Plants Affecting the Digestive System (Part III)

Table of Contents

Part I: Excessive Salivation
Part II: Gastrointestinal Impaction and Obstruction Caused by Plants
Part III: Vomiting
Part IV: Nightshades
Part V: Diarrhea

Leafy Spurge

Part VI: Lectins

Castor Bean, Precatory Bean, Black Locust, Mayapple, Privet

Part VII: Rhododendron Grayanotoxins

Rhododendron, Mountain Laurel, Japanese Pieris, Fetter-Bush, Maleberry, Common Box

Alphabetic Plant List
Glossary

Part V: Diarrhea

A variety of common plants may cause diarrhea when they are eaten by animals that do not have good quality forages available to them. Invasive pasture plants such as Euphorbia esula (leafy spurge), Iris missouriensis (wild iris), Equisetum arvense (horse tail, scouring rush), Helenium spp. (bitter weeds), pokeweed (Phytolacca americana), and a variety of Brassica spp. (mustards) may cause colic and diarrhea. English ivy, which can invade animal pastures and fence rows accessible to livestock, may cause gastroenteritis, colic, and diarrhea (Table 3-3).

Plants:

Leafy Spurge

Euphorbia esula - Euphorbiaceae (Spurge family)

Habitat

Introduced from Eurasia, leafy spurge has become a troublesome weed of North America where it has infested millions of acres in Canada and the north-central United States. It is listed as a noxious weed in most states because of its ability to proliferate and displace normal forages.

Habitat of Leafy Spurge. Euphorbia esula - Euphorbiaceae (Spurge family).

Description

Leafy spurge is a prolific perennial, up to 3 feet (1 meter) tall, that reproduces by seeds and an extensive root system. Leaves are alternate, narrow 1 to 4 inches (2 to 10 cm) long. Multiple stems arise from root crowns. The plant contains a milky sap in the stems and leaves. The flowers are small and yellowish green in color and are arranged in terminal clusters. Conspicuous yellowish green heart-shaped bracts (often mistaken as the flower) surround each flower (Fig. 3-31A). Seed capsules explode when dry, scattering the seeds widely, which aids in the plant's rapid proliferation.

Figure 3-31A. Leafy spurge (Euphorbia esula).

Other spurges are potentially toxic to animals and include the tropical pencil tree (Euphorbia tirucalli), and snow on the mountain (E. marginata) (Fig. 3-31B). Myrtle spurge (E. myrsinites) (Fig. 3-31C) has a particularly irritating sap that causes dermatitis in some people who handle the plant.

Figure 3-31B. Snow on the mountain (Euphorbia marginata).

Figure 3-31C. Myrtle spurge (Euphorbia myrsinites).

Principal Toxin

The specific toxin in leafy spurge has not been defined. Cattle, through negative feedback, learn to avoid eating the plant once they have initially consumed small amounts of the plant [85]. Terpenes appear to be the aversive chemical in the plant [86]. Even ensiling leafy spurge does not improve its palatability [87]. Sheep and goats readily eat leafy spurge and appear to be unaffected by it.

Clinical Signs

Spurges are usually not eaten by cattle when other forages are available. Sheep and goats, however, will eat the plants without apparent problem [88]. Spurges cause excessive salivation in some animals due to the irritant effects of the plant sap. Cattle frequently develop diarrhea if they are compelled to eat leafy spurge. Recovery is rapid once animals are provided more nutritious food.

Note

Leafy spurge is a noxious weed that should be vigorously controlled to prevent its rapid invasion of pastures and rangeland where it will displace nutritious forbes and grasses. Sheep are effective biologic controls for leafy spurge and can be profitably used to graze rangeland heavily infested with leafy spurge [89]. Sheep can eat diets containing up to 40 to 50 percent leafy spurge without any evidence of disease or decrease in weight gain [90]. The sheep can reduce the plant's biomass and density but will not eradicate it. Approximately 5 percent of leafy spurge seeds eaten by sheep remain viable in the feces, and, therefore, sheep can help spread the plant if not appropriately managed. Ideally sheep should be used to graze the leafy spurge before it flowers and the seeds are produced. If sheep are grazing the plant when it has seeds, they should be kept confined for at least 5 days before they are moved to leafy spurge-free areas [91].

Part VI: Lectins

A group of unrelated plants including castor bean (Ricinus communis), rosary pea (Abrus precatorius), and black locust (Robinia pseudoacacia) contain highly poisonous compounds called lectins that are capable of causing severe poisoning in humans and animals. Lectins are some of the most toxic of known plant compounds, and as glycoproteins (toxalbumins) are capable of binding to receptor sites on cells causing inhibition of protein synthesis and cell death. Lectins are concentrated in the seeds, and it is the consumption of the seeds that is most commonly the cause of poisoning in humans and animals. The seeds have a tough outer coating and unless it is disrupted through chewing, the seeds will pass through the digestive system without causing problems. Castor beans and rosary peas have a long history of causing poisoning in children and adults [92-95]. Cattle, goats, horses, poultry, and dogs have been poisoned by castor beans, and less frequently by rosary peas when they contaminate animal foods [95-101]. Cattle fed "cake" made from castor beans following the extraction of castor oil may be poisoned unless the cake is first treated with heat to destroy the ricin [95,102]. Properly detoxified castor bean meal is a useful protein source for cattle.

Principal Toxins

The principal toxins in castor beans, rosary peas, and black locust are the glycoproteins ricin, abrin, and robinin, respectively. Castor oil derived from the beans contains ricinoleic acid, an irritant that can cause severe intestinal irritation with profound purgation. Various other alkaloids and proteins are present in the seeds but are generally not toxic and have been used for a multitude of medicinal purposes [103]. Some of the proteins act as agglutinins and are capable of causing red blood cell agglutination in vitro [96]. Agglutination is not a feature of orally ingested castor beans, and ricin, when injected systemically, does not cause hemolysis, indicating that compounds other than ricin are involved [104].

Lectins, comprising two peptide chains joined by sulfide bonds, are capable of binding to certain cell receptor sites and inhibit cellular protein synthesis in the ribosomes [105]. Because this process takes time to occur, clinical signs of poisoning do not occur for several days after the ingestion of the lectins [105]. An additional property of lectins, being proteins, is their ability to induce antibody formation when injected into animals, a factor that has been explored in an attempt to develop antitoxins to ricin and abrin [104]. The allergic reaction encountered in humans exposed to dust from castor beans is not a reported problem in animals [103,107]. Ricin is also capable of inhibiting the growth of tumor cells that may have potential for treating some tumors [108].

Ricin and abrin are some of the most poisonous plant compounds known, especially when administered by injection. As little as 1 mg ricin is lethal to humans [93]. Reports of castor bean poisoning have varied considerably as to the number of beans that will induce poisoning and death [89]. This may be accounted for by variations in the quantity of ricin present in some castor beans and the degree to which the beans had been chewed before they were swallowed. Human poisoning has occurred when 2.5 to 20 castor beans have been eaten, and animals may be fatally poisoned with 4 to 11 beans [103]. A dose of 2 g/kg body weight of ground castor beans is reported as lethal in cattle [109]. Horses are reportedly fatally poisoned by as few as 60 seeds; ruminants appear to be less susceptible because abrin is broken down in the rumen [110]. Goats experimentally fed 1 to 2 g/kg body weight of ground A. precatorius seeds died 2 to 5 days later [96]. Thousands of wild ducks have been fatally poisoned by eating castor beans, and experimentally domestic ducks could be poisoned by three to four seeds [111]. Studies in mice and dogs in which pure abrin and ricin were injected experimentally demonstrated that the minimum lethal dose was 0.7 and 2.7 mg/kg body weight, respectively [104].

In reexamining the literature on castor bean poisoning in humans, Rauber and Heard propose a much less severe prognosis for poisoning in humans in light of modern medical practices [93]. Rapid removal of the castor beans from the stomach and aggressive fluid and electrolyte therapy to counteract the primary effects of diarrhea and dehydration greatly reduce the incidence of fatalities.

Plant parts of castor beans and rosary peas, other than the seeds, are rarely reported as a cause for poisoning in animals. Although the leaves of the castor bean plant are rarely eaten, they are reported to be toxic [112]. Cattle fed castor bean leaves develop signs distinct from those associated with ricin. Affected animals develop neuromuscular impairment characterized by muscle weakness, tremors, salivation, and excessive eructation [112]. Recovery may occur after a short period or the animal dies, presumably as a result of the quantity of leaves consumed.

Clinical Signs

The signs of castor bean and rosary pea poisoning are primarily associated with severe gastrointestinal irritation, and begin several days after the consumption of a toxic dose of lectins [96,100,101,109,110]. Affected animals stop eating and develop a severe hemorrhagic diarrhea. Lactation stops abruptly. Abdominal pain is often severe. In the case of black locust poisoning, horses, in particular, may also develop dilated pupils and cardiac arrhythmias [114]. Rapid loss of water and electrolytes through the diarrhea results in dehydration and hypovolemic shock. Increases in serum liver enzymes, creatinine, urea nitrogen, and sodium and potassium levels, and a decrease in serum total protein reflect the loss of fluid and electrolytes and the effects of the lectins on organ function [96]. Animals left untreated die from hypovolemic shock.

Postmortem findings include severe pulmonary congestion, ulceration of the stomach and intestines, and fatty degeneration and necrosis of the liver and kidneys [96].

Diagnosis

The diagnosis of castor bean or rosary pea poisoning can be difficult to confirm unless animals are observed eating the seeds or the intact seeds or parts thereof are identifiable in the digestive tract at postmortem examination. Because it resembles sunflower and cotton seed cake, castor bean meal can be recognized in animal feeds by microscopic examination for the characteristic seed hull fragments [110].

Treatment

Treatment is directed at removing the seeds from the stomach and digestive tract as quickly as possible. Vomiting can be induced in dogs and cats, or endoscopy can be used to remove the seeds from the stomach. Orally administered activated charcoal is of benefit. If cattle are known to have consumed feed contaminated with castor beans within the past day, purgatives such as magnesium hydroxide may be helpful in removing the toxin from the digestive system. Animals with diarrhea and resulting dehydration and hypovolemic shock should be given intravenous fluids and electrolytes. Such treatment has been the main reason that fatalities in humans who have consumed castor beans have been virtually eliminated [93,115]. The use of immune serum to treat ricin poisoning is rarely necessary [115].

Plants:

Castor Bean

Ricinus communis - Euphorbiaceae (Spurge family)

Habitat of Castor Bean. Ricinus communis - Euphorbiaceae (Spurge family).

Description

Castor bean is an annual herb or short-lived perennial, and small tree in warmer areas. It is often cultivated as a garden annual. The leaves are alternate, large, and palmate, with 5 to 11 serrate lobes (Fig. 3-32A). The petioles have conspicuous glands. New leaves are usually purple. The plants are monoecious. The flowers have no petals and are borne in terminal panicles with staminate (male) flowers below and pistillate (female) above. The calyx is of three to five parts, and the stamens are numerous, with many branched filaments. The ovary has three cells with one ovule in each cell; the styles are deep red with fine feather-like hairs. The fruit is a spiny capsule, which splits into three sections, each containing a shiny seed with gray and brown mottling (Fig. 3-32B).

Figure 3-32A. Castor bean plant with flower spike and spiny seed capsules (Ricinus communis).

Figure 3-32B. Castor beans (Ricinus communis).

Principal Toxin

A lectin, ricin, is the principal toxin. All parts of the plant are toxic with the seeds containing the highest concentration of ricin, a heat-labile glycoprotein (toxalbumin). Other compounds in the seeds are responsible for agglutination and hemolysis. Ricinoleic acid present in castor oil is primarily responsible for its purgative action.

Note

Castor oil cake is poisonous to ruminants unless it has been heat treated. Castor bean plants should not be planted in or near livestock enclosures.

Precatory Bean, Rosary Pea, Jequirity Bean, Crab's Eye

Abrus precatorius - Fabaceae (Legume family)

Habitat

A weed of fence rows, roadsides and citrus groves, precatory bean was introduced from tropical countries. It has become established in Florida.

Habitat of Precatory Bean, Rosary Pea, Jequirity Bean, Crab's Eye. Abrus precatorius - Fabaceae (Legume family).

Description

Precatory bean is a twining, perennial vine, 10 to 20 feet (3 to 6 meters) long, using other plants for support. Lower, older portions of the stem become gray; the younger portions remain green. The leaves are alternate, opposite pinnately compound with 8 to 15 pairs of leaflets. The flowers are in axillary racemes and are red to purple in color. The fruit is a legume pod, 2 inches (4 cm) long, and produces ovoid seeds that are glossy red with a jet black eye (Fig. 3-33A and Fig. 3-33B). Some varieties have seeds that are black with a white eye or are white with a black eye.

Figure 3-33A. Precatory bean vine and pods with seeds (Abrus precatorious).

Figure 3-33B. Precatory beans (Abrus precatorious).

Principal Toxin

Abrin, like ricin from castor beans, is a potent lectin found in highest concentration in the seeds. Other toxic compounds are also present in the seeds. Only if the seeds are chewed and swallowed is the lectin released. Abrin is one of the most toxic compounds known, requiring as little as 0.00015 percent of a person's body weight to be fatal. Animals are infrequently poisoned.

Black Locust

Robinia pseudoacacia - Fabaceae (Legume family)

New Mexican Black Locust

Robinia neomexicana - Fabaceae (Legume family)

Habitat

Usually around dwellings and along fence rows, black locust is common in the southwestern states. It occasionally forms dense stands. Robinia neomexicana often grows along streams and in valleys.

Habitat of Black Locust / New Mexican Black Locust. Robinia pseudoacacia / Robinia neomexicana - Fabaceae (Legume family).

Description

Black locust is a small tree up to 70 feet (21 meters) tall. The trunk is straight and slender; branches are spiny and glabrous when young. The leaves are alternate, pinnately compound with entire, elliptical leaflets in 3 to 10 pairs. The individual flowers are showy, white, and pealike, forming drooping clusters, 4 to 8 inches (10 to 20 cm) long (Fig. 3-34A). The fruit is a straight, flat, many-seeded brown legume pod.

Figure 3-34A. Black locust (Robinia pseudoacacia).

Robinia neomexicana differs from R. pseudoacacia in that it has rose-pink flowers, hairy leaflets, finely haired young twigs and glandular hairy pods (Fig. 3-34B).

Figure 3-34B. Black locust (Robinia neomexicana).

Principal Toxin

Robin, a lectin, is similar to but less toxic than ricin found in castor beans. The bark and seeds have the highest concentrations of lectins; the flowers are not toxic.

Note

Locust trees of the genus Gleditsia, commonly referred to as honey locusts, are unrelated to the black locust and are not poisonous.

Mistletoes (Phoradendron spp.) and Viscum spp. (English mistletoe) also contain toxic lectins that can cause severe gastrointestinal irritation resulting in vomiting and diarrhea. Cardiovascular collapse with brady- cardia and hypotension may occur when a large dose of mistletoe has been eaten. Animals are rarely poisoned by mistletoe. Children are most likely to be poisoned after eating the white berries when mistletoe is brought into the house for festive occasions.

Mayapple, Mandrake

Podophylum peltatum - Berberidaceae (Barberry family)

Habitat

Mayapple is an indigenous plant of eastern North America extending westward to Minnesota and Texas. It prefers moist, fertile soils of woodlands and pastures.

Habitat of Mayapple, Mandrake. Podophylum peltatum - Berberidaceae (Barberry family).

Description

Mayapple is a perennial herb, 1.5 to 2 feet (0.5 to 0.60 meters) tall, with a simple stem bearing two large umbrella-shaped, five to nine lobed, hairless leaves. A single, white, nodding, flower, with six to nine petals is produced at the junction of the two leaf stems. The fruit is a 1 to 2 inch (2.5 to 5 cm) fleshy berry that turns yellow when ripe (Fig. 3-35). The plant spreads by a fibrous creeping root system.

Figure 3-35. Mayapple, mandrake (Podophyllum peltatum).

Principal Toxin

Podophyllin, a bitter, resinous compound, is found in all parts of the plant The ripe yellow fruit, however, is edible. Podophyllin acts as an irritant and has strong laxative properties. It also interferes with cell division and may have anticancer properties [116]. Livestock generally will not eat the plant unless deprived of their normal forages. Human poisoning occurs more commonly when unripe may apples are eaten or when parts of the plant are inappropriately used as a medicinal herb.

Clinical Signs

Colic and diarrhea are the major signs of mayapple poisoning. Excessive salivation and swelling of the muzzle, intermandibular area, and eyelids may result from the irritant effects of the resinous toxin [117]. Excitement lasting about a day is a reported symptom of mayapple poisoning. Most animals will recover once they are prevented from eating the plant.

Privet

Ligustrum vulgare - Oleaceae (Olive family)

Description

Privet is a deciduous shrub, with opposite, lanceolate leaves 1 to 2 inches (2 to 5 cm) long. The leaves are dark green on the upper surface and paler underneath. Some varieties have yellow or white marbling. Numerous small, white flowers are produced in clusters at the ends of the branches (Fig. 3-36). The fruits are drooping clusters of black berries containing one to four seeds.

Figure 3-36. Privet (Ligustrum vulgare).

Principal Toxin

The toxin has not been identified. However, it has irritant properties that cause gastroenteritis, hypotension, and kidney damage. The berries and leaves are toxic. Animals rarely eat the plant unless they are hungry and deprived of normal forage.

Privet hedges should be avoided around livestock corrals or pastures and pruned leaves and branches should not be given to livestock.

Clinical Signs

Vomiting, abdominal pain, and diarrhea are common signs of privet poisoning. Hypotension and kidney failure will occur in severe cases, and death may occur within a day of eating a lethal amount of the plant [118].

Part VII: Rhododendron - Ericaceae (Heath family)

Rhododendrons and closely related species including azaleas (Rhododendronspp.), laurel (Kalmiaspp.), fetter-bush (Leucothoespp.), mountain fetter-bush (Pierisspp.), maleberry (Lyoniaspp.), mock azalea (Monziesiaspp.), and Labrador tea (Ledumspp.) are both wild and cultivated plants of North America. All are poisonous to animals that eat them [119-128]. The honey produced by bees feeding on the nectar of rhododendrons is also poisonous to people eating it [129,130].

Principal Toxin

Members of the Ericaceae (Heath) family contain grayanotoxins (andromedotoxin, deacetylandromedol, deacetylanhydroandromedol) that are water-soluble diterpenoid compounds. All parts of the plant, including the nectar of the flowers, contain the toxins.

Animals are most often poisoned during the winter because rhododendrons retain their green leaves year round in milder climates. As little as 0.2 percent of an animal's body weight of green leaves can cause poisoning. Cattle, sheep, goats, occasionally horses, and rarely other animals and birds have been poisoned by members of the Ericaceae [121,123,125,131]. Goats seem to be particularly susceptible to poisoning by rhododendrons Grayanotoxins act by binding to cell membranes, thereby affecting sodium channels and causing prolonged depolarization of cells. The primary effects are on the heart, nervous system, and gastrointestinal tract [132-134]. A glycoside, arbutin, present in the plants may contribute to the toxicity of the Ericaceae.

Clinical Signs

Animals poisoned by rhododendrons initially have clinical signs of digestive disturbances characterized by anorexia, excessive salivation, vomiting, colic, and frequent defecation [119-128]. In severe cases, muscle weakness, bradycardia, cardiac arrhythmia, weakness, paralysis, and coma may precede death. Regurgitation of rumen contents may result in inhalation pneumonia. Fetal mummification has been reported in goats following severe Japanese pieris poisoning [135]. Depression, vomiting, slow erratic heart rate, painful neck, and weakness are reported in people who have consumed "mad honey" made by bees feeding on rhododendrons or who have consumed tea made from the leaves of rhododendrons [124,130,135-137].

Diagnosis

A diagnosis of rhododendron and laurel poisoning is usually based on the clinical signs and evidence that the plant has been consumed. Postmortem findings are not specific and generally consist of multiple hemorrhages on internal organs. The detection of grayanotoxins in the rumen contents is also possible and is a means of confirming rhododendron poisoning [137].

Treatment

Animals should be removed from the source of the toxic plants and given supportive therapy. Osmotic laxatives such as magnesium sulfate and activated charcoal may be useful early in the course of poisoning to reduce further intestinal absorption of the toxins. Oral and intravenous fluids should be given as necessary to counteract the effects of vomiting and diarrhea. If cattle, sheep, or goats are observed eating significant quantities of rhododendron or other related plants containing grayanotoxins, a rumenotomy may prove life-saving to remove the rhododendron leaves and prevent further absorption of the toxins. If severe bradycardia is present, atropine to increase the heart rate is indicated.

Plants:

Rhododendron (Azalea)

Rhododendron spp. - Ericaceae (Heath family)

Habitat and Description

There are at least 250 species of rhododendrons found mostly in the acidic soils of western and eastern North America. Many hybrids have been developed for their showy flowers. Generally they are large shrubs or open trees growing to heights of 30 feet (10 meters) or more. The leaves are alternate, simple, leathery, lanceolate, and often evergreen. The flowers are produced in large, showy, terminal clusters, ranging in color from white to purple, to red (Fig.3-37A and Fig.3-37B). The fruits are elon- gated capsules that split into five sections to release the small, scalelike seeds.

Habitat of Rhododendron (Azalea). Rhododendron spp. - Ericaceae (Heath family).

Figure 3-37A. Catawba rhododendron (Rhododendron catawbiense).

Figure 3-37B. Great laurel (Rhododendron maximum).

Azaleas are considered by some to be a subgenus of rhododendron (Fig. 3-37C). Azaleas are generally deciduous and have been extensively hybridized to produce showy garden and house plants in a wide spectrum of colors.

Figure 3-37C. Flame azalea (Rhododendron calandulaceum).

Principal Toxin

All parts of the plant including the nectar contain grayanotoxins. Most poisoning occurs in the winter months because the leaves are generally evergreen and are attractive to animals when other forages are unavailable. Animals eating approximately 0.2 percent of their body weight of leaves are likely to develop signs of poisoning.

Mountain Laurel

Kalmia latifolia - Ericaceae (Heath family)

Habitat and Description

Laurels are common to the eastern and southern areas of North America. They 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.3-38A and Fig.3-38B).

Habitat of Mountain Laurel. Kalmia latifolia - Ericaceae (Heath family).

Figure 3-38A. Mountain laurel blooming shrub (Kalmia latifolia).

Figure 3-38B. Mountain laurel flowers (Kalmia latifolia).

Principal Toxin

Grayanotoxins (andromedotoxin) and a glycoside arbutin are the principal toxins present in all parts of the plant. Similar toxins are also present in the genera Rhododendron (azalea), Leucothoe(fetter-bush), Pieris (mountain fetter- bush), and Lyonia (maleberry). The principal actions of the toxin are gastrointestinal irritation and disruption of myocardial activity.

Clinical Signs

All animals are susceptible to laurel poisoning. Affected animals may show excessive green frothy salivation, vomiting, colic, frequent defecation, depression, weakness, and ataxia. Depending on the quantity of laurel that has been eaten, affected animals may become recumbent and comatose before death.

Treatment

Mineral oil via nasogastric tube and intravenous fluid therapy should be administered as necessary.

Japanese Pieris

Pieris japonica - Ericaceae (Heath family)

Habitat and Description

Introduced from Japan, P. japonica is grown as an ornamental flowering shrub in the acidic soils of eastern and western North America. Several species of Pieris are indigenous. Leaves are generally alternate, dark green, toothed, and evergreen. New foliage is bronze in color. The terminal flowers are in drooping pannicles and white to pink in color (Fig. 3-39).

Habitat of Japanese Pieris. Pieris japonica - Ericaceae (Heath family).

Figure 3-39. Japanese pieris (Pieris japonicus).

Principal Toxin

Grayanotoxins (andromedotoxin) are the principal toxins and are present in all parts of the plant.

Fetter-Bush, Black Laurel

Leucothoe spp. - Ericaceae (Heath family)

Habitat and Description

Several species are grown for their attractive foliage and flowers in the eastern and western regions of North America. Shrubs 4 to 6 feet (1 to 2 meters) in height, with leaves evergreen or deciduous, alternate, and carried on arching branches. Some cultivars have reddish purple leaves. Flowers are white to pink, borne along or at the tips of branches, and with five small teeth at the top of the flower (Fig. 3-40).

Habitat of Fetter-Bush, Black Laurel. Leucothoe spp. - Ericaceae (Heath family).

Figure 3-40. Fetter-bush (Leucothoespp.).

Principal Toxin

Grayanotoxins (andromedotoxin) are the principal toxins in fetter-bush and are present in all parts of the plant.

Maleberry

Lyonia ligustrina - Ericaceae (Heath family)

Description

These shrubs are 2 to 3 feet (0.5 to 1 meter) tall with alternate, deciduous, hairless, elliptical leaves, growing mostly in the southeastern region of North America. Flowers are white, 0.3 to 0.5 cm (3 to 5 mm) in length, in clusters at the ends of branches. Fruits are round capsules (Fig. 3-41).

Figure 3-41. Maleberry flowering branch (Lyonia ligustrina).

Principal Toxin

Grayanotoxins (andromedotoxin) are present in all parts of the plant.

Common Box

Buxus sempervirens - Buxaceae (Box family)

Habitat

Originally from Europe and Asia, box is widely grown in North America as an ornamental shrub or hedge.

Habitat of Common Box. Buxus sempervirens - Buxaceae (Box family).

Description

Box is a heavily branched, perennial woody shrub, with dark green, opposite, leathery leaves up to 1.5 inches (4 cm) in length (Fig. 3-42). The undersides of the leaves are lighter green or grayish in color. Small star-shaped yellow-green flowers are produced in the leaf axils.

Figure 3-42. Box (Buxus sempervirens).

Principal Toxin

All parts of the plant contain toxic alkaloids, the mode of action of which is yet to be defined. Horses, cattle, sheep, pigs, and camels are susceptible to poisoning from Buxus spp. [138]. Approximately 1.5 lb of green leaves may be lethal to an adult horse. Most poisoning occurs when box clippings are carelessly fed to animals or when box hedges are placed around animal enclosures.

Clinical Signs

Severe gastroenteritis, colic, and hemorrhagic diarrhea can be expected in poisoned animals. In acute poisoning, death results from respiratory failure [138].

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