Plants Affecting the Digestive System (Part I)

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

Part VI: Lectins

Part VII: Rhododendron Grayanotoxins

Alphabetic Plant List

Glossary

Numerous toxic plants cause digestive problems in animals either through direct effects of the plant on the gastrointestinal system or indirectly by affecting other organs with a secondary effect on the digestive system. In this chapter, only plants that have a direct effect on the digestive system will be discussed. Excessive salivation, abdominal pain (colic), impactions of the stomach or intestines, bloat, constipation, and diarrhea are all signs that can be attributed to plants affecting the digestive system.

Part I: Excessive Salivation

Excessive salivation, characterized by drooling or frothy saliva around the lips, may be caused by a variety of things including chemical irritants fungal toxins, virus and bacterial diseases affecting the mouth, teeth problems, choking caused by esophageal obstruction, and various toxic or injurious plants. Grazing animals that eat sharp grass awns, spiny plants such as the prickly pear cactus (Opuntia spp.) (Fig. 3-1A), or those with burs such as burdock (Arctium minus) (Fig. 3-1B) and cocklebur (Xanthium spp.) (Fig. 3-1C) may injure the oral mucosa. Some common grasses such as foxtail barley (Fig. 3-2A), bristle grass (Fig. 3-2B) and sandbur (Fig. 3-2C) have seeds with sharp awns that can become embedded in the tongue and gums of animals eating them. Initially excessive salivation may be noticed, but in time the grass awns or spines that are imbedded in the mucosae create large ulcers. The awns are not easily visible in the ulcers because they become embedded in the granulation tissue filling the ulcer. It is not uncommon for some sharp grass awns to penetrate the skin of animals, migrate through the tissues, and act as a foreign body causing abscesses and draining wounds far from the site of penetration [1]. Grasses with sharp awns that commonly become embedded in the mouth, ears, and skin of animals are included in Table 3-1.

Figure 3-1A. Prickly pear (Opuntia spp.).

Profuse salivation has been observed in horses and other livestock eating clover or alfalfa pasture or hay that is infected with the fungus Rhizoctonia leguminicola. The mycotoxin responsible for the "slobbering" that animals exhibit has been identified as slaframine, an indolizidine alkaloid produced most commonly by the fungus R. leguminicola growing on red clover [2,3]. Slaframine is chemically similar to the alkaloid swainsonine produced by plants of the genera Astragalus and Oxytropis that are responsible for causing locoism. Under wet or humid conditions the fungus grows on the leaves producing black or brown spotting. After they eat the fungus-infected clover for several days, horses begin to salivate excessively and lose weight; pregnant mares may abort if they continue to consume the infected clover. Recovery occurs rapidly once horses are removed from the infected hay. Problem pastures can be used for animals if they are mowed, the affected hay is removed, and the regrowth has no brown spotting on the leaves.

Figure 3-1B. Burdock (Arctium minus).

Figure 3-1C. Cocklebur (Xanthium strumarium).

Miscellaneous plants cause irritation to the mouth of animals through the action of oxalate crystals present in the plants leaves and stems. The oxalate crystals become embedded in the mucous membranes of the mouth causing severe inflammation and swelling, excessive salivation, and difficulty in swallowing. In addition the soluble oxalates in the plants can induce kidney failure (see Chapter 7).

Figure 3-2A. Foxtail barley (Hordeum jubatum).

Protoanemonins

Plants including buttercups (Ranunculus spp.) and related species such as marsh marigold (Caltha palustris) (Fig. 3-3A), clematis (Clematis spp.) (Fig. 3-3B), anemone, and baneberry (Actaea arguta) contain substances that cause mouth irritation, excessive salivation, and diarrhea if eaten in quantity [4]. The buttercup family (Ranunculus spp.) contains an oily glycoside, ranunculin, that when converted by plant enzymes to protoanemonin becomes a strong irritant [5-7]. It primarily causes irritation to the mucous membranes of the mouth and digestive system and can blister the skin and cause liver damage and secondary photosensitization [8-9]. Sheep have been fatally poisoned by bur buttercup (Ceratocephalus testiculatus) [10] (see Fig. 3-5). Protoanemonin is rapidly polymerized to anemonin, which is nontoxic, and accounts for the fact that hay-containing plants with protoanemonins are not toxic. Feeding trials with cattle and sheep have shown that buttercups vary in their toxicity and do not seriously affect animals under most circumstances [11,12].

Figure 3-2B. Bristle grass (Setaria spp.).

Figure 3-2C. Sandbur (Cenchrus longispinus).

Clinical Signs

Protoanemonins are toxic to all animals and cause reddening of the oral mucous membranes, salivation, gastroenteritis, colic, and diarrhea. In lactating animals, especially cows, protoanemonins produce a bitter taste to the milk and because of their irritating effects may cause blood to appear in the milk and urine.

Treatment

Because there is no specific treatment, severely affected animals should be given intestinal protectants until the toxic plant material is eliminated from the digestive tract.

Figure 3-3A. Marsh marigold (Caltha palustris).

Figure 3-3B. Clematis (Clematis ligusticifolia).

Plants:

Blister Buttercup

Ranunculus sceleratus - Ranunculaceae (Buttercup family)

Habitat

Blister buttercup is a plant of early spring that prefers borders of lakes, ponds, and streams and in general wet areas, from Alaska south to Iowa, New Mexico, and California.

Description

Blister buttercups are perennial herbaceous plants with fibrous roots. Stems are erect, stout, and glabrous or nearly so. The basal leaves are kidney-shaped, long petioled, and three-parted. The upper leaves are sessile or short-petioled. Flowers are few, sepals five, petals yellow, stamens number 10 to many, pistils many, and the fruit is an achene.

Principal Toxin

An oily glycoside, ranunculin, is converted to protoanemonin by the action of plant enzymes released when the plant is chewed. The protoanemonin irritates the mouth, causing excessive salivation and intestinal irritation that may result in diarrhea.

Signs of Poisoning

Signs of poisoning include excessive salivation, reddening of oral mucous membranes, and diarrhea. Cattle that consume excessive quantities of certain buttercup species may develop a severe gastroenteritis and hemorrhagic diarrhea that can be fatal. The bitter taste of the protoanemonin can also be passed into the milk of lactating animals.

Among the buttercups considered more toxic to animals than others are R. sceleratus, R. flammula, R. parviflora, R. acris, R. abortivus, R. cymbalaria, and R. repens (Fig. 3-4).

Figure 3-4. Creeping buttercup (Ranunculus repens).

Bur Buttercup

Ceratocephalus testiculatus - Ranunculaceae (Buttercup family)

Habitat

Introduced from Europe, bur buttercup has become established commonly along roadsides and in disturbed areas in northwestern North America. It is a plant of spring and early summer.

Description

Bur buttercups are annual plants with stems 1 to 3 inches (3 to 10 cm) tall (Fig. 3-5). The flower-bearing stems have simple, three-parted, gray-green, hairy, basal leaves with lateral segments, cleft into linear divisions and a winged petiole. The five sepals are green and hairy. The five petals are yellow. The fruits are burlike, consisting of numerous individual seed capsules, each three-chambered, but with the two lateral chambers empty.

Figure 3-5. Bur buttercup (Ceratocephalus testiculatus) (Courtesy of Dr. Michael H. Ralphs, USDA Poisonous Plants Research Laboratory, Logan, Utah).

Principal Toxin

The glycoside, ranunculin, which is converted to protoanemonin by the action of plant enzymes released when the plant is chewed, is responsible for oral irritation causing excessive salivation and intestinal irritation that may result in diarrhea. Sheep are particularly susceptible to bur buttercup poisoning, and large numbers of sheep have died from eating as little as little as 500 g of the plant [10-12]. Affected sheep develop watery diarrhea, labored breathing, and weakness and cannot rise when approached. Hypocalcemia is not the cause of the muscle weakness and recumbency. Postmortem findings include inflammation of the rumen; congestion of the lungs, liver, and kidneys; and excessive fluid in the thoracic and abdominal cavities [10].

Baneberry

Actaea rubra - Ranunculaceae (Buttercup family)

Habitat

Baneberry prefers rich, moist soils of woodlands, often in deep shade of trees. It is found in most areas of North America except in the desert southwest.

Habitat of Baneberry. Actaea rubra - Ranunculaceae (Buttercup family).

Description

Baneberry is an erect perennial herbaceous plant with thick root stalks. The leaves are large with the lower ones petioled and the upper nearly sessile. They are ternate with the divisions long petioled and pinnate. The leaflets are ovate-lanceolate and serrate, with three to five lobes. The raceme elongates in the fruit, often up to 4 inches (10 cm). The petals are shorter than the stamens and are white. Stamens are numerous with the filaments flattened. The pistil has one locule and is sessile. The fruiting pedicels are elongated up to 2 cm (20 mm) long with red or white berries (Fig. 3-6A and Fig. 3-6B).

Figure 3-6A. Baneberry (Actaea rubra).

Figure 3-6B. White baneberry (Actaea rubra).

Principal Toxin

As a member of the buttercup family, baneberries contain the glycoside ranunculin and as yet other unidentified irritant compounds. Human or livestock fatalities associated with baneberry have not been recorded in the United States, but in Europe references are found concerning the death of children who have eaten the conspicuous red or white berries.

Tung Nut

Aleurites fordii

Candle nut (A. moluccana)

Lumbang nut (A. trisperma)

Euphorbiaceae (Spurge family)

Habitat

The tung tree was originally imported from China and grown in Florida and along the Gulf Coast to east Texas for the purpose of producing tung oil. Although the tung oil industry is no longer of major significance, many of the trees have persisted and are grown as ornamentals.

Habitat of Tung Nut. Aleurites fordii - Candle nut (A. moluccana), Lumbang nut (A. trisperma), Euphorbiaceae (Spurge family).

Description

The tung tree may attain a height of 50 feet (20 meters) with stout branches, often in whorls. The leaves are simple, alternate deciduous, and palmately veined, reaching 12 inches (30 cm) in length (Fig. 3-7). Ivory-colored male and female flowers appear in the spring before the leaves. The lumbang nut tree (A. trisperma) has white flowers tinged with red. The fruits are conical and 2 to 3 inches (5 to 7 cm) long, turning brown when ripe. The thin shell splits open to reveal three to four round dark brown seeds that are white on the inside.

Figure 3-7. Tung nut (Aleurities).

Principal Toxin

Saponins and possibly a toxalbumin are found in highest concentration in the tung nuts and leaves but not in the oil [13-15]. The toxicity of the various species is variable, the tung nut being the most toxic. Experimentally 0.35 percent of an animal's body weight of fresh macerated leaves induced a hemorrhagic diarrhea. Cattle do not readily eat the leaves off of the tree, but they will eat prunings. Most poisoning has been reported in people who have eaten the white-fleshed seeds [16].

Clinical Signs

Cattle become depressed and anorexic and develop an atonic rumen. A hemorrhagic diarrhea often develops after several days of consuming either the tung nuts or the leaves [17]. Chronic watery diarrhea and emaciation often develop in animals that do not die and can mimic chronic bovine virus diarrhea.

On postmortem examination the most common finding is hemorrhagic gastroenteritis, the abomasum and proximal small intestine being most severely affected.

Treatment

There is no specific treatment for tung oil poisoning. Affected animals should be removed from the source of the plant and given supportive oral and intravascular fluid therapy.

Chinaberry, Paraiso

White cedar, syringa berry, Persian lilac

Melia azadarach - Meliaceae (Mahogany family)

Texas umbrella tree - M. azadarach var. umbraculiformis

Habitat

The chinaberry tree is a fast growing tree that was introduced from China and has become established in the Southern United States from Florida to Southern California, Hawaii, and Mexico. The tree has escaped from cultivation and is commonly found growing in hedgerows and waste areas where birds have dropped the seeds.

Habitat of Chinaberry, Paraiso. Melia azadarach - Meliaceae (Mahogany family).

Description

The chinaberry tree is a fast growing tree up to 40 feet (20 meters) in height, with compound, opposite leaves, 1 to 3 feet (0.5 to 1 cm) in length, each leaflet being serrated and 1 to 3 (2 to 6 cm) inches long. The tree is deciduous, with the leaves turning yellow before falling. The white to lavender inch-sized flowers with 5 to 6 petals are produced in clusters and are heavily and pleasantly fragrant. The smooth green fruits (drupe) hang in clusters, turn yellow when ripe, and have a ridged pit surrounded by a little pithy flesh. Fruit clusters often remain hanging on the tree even in winter (Fig. 3-8). Fruit production is especially heavy in high rainfall years.

Figure 3-8. Chinaberry (Melia azedarach).

Principal Toxin

Uncertainty exists as to the exact nature of the toxic compounds found in chinaberry, but saponins, alkaloids (azaradine, margosine, mangrovin), and tetranortriterpenes (meliatoxins) are thought to be responsible for the gastroenteric and neurologic signs [18-21]. All parts of the tree are poisonous, but most poisoning is associated with the consumption of the fruits. Humans as well as pigs, cattle, sheep, goats, rabbits, guinea pigs, poultry and dogs are susceptible to poisoning from chinaberries [18-20]. Pigs are most frequently fatally poisoned after consuming as little as 100 g of the fruits.

Clinical Signs

The usual signs associated with chinaberry poisoning are associated with either the gastrointestinal system (vomiting, constipation, hemorrhagic diarrhea, colic) or the nervous system (weakness, muscle trembling, ataxia, and generalized paresis leading to recumbency, coma, respiratory failure) [18-21]. Rumen impaction may develop in cattle eating large quantities of the ripe fruits that drop to the ground. Signs develop within a few hours to a day or two later depending on the quantity of fruits consumed. Death may occur 1 to 2 days after the onset of signs if a lethal dose of chinaberries was consumed.

Chinaberry poisoning has no known specific treatment and affected animals must be treated symptomatically. This may include inducing vomiting or gastric lavage in people and dogs to remove the berries from the stomach, oral administration of activated charcoal, and intravenous fluid therapy to counteract shock and maintain renal function.

At postmortem examination, the fruits and seeds may be evident in the stomach, which is often congested and hemorrhagic. The intestinal tract is usually congested and hemorrhagic. The meninges of the brain are often congested. Histologically the liver, kidneys, and heart show varying degrees of degeneration and coagulative necrosis.

Chinaberry trees should not be planted in or around livestock enclosures because of the high risk of poisoning.

Pokeweed, Pokeberry

Phytolacca americana - Phytolaccaceae (Pokeweed family)

Habitat and Description

Pokeweed grows mostly in the eastern and southern United States. It is a perennial branching herb from 3 to 10 feet (1 to 3 meters) tall, with a large tap root, green or purple stems, and large alternate, petioled, and ovate leaves. The flowers are small, white in color and without petals. The distinctive fruits are shiny purple-black berries carried on red stems (Fig. 3-9).

Habitat of Pokeweed. Phytolacca americana - Phytolaccaceae (Pokeweed family).

Figure 3-9. Pokeweed (Phytolacca americana).

Principal Toxin

All parts of the plant contain saponins, oxalates, and the alkaloid phytolacine with greatest concentrations in the roots and seeds. Pokeberry also contains a protein lectin, (a mitogen) that can have wide effects on the immune system. Pokeweed mitogen affects cell division and stimulates B- and T-cell lymphocyte proliferation. The plant should be handled with gloves because the mitogen can be absorbed through cuts and abrasions on the skin.

Clinical Signs

Depending on the amount of the plant consumed, animals may show mild to severe colic and diarrhea. Fatalities are rare unless large quantities of the plant are consumed. Other species of Phytolacca found in South America and Africa have been associated with higher mortality rates [22]. Humans appear to be more severely poisoned by pokeweed and develop mouth irritation, stomach cramps, vomiting, and diarrhea. Death may occur in children eating large amounts of the plant or berries.

Sheep, cattle, goats, horses, pigs, and poultry are susceptible to the toxic effects of pokeweed [23-26]. The signs of poisoning are varied and include oral irritation, excessive salivation, vomiting, colic, bloody diarrhea, depression, prostration, and death. Mild to severe gastroenteritis with ulceration of the gastric mucosa are common nonspecific findings on postmortem examination.

Treatment

Intestinal protectants and other supportive treatments should be given as appropriate.

Corn Cockle

Agrostemma githago - Caryophyllaceae (Pink family)

Habitat

Corn cockle was introduced from Europe and has become a common weed of wheat fields throughout North America. Its seeds become a problem to livestock when they contaminate grains fed to them. Wheat screenings are particularly hazardous to livestock because the corn cockle seeds tend to be concentrated in the screenings.

Habitat of Corn Cockle. Agrostemma githago - Caryophyllaceae (Pink family).

Description

The corn cockle is an erect annual, with hairy stems, branching above and growing to 3 feet (1 meter) in height. The leaves are alternate, lanceolate, and grayish green due to the heavy covering of hairs. Flowers are showy, terminal, and purplish red in color with green sepals longer than the colored petals (Fig. 3-10). The urn-like seed capsules contain relatively large 0.2 to 0.3 cm (2 to 3 mm) black seeds, rounded with a flat side and covered by rows of sharp tubercles.

Figure 3-10. Corn cockle (Agrostemma githago).

Principal Toxin

A saponin, githagenin, which can comprise 5 to 7 percent by weight of the seeds, appears to be the toxin that causes gastrointestinal irritation and diarrhea [27]. Poultry, cattle, sheep, pigs, and horses are susceptible to corn cockle poisoning. Similar saponins are found in members of the genus Drymaria (Alfombrilla) common in Mexico.

Bouncing Bet

Saponaria officinalis - Caryophyllaceae (Pink family)

Habitat and Description

Widely distributed throughout the United States, Saponaria spp. are perennial erect herbs with jointed stems, opposite, lanceolate, simple leaves, which are sessile. The leaves are prominently veined. The white or pink flowers are produced in terminal clusters, with a calyx of five sepals that is green and tubular (Fig. 3-11). The flower has five petals, 10 stamens, and two styles.

Habitat of Bouncing Bet. Saponaria officinalis -  Caryophyllaceae (Pink family).

Figure 3-11. Bouncing bet (Saponaria officinalis).

Principal Toxin

Saponins are the primary toxins present in Saponaria spp. If eaten in sufficient quantity, the saponins may cause acute liver degeneration and death [28]. The seeds, which are especially toxic, may be a contaminant of cereal crops. Cow cockle (Vacaria pyramidata, or Saponaria vacaria) is an annual weed introduced from Europe that is common in grain fields and has similar toxic properties.

Sesbania, Coffee Weed, Bladderpod

Sesbania ssp. (Daubentonia and Glottidium) - Fabaceae (Legume family)

Habitat

Various species of Sesbania are found in North America, most of which grow in the warmer climates from Florida to California and Hawaii. Some are vigorous annuals that form dense stands in the damp soils along streams. Sesbania punicea, red or purple sesbania (Fig. 3-12A), S. drumondii (coffee bean, rattlebox) (Fig. 3-12B), and S. vesicaria (annual bladderpod) are some of the more prevalent species [29]. Synonyms for the genus Sesbania include Daubentonia and Glottidium.

Figure 3-12A. Sesbania (Sesbania punicea).

Figure 3-12B. Rattlepod sesbania (Sesbania drummondii).

Description

Sesbania plants are perennial shrubs or small trees growing to 12 feet (3.5 meters) tall. Leaves are alternate, pinnately compound with 12 to 40 leaflets. Red, orange, and yellow flowers are produced in showy pendant racemes. Pods are hairless, fourwinged, and contain glossy, kidney-shaped seeds.

Principal Toxin

Saponins are believed to be the principal toxins present in all parts of the plants and especially the seeds. The green seeds are most poisonous, and the seeds remain toxic for years. The leaves appear to be least toxic. Birds, with the exception of ducks, are especially susceptible to poisoning. Sheep, cattle, and goats are also susceptible to poisoning, sheep being fatally poisoned after eating less than 2 oz of seeds per hundred weight [29]. As few as 10 seeds of S. punicea are lethal to poultry. The primary effects of the toxin are severe gastrointestinal irritation and liver degeneration [30]. Hemolysis may also occur when large quantities of seed are consumed.

Clinical Signs

Severe hemorrhagic diarrhea is often the presenting sign of Sesbania poisoning in cattle and sheep. Anorexia, abdominal pain, dehydration, and prostration may also be observed before death. Poultry develop similar signs of poisoning.

Postmortem findings include a severe hemorrhagic abomasitis, enteritis, and liver and kidney degeneration with necrosis. Diagnosis of poisoning is based on the signs and evidence that the plant or the seeds have been consumed. The finding of Sesbania seeds in the rumen, coupled with the clinical and post mortem signs is strongly supportive of a diagnosis Sesbania poisoning.

Treatment

Laxatives to evacuate the intestinal tract, activated charcoal via stomach tube, and intravenous fluids are helpful in treating the effects of the hemorrhagic diarrhea. The prognosis is poor if extensive liver and kidney degeneration occurs.

Prevention

Mowing of the plants before the formation of seed pods is the best way to contain the plants. Herbicides (2,4-dichlorophenoxyacetic acid) are effective in controlling young plants.

Part II: Gastrointestinal Impaction and Obstruction Caused by Plants (click here to go to this part)

Part III: Diarrhea (click here to go to this part)

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