Plant Toxicities

Bitterweed Poisoning

Hymenoxys odorata, an annual of the Texas range, is a major cause of economic loss in sheep and also affects Angora goats. The plant, known as western bitterweed or bitter rubberweed, is most common in southwest Texas, especially on the Edwards Plateau.

A second plant, Hymenoxys richardsoni, known as pingue or Colorado rubberweed, can also produce the disease and is found more extensively in the west from Kansas to Mexico. The major toxin, hymenoxon, a sesquiterpine lactone, is a cumulative toxin that inhibits cellular function by alkylating sulfhydril groups of cellular enzymes. The principal signs are gastrointestinal and neurologic. In sheep, the LD₅₀ of H. odorata is just 1.3% of bodyweight. Goats are reported to be slightly more resistant, requiring 1.8 times more plant material than sheep to produce death (Rowe et al. 1973).

Acute, subacute, and chronic disease states can occur. The acute form is seen mostly under experimental conditions, after a single large ingestion. The clinical course is one to four days and leads to death. Early signs include bloat, anorexia, arching of the back, teeth grinding, and marked depression. Affected animals become increas­ingly depressed and may show regurgitation, fine muscle tremors, mucous nasal discharge, mild dyspnea, and head pressing. Terminal animals become recumbent with inter­mittent paddling, tonic convulsions, opisthotonos, tachy­cardia, severe dyspnea, and regurgitation.

The subacute and chronic forms are more likely under field conditions, usually after approximately one month of low-level exposure to the plant.

Though there is no specific therapy, a gradual recovery can occur if affected animals are removed from the plant source and fed fresh feed and water. In severe cases, oral administration of activated charcoal may improve chances of recovery. Control of bitterweed poisoning involves avoidance of overgrazing and reduction of bitterweed or pingue by mowing and burning, fencing, or applying herbi­cides to reduce plant populations.

Coyotillo Poisoning

Karwinskia humboldtiana, or coyotillo, is a woody shrub indigenous to southern Texas and California and northern Mexico. It grows on gravelly hills and ridges and in can­yons, gullies, and river valleys. The leaves and fruit are toxic, and spontaneous poisoning has been reported in goats, sheep, cattle, and humans, especially in winter when the plants are heavy with fruit and other forage is scarce. Losses of more than 1000 goats caused by coyotillo poison­ing have been reported on Texas ranches (Sperry et al. 1962). Consumption of whole fruit in quantities as little as 0.3% of the goat's bodyweight is lethal. The toxicity is due to four dimeric anthracenone toxins which have been, character­ized (Jaramillo-Rangel et al. 2020). The toxic action is pri­marily on striated muscle cells and Schwann cells, leading to cellular degeneration.

Early signs in goats include increased alertness, hyper­sensitivity to sound and touch, generalized fine tremors, and a humpbacked posture, soon followed by distur­bances of gait. The stride becomes shortened and jerky or hypermetric. These abnormalities are aggravated by forced exercise.

Gross lesions in coyotillo poisoning of goats are not described. Histologically, lesions of the nervous system are found in the peripheral nerves and the cerebellum. There is extensive Schwann cell degeneration and demyelination, and to a lesser extent Wallerian degeneration of axons. Secondary axonal degeneration is most prominent in distal sections of long motor nerves (Charlton and Pierce 1970). Axonal dystrophy of Purkinje cells is also prominent in the cerebellum of affected goats (Charlton et al. 1970). Myodegeneration of heart and skeletal muscle may also be observed, as well as fatty degeneration of the liver (Dewan et al. 1965). The muscle lesions are similar to those seen in nutritional muscular dystrophy.

Treatment is non-specific and involves removal of affected goats from the plant and providing adequate feed and water. Some recoveries can occur. Goats should not be turned into infested areas for grazing when the plant is in fruit.

Astragalus Poisoning (Alpha Mannosidosis; Locoism)

Several distinct disease syndromes of differing pathogene­sis are associated with livestock consumption of legumi­nous plants of the genera Astragalus and Oxytropis. Three of these syndromes produce signs of nervous disease and have been identified in goats. The first, locoism, is a chronic poisoning that results from prolonged consumption of spe­cies containing the indolizidine alkaloid swainsonine. This alkaloid produces an acquired lysosomal storage disease, alpha mannosidosis, by inhibiting lysosomal alpha man- nosidase, which leads to vacuolation and degeneration of the CNS.

Other plants also contain swainsonine and can induce acquired alpha mannosidosis in grazing livestock. These include Swainsona spp. and Sphaerophysa spp., which are, like Astragalus and Oxytropis, in the family Fabaceae; Ipomoea spp. and Turbina spp. in the family Convolvulaceae; and Sida spp. in the family Malvaceae. Ingestion of Ipomoea carnea (Schumaher-Henrique et al. 2003), Ipomoea Verbascoidea (Mendonςa et al. 2012), Turbina cor- data (Dantas et al. 2007), and Sida carpinifolia (Colodel et al. 2002) is reported to cause acquired alpha mannosido- sis in goats in Brazil, and I. carnea consumption has been associated with the disease in goats in Mozambique as well (Balogh et al. 1999). A similar acquired lysosomal storage disease in goats has been reported in association with con­sumption of Ipomoea hieronymi in Argentina (Rodriguez Armesto et al. 2004). Several Oxytropis spp. in China and Swainsona spp. in Australia have also been associated with acquired alpha mannosidosis in grazing livestock, but cases specifically in goats, though possible, have not been reported.

The second syndrome is an acute poisoning resulting from short-term consumption of plant species possessing nitro-containing glycosides, notably miserotoxin. The third syndrome is blind staggers, or alkali disease, a condition long thought to be due to chronic selenium poisoning asso­ciated with consumption of plant species such as Astragalus that act as selenium accumulators. The condition has been known in western rangelands of the United States for more than a century, but in recent years the role of selenium in this disease has been called into question, and the theory proposed that this condition is actually a manifestation of PEM resulting from excessive sulfur intake (O'Toole et al. 1996).

Species of Astragalus and Oxytropis that cause locoism are found in temperate regions worldwide, but the disease is of particular concern in grazing stock in the western United States, particularly on open plains in winter.

While reports of spontaneous locoism in goats in the United States are scarce and the economic impact minor, the clinical effects of two Texas locoweeds, Astragalus earlei and Astragalus wootoni, have been documented (Mathews 1932). Goats ate 335% of their bodyweight of A. earlei over 54 days to produce locoism, but refused to eat A. wootoni. Early signs include hindlimb weakness charac­terized by inability to extend the hocks and an intermittent, weaving rear gait. Startled goats may stumble or suddenly collapse onto their hindquarters, but remain supported on the forelimbs. Paresis and ataxia are progressive, eventu­ally involving the forelimbs as well. In advanced stages, goats become sternally recumbent with intermittent opis­thotonos, nystagmus, and shaking of the head. There is progressive weight loss. Goats may remain bright and alert until just a few days before death. In comparison, sheep almost always show profound depression in locoism.

Documentation of abortion in goats caused by locoism, a common problem in sheep, is lacking. At necropsy, gross lesions are limited to emaciation and possibly abomasal ulceration. Histologically there is vacuolation of neurons in the CNS.

Goats may recover from locoism if they are removed from locoweeds early in the course of the disease and then are well fed and watered. However, they may seek out and resume eating locoweed if allowed subsequent access, due to the habituation that occurs.

The acute neurologic form of Astragalus poisoning caused by nitro-containing compounds has been reported in cattle and sheep in Texas and reproduced experimen­tally in goats by feeding Astragalus emoryanus, the red­stemmed peavine (Mathews 1940).

“Blind staggers” has been reported in goats and sheep in Iran after prolonged grazing of Astragalus spp. (Hosseinion et al. 1972). This form of Astragalus toxicity has been ascribed to its role as a selenium accumulator. Emaciation, rough haircoat, anorexia, separation from the flock, impaired vision, circling, and a staggering gait were observed, as were foamy salivation, lacrimation, severe constipation, and signs of abdominal pain. The mortality rate was approximately 4%. Selenium concentration of the weeds was 500 ppm.

GuajiLLo Poisoning

Acacia berlandieri, or guajillo, is a perennial shrub of range­land in southwest Texas and Mexico. The plant is palatable and routine grazing by goats and sheep is generally permit­ted. However, it may cause toxicity under drought condi­tions when the diet is monotonous and consumption extends for six months or longer. The toxic principles are sympatho­mimetic amines, N-methyl-beta-phenylethylamine (Camp and Lyman 1957), and tyramine. Affected animals retain their appetites and remain bright and alert. The predomi­nant clinical sign is a progressive ataxia, which eventually leads to recumbency and death secondary to starvation and thirst. The condition is known locally as limberleg or gua- jillo wobbles. There are no significant lesions found at necropsy. Recoveries can occur if the condition is identified early and animals removed from the plant.

Hairy CaLtrop Poisoning

Kallstroemia hirsutissima, known as hairy caltrop, is a low- lying, ground-hugging weed of disturbed soils in western North America from Kansas south to northern Mexico. Though not palatable, the plant may be consumed by graz­ing livestock in summer during periods of drought. Natural cases of poisoning in goats are not documented, but experi­mental poisoning has been reported (Mathews 1944). The toxic principle is unknown. The susceptibility of goats is variable, with clinical disease seen in one goat eating the plant at a rate of 11% of bodyweight, and no signs seen in another eating 177% of its weight in carpetweed. After three days of consumption, the affected goat showed signs of marked paresis, being unable to stand normally and walking on the carpi in front with the hocks flexed behind. The animal was euthanized and no gross lesions were observed. Cattle and sheep also showed marked paresis and walked with prominent knuckling of the fetlocks.

MiLkweed Poisoning

There are numerous species of milkweed in the genus Asclepias and many are toxic to livestock. Many are distrib­uted widely throughout the United States. These plants are not normally eaten, except in times of drought or limited forage. They also may be baled into hay and retain their toxicity when dry. Goats are poisoned by milkweed (Kingsbury 1964). Consumption of various Asclepias spp. in doses from 0.25 to 2% of bodyweight can be toxic. Clinical signs appear within a few hours of ingestion of a toxic dose and include profound depression, weakness, and a staggering gait. Bloat and dyspnea may also occur. Severely affected animals go down and exhibit intermittent tetanic convulsions. Pupils become dilated, coma ensues, and death usually occurs between one and two days after the onset of signs. The milkweeds contain toxic resins and steroid glycosides, including cardiac glycosides, but the specific mechanism of neurotoxicity is not known. Non­specific lesions at necropsy include congestion of liver and kidneys and irritation of intestinal mucosa. There is no known treatment and poisoning is controlled by reducing access to milkweed and by maintaining pastures in good condition.

Cycasin Toxicity or Zamia Staggers

Cycasin is a toxic pseudocyanogenic glycoside found in the nuts, leaves, and young shoots of various tropical cycad palms. Poisoning of cattle has been associated with con­sumption of leaves or young shoots of four genera: Cycas, Macrozamia, Zamia, and Bowenia in Puerto Rico, the Dominican Republic, Japan, and Australia. The poisoning of goats with Cycas media is a serious problem in parts of Australia, notably Groote Eylandt (Hall 1964). Clinical neurologic disease associated with ingestion of the seeds of the King Sago palm tree, Cycas revoluta, has been reported in dogs in the southern United States, so the potential for goat exposure exists there (Albretsen et al. 1998) as well as elsewhere in the country, since cycads are commonly sold as houseplants throughout the United States.

Chronic consumption leads to incoordination, character­ized by a lack of proprioception, with abnormal placement of feet, knuckling, and stumbling or falling. Pain responses, motor control, and withdrawal reflexes remain intact. Once signs are observed, the condition is irreversible (Baxendell 1988). Goats experimentally poisoned with cycasin extracts also show marked depression, anorexia, weight loss, and anemia. At necropsy, histologic lesions of the spinal cord include axonal swelling and death, with demyelination most prominent in the lateral and ventral funiculi. Hepatic necrosis, biliary hyperplasia, and pancre­atic atrophy were additional necropsy findings in experi­mentally poisoned goats (Shimizu et al. 1986).

Miscellaneous Plant Poisonings

Nervous disease in goats associated with plant ingestions has been reported sporadically from various places in the world. Solanum spp. have been reported to produce neuro­logic dysfunction in goats in Australia (Bourke 1997) and Florida (Porter et al. 2003). In Australia, the implicated plant was Solanum cinereum (Nawarra burr), and in Florida, Solanum viarum (tropical soda apple). The clinical presentation was similar in both instances and strongly suggested involvement of the cerebellum, with grazing goats showing signs of head tremor, wide-base stance, hypermetria, incoordination, nystagmus, and propriocep­tive deficits. At necropsy, CNS lesions were restricted to the cerebellum and were characterized by cytoplasmic vacuo­lation, degeneration, and loss of Purkinje fibers. The Solanum spp. may contain several toxic principles, includ­ing the steroidal glycosides solasonine and solasodine as well as beta-carboline alkaloids. The exact cause of the cer­ebellar degeneration is not fully clarified.

Albizia is a genus of legumes in the family Mimosaceae. Seed pods of the toxic species in this genus contain 4-methoxy-pyridone, a pyridoxine (vitamin B₆) analog that causes neurologic dysfunction as well as cardiomyopathy and pulmonary edema. An outbreak of Albizia versicolor poisoning of goats and sheep eating ripe, dry seed pods was reported from Malawi, and was confirmed by experimental oral challenge of goats and sheep with dried seed pods (Soldan et al. 1996). Sheep were more susceptible than goats. Signs of intoxication included hyperesthesia, wild running, lateral recumbency with rapid leg movements, nystagmus, and rapid blinking. The condition is reported to be treatable in sheep with 20-25 mg/kg pyroxidine hydrochloride/kg bw given twice at an eight-hour interval, even after clinical signs are apparent and well advanced (Gummow et al. 1992).

Another legume with seed pods toxic to animals is ProsopisJuliflora or mesquite. It is native to Mexico, South America, and the Caribbean, but has become established as an invasive species in Asia, Africa, and Australia. Ingestion of the pods is known to cause a syndrome of dys­phagia in cattle associated with degeneration of the mas­seter muscles, slackening of the mandible, protrusion of the tongue, and difficulty chewing. In Brazil the condition has been reported in both cattle and goats in the northeast region and reproduced experimentally in goats (Tabosa et al. 2000). Affected goats fed 60-90% of their ration as seed pods for seven months showed difficulty eating, with mandibular tremors and chewing on one side of the mouth. At necropsy, there was evidence of neuronal degeneration with vacuolation in some cranial nerves, most notably in the motor nuclei of the trigeminal nerve. There was associ­ated denervation atrophy of masseter, temporal, and other muscles of the face and tongue.

In Togo, grazing on the shrub Byrsocarpus coccineus - especially young shoots - at the beginning of the rainy sea­son in March and April produces toxicity in goats. Clinical signs include anorexia, weight loss, separation from the flock, dizziness, staggering gait, circling, and frantic, aim­less flight. In peracute cases, tetanic convulsions are observed. Recovery occurs if goats and sheep are removed to pastures where the shrub is absent (Amegee 1983).

In Tanzania, ingestion of the seeds or leaves of the decidu­ous shrub Burttia prunoides has produced neurologic signs in goats, including circling, bleating, lateral recumbency, teeth grinding, convulsions, coma, and death. The disease has been observed naturally and produced experimentally (Msengi et al. 1987). In Sudan, Azadirachta indica is reputed to cause toxicosis in livestock. Experimentally, continuous feeding of leaves of this plant to goats led to weight loss, weakness, diar­rhea, and, terminally, ataxia and tremors (Ali 1987).

In Holland, ingestion of fool's parsley (Aethusa cyn- apium) by goats led to signs of ataxia, indigestion, and hyperpnea. Affected goats were treated orally with oak bark, tannalbumin, and purgative salts, and recovered in several days (Swart 1975). This annual weed also occurs in northeastern North America and is found locally in waste places and gardens.

Diplodiosis is a neuromycotoxicosis of cattle and occa­sionally sheep in South Africa. It occurs when livestock consume maize contaminated with the fungus Diplodia maydis. Goats are susceptible based on experimental toxi­cosis, showing typical signs of ataxia, paresis, and paralysis (Kellerman et al. 1985). The fungus may contaminate corn and cause livestock disease elsewhere in the world, as has been reported in cattle in Argentina (Odriozola et al. 2005).

Larkspurs (Delphinium spp.) are an important cause of cattle mortality during spring and early summer grazing in western North America. The plant is readily eaten. Goats are presumed to be susceptible. Toxic alkaloids in larkspurs block postsynaptic cholinergic receptors. Signs of toxicity include sudden death, or a staggering gait, wide-base stance, collapse, difficulty rising, muscle twitching, abdom­inal pain, constipation, and bloat. Removal from the plant and early treatment with neostigmine at 0.01-0.02 mg/kg bw IM, repeated as needed, may be effective (Knight 1987).

Plant poisonings that produce signs of nervous dysfunc­tion via the mechanism of hepatoencephalopathy second­ary to phytogenous hepatosis are discussed in Chapter 11. Plants causing blindness are discussed in Chapter 6.

A number of additional plants have been identified as causing neurologic symptoms in small ruminants (Brewer 1983). While their toxicity in sheep is well estab­lished, documentation of goat poisonings is often lacking. These plants include Solanum esuriale, the cause of “humpy back” in Australia; Kochia scoparia, or Mexican fireweed, found in the western United States; and the lupines of the western United States and Australia. In addi­tion, phalaris, paspallum, rye, and dallis grasses have been associated with “grass staggers” in sheep, but the condition in goats is not well defined. Periodically, Bermuda grass (Cynodon dactylon) has been associated with cattle losses in the southern United States, producing ataxia, tremors, and sometimes death. The toxicity for goats has been dem­onstrated experimentally (Strain et al. 1982). Convulsive ergotism, well documented in other livestock species, is poorly substantiated in goats.

In a recent review of neurotoxicoses of ruminant ani­mals, additional plants were identified with potential toxic­ity for goats in the United States (Niles 2017). In the southern United States, these include affine or Texas sophora (Styphnolobium [Sophora] spp.), Carolina bristle mallow (Modiola carolina), China berry (Melia azedarach), Jimmy fern (Astrolepis chohisensis), and Carolina jessa­mine (Gelsemium sempervirens). For the eastern United States, plants listed included prickly ash (Zanthoxylum sp.), Ohio buckeye and horse chestnut (Aesculus sp.), Carolina allspice (Calycanthus floridus), and white snake­root (Ageratina altissima). Plants widely distributed in the United States that may produce toxicity in goats include water hemlock or spotted cowbane (Cicuta maculata), hairy vetch (Vicia villosa), black locust (Robina pseudoaca­cia), and death camas (Zigadenus spp. and Toxicoscordion spp.). When potentially toxic trees, bushes, vines, or brush are cut, trimmed, or cleared, goats and other livestock should not be allowed access to them. For example, poison­ing has been reported in a goat eating from a downed and shredded horse chestnut tree (Harwood et al. 2010) and in three goats consuming cuttings of Carolina jessamine (Gelsemium sempervirens) (Thompson et al. 2002).