fatal in most affected animals. The plants that are most frequently associated with secondary photosensitization in horses in North America are discussed in the next section on “Liver Disease-Inducing Plants,” and are listed in Table 18–4. Those most commonly responsible for causing primary photosensitization in horses, buckwheat and St. John’s wort, are described here.

TABLE 18–4 Hepatotoxic Plants

^a In addition to signs of liver failure, often first noted by abnormal behavior followed by weight loss, icterus, bloody urine, anemia, and photosensitization (Fig. 18–18), the pyrrolizidine alkaloids also cause cancer, birth defects, and abortion with effects often not occurring for months after its ingestion.

^b Currently not found in North America, but could be introduced and become a problem. Salvation Jane has been introduced into California; if it escapes, it may become a problematic toxic plant in North America.

^c Several weeks of eating indigo may also result in incoordination, depression, corneal opacity, difficulty breathing, and abortion.

^d Horses on contaminated pastures (not hay) during warm, humid weather characteristically develop acute photosensitization of thin haired and white-skinned areas (Fig. 18–18) especially around the lips, nose, and feet, which has been referred to as “dew poisoning.”

Treatment of the dermatitis due to photosensitization, whether it is primary or secondary, is to keep the animal completely out of the sun, preferably stalled. Sunlight through a glass window isn’t harmful, as ultraviolet rays are filtered out by the glass. Gentle daily cleaning of the skin with a mild organic iodide solution will aid recovery. Antibiotic therapy may be necessary if there is secondary bacterial infection of the skin.

St. John’s Wort or Klamath Weed

St. John’s wort (Hypericum perforatum) grows throughout North America. It is an erect perennial herb that grows up to 3 ft (1 m) tall with woody lower stems. The branches are opposite and sterile. Usually both stems and branches are two-edged or winged. The leaves are opposite, sessile, linear-oblong, ¾ inch (2 cm) long, and spotted with tiny dots which are translucent when held against the light. The flowering part of the plant has a cyme arrangement with numerous flowers ½ to ¾ inches (1 to 2 cm) in diameter with five bright yellow petals, five green sepals, many stamens in clusters of three to five and an ovary with three widely spreading styles (Fig. 18–19). The petals have fimbriatc margins and may have black glandular dots on the margins. These dots contain the toxin, hypericin.

Fig. 18–19. St. John’s wort or Klamath weed (Hypericum perforatum)

Hypericin is a photodynamic pigment that remains chemically intact through digestion and is readily absorbed into the blood. It has no effect on the liver or other organs unless it is exposed to ultraviolet rays. This occurs especially in nonpigmented skin, causing primary photosensitization. Its presence in the glandular dots on the leaves suggests that all Hypericum spp. plants with similar glands are potentially capable of causing primary photosensitization. The young plants are as toxic as the mature plants and more palatable to livestock; they are thus more likely to cause poisoning in grazing animals. However, the toxin is not destroyed by drying and, therefore, hay containing it may also cause poisoning.

Buckwheat

Buckwheat (Fagopyrum esculentum) is a glabrous, herbaceous annual plant with erect stems, alternate with hastate or cordate leaves. The stipules are united as a sheath (ochrea) around the stem at the nodes. The greenish white flowers occur as terminal or axial panicles, and have eight stamens and 3-parted styles, which form 3-angled brown-colored seeds from which buckwheat flour is made (Fig. 18–20). Commonly grown as a cover crop to be plowed under for soil enrichment, it has escaped in many areas to become a weed of waste places.

Both the green and dried plant contain the pigment fagopyrin, which, when ingested in sufficient quantities and then exposed to sunlight, is capable of producing primary photosensitization in all domestic livestock.

Fig. 18–20. Buckwheat (Fagopyrum esculentum) showing the typical heart-shaped leaves and white flowers

LIVER DISEASE-INDUCING PLANTS

Surprisingly, few plant toxins cause liver disease, probably because the liver has tremendous capabilities for detoxifying many compounds that are absorbed from the gastrointestinal tract. Furthermore, the liver has a great reserve capacity and will continue to function at near optimal levels until approximately 80% of it is destroyed. Only then will clinical signs of liver failure such as weight loss, depression and abnormal behavior, icterus, bloody urine, anemia, and photosensitization be observed. Photosensitization occurs because of the damaged liver’s inability to eliminate the body’s normal breakdown products of plant chlorophyll, which then accumulate in the blood. When these photosensitive substances are exposed to sunlight, they fluoresce, causing the skin damage responsible for secondary or hepatogenous photosensitization (Fig. 18–18). As described in the previous section, photosensitization may also be caused by the ingestion of plants, such as buckwheat (Fagopyrum esculentum) or St. John’s wort (Hypericum perforatum), that contain photosensitive pigments but do not cause liver damage. Because signs of secondary or hepatogenous photosensitization, or other clinical signs of liver disease, appear only when a majority of the liver’s functions are destroyed, horses showing clinical signs as a result of any plant-induced liver disease have a guarded to poor prognosis.

The most important plant toxins responsible for causing secondary photosensitization, as well as other manifestations of liver damage, are pyrrolizidine alkaloids.

Pyrrolizidine Alkaloid Poisoning

Plants Causing Pyrrolizidine Alkaloid Liver Damage

Pyrrolizidine alkaloids (PA), the major plant toxins harmful to the liver are present in a variety of plants listed in Table 18–4. The most common in North America are the many different species of Senecio.

TABLE 18–5 Toxic Senecio Species Plants in North America

Senecio spp.

There are some 1200 different species of Senecio that are distributed throughout the world, with about 70 species occurring in North America. Approximately 25 of these are known to be poisonous, but all species of Senecio should be considered toxic unless known otherwise. Those most commonly responsible for causing poisoning in horses in North America are listed in Table 18–5. The Senecio species have a wide overlapping geographical range in which they grow, but are selective in their habitats, some preferring high altitude, subalpine, moist conditions, while others prefer dry, rocky, sandy soils at lower elevations.

Identification of individual Senecio species is difficult. However, recognition of a plant as a member of the genus Senecio can be based on the presence of a single layer of touching, but not overlapping, greenish bracts surrounding the flower head (Fig. 18–21). Senecio species have alternate leaves that are generally lanceolate to ovate, dentate, and often irregularly and deeply pinnately divided. Some species are densely covered with white hairs. The composite heads are flattened terminal clusters with showy yellow ray and disk flowers. Seeds have a dense ring of white hairs (pappus) at one end to aid in wind distribution.

Fig. 18–21. Senecio flower showing the characteristic single layer of green bracts surrounding the yellow petals

Fig. 18–22. Tansy ragwort or stinking willie (Senecio jacobaea)

The PA concentration and thus toxicity of Senecio species vary considerably with the stage of growth, the mature plant being the most toxic. Ridell’s ragwort (S. ridellii), when near maturity, contains exceptionally high concentrations of PA (10 to 18% dry weight). Acute poisoning and death in 1 to 2 days has been associated with a few clays’ consumption of Senecio plants high in PA concentration in amounts of green plant equal to 1 to 5% of the animal’s body weight. Chronic poisoning, however, is more common in horses and cattle, and is usually associated with ingestion of smaller amounts of Senecio over a period of 3 weeks or longer.

Horses eating green tansy ragwort or stinking willie (S. jacobaea) (Fig. 18–22) in amounts in excess of that equal to 1 to 2% of their body weight develop clinical signs 20 days to 5 months later. This equates to a minimum 20-day cumulative or total dose equal to 2% of the animal’s body weight of plant dry matter.

Hound’s tongue (Cynoglossum officinale)

is a PA-containing common biennial weed of cultivated and waste areas that grows up to 3 ft (1 m) tall with alternate tongueshaped, hairy basal leaves up to 20 inches (0.5 m) long (Fig. 18–23). The upper leaves are lanceolate and sessile. The flowers are small, regular, reddish purple, and produced on terminal racemes. The fruits separate into four brown nutlets at maturity, which are covered with hooked barbs that readily attach to animal hair, aiding in their dispersal (Fig. 18–24). Hound’s tongue contains the pyrrolizidine alkaloids heliosupine and echinatine, with the greatest concentration (2.1% dry weight) in the preflowering rosette stage. Although reduced in quantity, the alkaloids remain present in the dried plant.

Fig. 18–23. First-year growth or rosette stage of Hounds tongue (Cynoglossum officinale)

Fig. 18–24. Flowers and fruits of Hounds tongue (Cynoglossum officinale)

Fig. 18–25. Fiddleneck (Amsinckia intermedia) showing its characteristic fiddleneck and flowers on one side of the inflorescence

Fiddleneck or Tarweed (Amsinckia intermedia)

is an erect, sparsely branched annual weed that grows up to 3 ft (1 m) tall and is covered with numerous, fine white hairs. Leaves are hairy, lanceolate, and alternate. The perfect five-parted, small, orange to yellow flowers are born terminally on a characteristic fiddleneck-shaped raceme, with the flowers all inserted on one side of the axis (Fig. 18–25). Mature fruits separate into two to four black-ridged nutlets.

Horses, cattle, and pigs have been poisoned by eating fiddleneck plants, especially the seeds. The symptoms and lesions in all species of animals consist of liver damage and fibrosis characteristic of pyrrolizidine alkaloid poisoning. Amsinckia species have also been reported to accumulate levels of nitrate potentially toxic to ruminants but probably not horses (see section on “Nitrate Poisoning” in Chapter 19).

Rattlebox or Rattlepod (Crotalaria spp.)

are erect, herbaceous, variably hairy plants that may be annuals or perennials. The leaves are simple, alternate, lanceolate to obovate, with a finely haired undersurface. The flowers are yellow, with the leguminous calyx longer than the corolla (Fig. 18–26). The fruit is a leguminous pod, inflated, hairless, becoming black with maturity, and containing 10 to 20 glossy, black, heart-shaped seeds, which often detach and rattle within the pod. Several species of Crotalaria have been associated with livestock poisoning, including C. sagittalis, C. spectabilis, and C. retusa.

Fig. 18–26. Rattlebox or rattlepod (Crotalaria spectabiiis) showing the pea-like flowers and dark seed pods

Crotalaria species contain pyrrolizidine alkaloids, the most notable of which is monocrotaline. It is present in greatest quantity in the seeds, lesser amounts being present in the leaves and stems. All livestock, including domestic fowl, are susceptible to poisoning. Although acute deaths will occur from eating large quantities of the Crotalaria seeds or plant, more often, as with other pyrrolizidine alkaloid-containing plants, clinical signs typical of this toxin develop from a few days to up to 6 months later.

Effects of Pyrrolizidine Alkaloids

Variations in the PA content of plants, the quantity eaten, and susceptibility of individual animal species result in wide variations in the severity of PA poisoning in animals. Flowers tend to contain the greatest amount of the alkaloid, although seeds of rattlebox or rattlepod, fiddleneck, and tarweed contain high levels of PA.

Pigs are the most susceptible to the effects of PA, followed by poultry, cattle, horses, goats, and sheep. Sheep can eat approximately 20 times the amount of Senecio it would take to poison a cow on an equivalent bodyweight basis. Horses show about the same susceptibility to pyrrolizidine toxicosis as do cattle. The chronic lethal dose of dried tansy ragwort (S. jacobaea) in cattle is only 0.02 to 0.05 mg/kg body weight fed over several months. This would equate to a 1000 lb (450-kg) horse eating about 5%. of its body weight of green tansy ragwort over a period of 1 to 3 months.

Fortunately, herbivores will not readily eat plants containing PA unless they are forced to do so through lack of other feed. However, the dried plants, which have only a minimal reduction in their alkaloid content, are more palatable, making them a particular risk when present in hay. Although acute poisoning and death can occur from a few days’ consumption of plants high in PA, chronic poisoning is more common. The effects of PA are cumulative, so symptoms of liver disease and photosensitization may not appear for many months after animals have eaten toxic quantities of PA-containing plants. This makes identification of the suspected poisonous plants difficult, since the plants will often not be present in the pasture or hay when clinical signs become evident in the horse.

Pyrrolidizine alkaloids are readily absorbed from the digestive tract of horses and are converted in the liver to toxic substances that bind to cellular proteins, causing rapid liver cell death. Similar cellular damage may also occur in the kidneys, intestinal tract, and lungs. Pyrrolizidine alkaloids may also induce cancer, birth defects and abortion. Although secretion of PA in mare’s milk has not been established, there is potential risk to the suckling foal, as PA has been shown to be present in small quantities in the milk of cows and goats fed tansy ragwort (Senecio jacobaea).

Acute PA poisoning occurs occasionally in horses that ingest large amounts of alkaloid-containing plants over a few days. Affected animals may show only depression, coma, and death as a result of severe liver damage.

Chronic PA poisoning, which is more common, is characterized by irreversible liver disease clinically manifested by one or more of the following clinical signs: weight loss, nervous signs, icterus, anemia, bloody urine, and photosensitization. Nervous signs due to liver damage are often the first clinical indication of PA poisoning, and may include drowsiness, head pressing, blindness, aimless wandering or “walking disease,” frequent yawning, and incessant licking of objects. The first sign of PA poisoning in a small percentage of horses is difficulty in breathing in, destruction of red blood cells and a bloody urine. Photosensitization may occur in some horses that have areas of nonpigmented skin (Fig. 18–18). In these horses, severe dermatitis that develops when the horses are exposed to sunlight results from the liver’s failure to excrete phyloerythrin, a photoreactive by-product of chlorophyll breakdown. Photosensitization is described earlier in this chapter in the section on primary photodermatitis.

Pyrrolizidine alkaloid poisoning is usually not suspected and, therefore, not detected until severe liver damage has occurred and clinical signs of liver failure are evident. At the present time, the only widely available and reliable means of confirming PA-induced liver failure is detecting specific microscopic alterations in a liver biopsy. The only other disease to mimic these alterations is aflatoxin poisoning, which occurs when horses eat moldy grains containing aflatoxins, but which, as described in Chapter 19, is uncommon in horses.

Horses showing signs of liver disease should be fed as described in that section of Chapter 17. However, the prognosis is poor for confirmed cases of PA poisoning.

Animals showing signs of photosensitization should be provided shelter from the sun and preferably kept stalled completely out of sunlight. Sunlight through glass will not induce photosensitization as it blocks ultraviolet rays. Gentle daily cleaning of the affected skin with a mild organic iodine antiseptic solution will aid in the healing process. Antibiotics may be indicated in cases where there is severe secondary bacterial infection of the skin.

Nonpyrrolizidine Alkaloid Liver Poisoning Plants

Indigo

Creeping indigo (Indigofera spicata) is a legume that was introduced into southern Florida, where it has become well established. It causes a fatal neurologic disease resulting from liver failure. The disease of horses known in Florida as “grove poisoning,” originally thought to be due to chemicals used in the citrus industry, is now known to be due to horses’ eating creeping indigo. In Australia, a similar disease of horses and other livestock referred to as “Birdsville disease” is caused by Birdsville indigo (Indigofera dominii).

Creeping indigo is a prostrate plant of tropical and subtropical areas with many branched runners fanning out from a crown of a white tapering taproot that may be up to 3 ft (1 m) in length. The stems are usually pale green with alternate pinnate leaves and alternate ovate leaflets on a short petiole (Fig. 18–27). The pink to dark red flowers are produced on short spikes from the leaf axils. The pointed seed pods are produced in downward-pointing clusters. The plant is a prolific seed producer and tends therefore to be capable of spreading readily.

The liver poison amino acid indospicine is present in various species of Indigofera. The leaves may contain from 0.1 to 0.5% of this toxin in their dry weight, and the seeds as much as 2.0%. Horses apparently find the plant highly palatable and seek it out. The toxin acts as a specific antagonist of the amino acid arginine and, therefore, is an inhibitor of protein synthesis. Horses fed sufficient peanut meal or cottonseed meal, both of which are rich in arginine, are protected from the effects of this toxin. Arginine constitutes 10 to 12% of the protein in these two protein supplements as compared to 4 to 7% in other horse feeds (Table 18–6).

Fig. 18–27. Creeping indigo (Indigofera spicata): young flowering plant showing prostrate form (Courtesy of Dr. Julia F. Morton, University of Miami, Coral Gables, FL)

TABLE 18–6 Protein, Sulfur-Containing Amino Acid, and Arginine Content of Horse Feeds

After consuming creeping indigo for several weeks, affected horses develop incoordination, difficulty in turning, and inability to walk in a straight line; they eventually collapse. They become severely depressed, lose weight, and have been reported to develop corneal opacity and respiratory difficulty. Affected pregnant mares may abort. Death results from liver failure. Animals eating meat from horses that have been poisoned by creeping indigo may suffer similar fatal poisoning.

Alsike Clover and Klein grass

Occasionally horses grazing clover, generally alsike clover (Trifolium hybridum), during wet or humid weather, develop a photosensitivity and hepatitis referred to as tri-foliosis. A similar condition may also occur in horses or sheep grazing klein grass (Panicum coloratum) pastures during wet or humid weather. The toxin responsible for either trifoliosis or klein grass poisoning has not been identified, but the sporadic nature of the diseases and their occurrence only during wet humid weather suggest that mycotoxins, or plant metabolites produced under humid, high-moisture growth conditions, may be responsible.

Affected horses on clover pasture characteristically develop an acute photosensitization involving thinly haired and white-skinned areas (see Fig. 18–18), especially around the lips, nose, and feet. The condition has been referred to as “dew poisoning” because there is an association between the location of the dermatitis and contact with moisture present on the dew-laden clover pasture. Affected horses may exhibit icterus and other signs of liver disease. In such cases, there may be significant liver enlargement and evidence of liver degeneration. Horses generally recover rapidly from the photosensitivity if they are removed from the toxic pasture. Horses may graze the pasture again without problem under different growing conditions in subsequent years or after the pasture dries out.

NEUROLOGIC DISEASE-INDUCING PLANTS

Behavioral alterations, blindness, inability to ingest and chew food, incoordination, depression, convulsions, and other physical abnormalities are all indicators of nervous system disorders. The brain, spinal cord, and peripheral nervous systems are susceptible to a variety of infectious, toxic and congenital diseases that are often indistinguishable clinically. A variety of plants that grow throughout North America are known to produce neurologic abnormalities in horses and, therefore, should be considered in the differential diagnosis of nervous system disorders. These plants, along with the major clinical signs they cause in poisoned horses, are listed in Table 18–7.

Sagebrush

The sagebrushes (Artemisia spp.) of the western United States are perennials ranging from the woody-stemmed 3 to 10 ft (1 to 3 m) tall big sagebrush (A. tridentata) to the smaller sand sage (A. filifolia) (Fig. 18–28) and the low-growing fringed sage (A. frigida) (Fig. 18–29). Considerable variation exists in the 200 or more species of sagebrush. Leaves are usually alternate, covered with very fine hairs that give the leaves a silvery green appearance, and when crushed give the characteristic smell of sage. Flowers are usually inconspicuous and born on panicles from the leaf axils.

The toxins in sagebrush are volatile monoterpenoid oils, which vary considerably in quantity depending on growing conditions and season, being highest in the fall and winter months.

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.” Budsage (A. spinescens) has been reported to cause similar problems in California and Nevada. Recently the author encountered a neurologic disease of horses that were wintered on an overgrazed range in Colorado where fringed sage (A. frigida) was the predominant forage available.

TABLE 18–7 Neurotoxic Plants and Their Effects on Horses

Fig. 18–28. Sand sage (Artemisia filifolia)

Although the actual toxin that causes sage sickness has not been defined, some monoterpenes present in Artemisia species are known to be toxic to the nervous system. Thujone, a monoterpene present in wormwood (A. absinthium), has been associated with a neurologic syndrome in people who chronically consume absinthe, the alcoholic beverage produced from wormwood. A similar poisoning is presumed to develop in horses that consume a sufficient quantity of sage.

Horses appear to develop neurologic signs after they are forced to eat sagebrush because 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 incoordination and a tendency to fall down or react abnormally to stimuli that would not normally have elicited such a response. Tying an affected 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 act relatively normal. Incoordination is particularly noticeable in the forequarters, with the hindquarters seemingly normal. Some animals may circle incessantly; others may become excitable and unpredictable. The characteristic smell of sage is often noticeable on the breath and in the feces. Sage-poisoned horses maintain an appetite and have a normal temperature, pulse, and respiration. The clinical signs closely resemble those of a horse that has been poisoned by loco-weed. However, unlike “locoed” horses that do not recover, “saged” horses tend to recover in 1 to 2 weeks after they stop eating sage and are fed a nutritious diet. Supportive therapy, including protection from extreme climatic conditions will aid in the recovery. They should not be ridden until fully recovered and evaluated for normal behavior and neurologic function.

Fig. 18–29. Fringed sage (Artemisia frigida)

Locoweeds and Milkvetches

Several hundred species of locoweed and milkvetch (Astragalus spp.) occur in North America, many of which are known to cause severe poisoning of livestock. This large group of legumes is taxonomically very difficult to identify, even by the experienced botanist. The genus Oxytropis, which like many Astragalus spp. is also commonly called locoweed, is a closely related genus and produces identical locoism in horses, cattle, sheep, and elk. However, not all species of Astragalus are toxic, and some are useful forage plants.

Astragalus spp. are perennial legumes growing to a height of up to 3 ft (1 m), with branching stems from a stout crown and extensive taproot. The leaves are alternate, pinnately compound, with each leaflet being elliptical or oval and minutely hairy. The racemes are usually produced at the ends of the branches and are densely covered with white to purple pea-like flowers, depending on the species. The leguminous seed pods vary considerably in shape and contain many bean-shaped seeds (Fig. 18–30).

Oxytropis species differ from Astragalus in that their hairy leaves and flower stems arise directly from the taproot crown. The leaves are pinnately compound, with each having a single apical elliptical leaflet. The flowers are either white (O. sericea) or purple (O. lambertii) in color and have a characteristic pointed keel (Figs. 18–31 and 18–32).

Fig. 18–30. Locoweed (Astragalus spp.) showing the typical flowers, leaves and pea-like seed pods (see also Fig. 18–60)

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