TOXIC AND NOXIOUS PLANTS THAT AFFECT ANIMALS
Lecturer: Dr. Donal O'Toole
For someone from western Europe, North America is remarkable in the variety and toxicity of its native plants, particular on western rangelands I will not inflict on you all toxic plants endemic to the High Plains and Northern Rocky Mountains. But I want you to be aware of some of the important ones, and to be able to recognize them when you see them. Many are native but some are introduced. Introduced toxic weeds include as yellow star thistle (Centaurea solstitialis), Russian knapweed (Centaurea repens), both of which cause a distinctive (unique) CNS disease in horses, and houndís tongue (Cynoglossum officinale)
If you think you are dealing with a plant toxicity problem, there are several excellent resources. Until recently the bible was Kingsbury's book Poisonous Plants of the United States and Canada (Prentice-Hall; 1964). It does an excellent job of critically reviewing much of the old literature that was put out by agriculture experiment stations at the turn of the 1900s. The UW library has many of these monographs in the basement; they are a pleasure to read, and a reminder of the painstaking work done by early range specialists, botanists and veterinarians on the frontier. The study of toxic plants was a major activity and scientific product of early land-grant universities, including UW. A relatively new textbook put out by a plant specialist and a veterinary toxicologist is Toxic Plants of North America (Iowa University Press; 2001) - this book scuttled my tentative retirement plans to write an updated version of Kingsbury. Dr. Tom Whitson in UW wrote an excellent paperback that focuses on the plants as weed, with good color illustrations - the book Weeds of the West (Pioneer of Jackson Hole) is available in the university bookstore. Dr. Tony Knight and Richard Walter recently wrote a combined paperback/CD-ROM called A Guide to Plant Poisonings of Animals in North America - the CD is excellent. Dr. Knight is former director of the veterinary teaching hospital at CSU and has had a lifelong fascination with toxic plants. The USDA's Poisonous Plants Research Laboratory in Logan UT has a good web site on plants relevant to our area - go to the poisonous plants link at the top of the page. It also has Powerpoint notes on toxic plants from a class offered in 2008. Our laboratory's toxicologist, Dr. Merl Raisbeck, as well as Dean Frank Galey have considerable experience and interest in toxic plants. Merl's laboratory has done a series of studies on selenium in particular, since much erroneous literature was generated during the early 1900s, some of it unfortunately in the University of Wyoming. Last but not least, don't forget your neighbors. Long time residents are an excellent source of information about toxic plants local to an area. Most will know when plants are most toxic and how to avoid them.
||Death camas is one of the first plants to begin growth in the early spring. In foothills, death camas flowers in April-May. At higher elevations, the plant flowers in late June and July. Unless there is sufficient good quality forage, death camas may be heavily grazed and can cause severe losses. Sheep are most likely to eat death camas and they are poisoned more frequently than cattle and horses. It resembles native wild onion. Sheep show signs of poisoning after eating as little as 0.5 lb of the green plants. Convulsions, coma, and death soon occur if sheep eat 2 - 2.5 lb of green plant per 100 lb body weight. There are no specific lesions at necropsy. Diagnosis of death camas poisoning is usually made by eliminating other causes of sudden death, the presence of Zigadenus species in the animal's environment, and detection of Zigadenus alkaloids in the rumen contents using thin-layer chromatography.|
||Larkspurs are wild species corresponding to the common garden delphinium. You see ornamental varieties around campus during early summer, such as in the flowerbeds west of Old Main. The wild cousins are divided into the tall, low and plains larkspurs, based on height at maturity and geographic location. Many toxic plant specialists consider the tall larkspur most toxic. Flowers are blue-purple and have a characteristic spur. Both low and plains larkspurs begin growing in early spring, often before grasses start their spring flush. Under these conditions, larkspur may be the only green herbage available. Larkspur can cause heavy losses among cattle - historically many areas of Wyoming, including the Laramie valley, had larkspur control associations to work around the problem. Unlike most toxic plants, larkspur it is palatable for part of its growing season. Losses occur when cattle graze larkspur-infested ranges, especially where the plant is abundant or grows in large, dense patches. Clinical signs are nervousness, weakness, staggering, bloat and death. Excitement and physical exercise intensify the signs of poisoning. The best treatment for affected downer cattle is to get them into sternal recumbency with their heads uphill to reduce bloating, treating bloat if it develops, and prevent them from becoming unduly excited until they clear the toxins from their system. Lesions at necropsy are minimal, as with many toxic plants - the rumen contents have to be checked. Larkspur in its early vegetative growth stage is not palatable, therefore grazing early before plants flower may be an option in some areas. Once plants begin flowering, keep cattle off ranges until plants mature (after pod stage), then allow them to graze larkspur areas. Using sheep to graze or trample larkspur patches ahead of cattle grazing may also reduce cattle losses.|
||Sweet clover in itself is not poisonous. But if it becomes moldy, some fungal species are capable of converting coumarin in the plant to dicoumarol, a potent anticlotting agent related to the common rodenticide warfarin. You've smelt coumarin - it is the compound responsible for the smell of freshly cut grass. Moldy sweet clover poisoning is most common in cattle, but occasionally it affects horses; sheep are resistant. Signs may not appear for up to 3 weeks after feeding moldy sweet clover hay, and depend on the quantity of dicoumarol consumed. Dicoumarol interferes with the metabolism of vitamin K, which in turn affects four coagulation factors so that clotting of blood is compromised. Affected animals bleed uncontrollably both internally and externally. Calves are more severely affected than adult cattle. In a large recent episode in Riverton we saw it in newborn calves since dicoumarol crosses the placenta; calves were born fine, but then bled from the umbilicus and anus within 24 hours, and many died Early signs of sweet clover poisoning are not easily recognized because affected animals may just seem weak and depressed from the internal bleeding. The sudden appearance of subcutaneous swellings, bleeding from the nose, and blood in the stool are common in sweet clover poisoning. Subcutaneous hematomas, especially ventrally and over areas that are easily traumatized like the carpus, frequently develop. Affected animals do not have a fever and maintain a good appetite. Mortality can be high. To prevent moldy sweet clover poisoning, sweet clover hay or haylage should not be fed for at least 3 weeks before parturition or elective surgery such as castration, dehorning or tail docking. There are cultivars of sweet clover that contain low levels of coumarin; hay from these varieties is safe, even when moldy. Properly cured sweet clover silage is low in dicoumarol because dicoumarol-producing fungi require oxygen. Affected animals can be treated with vitamin K.|
||Sheep are frequently poisoned by eating lupine seeds and pods. Losses may be heavy when hungry sheep are trailed through lupine ranges in late summer. Lupine hay remains toxic and can poison sheep. Clinical signs are nervousness, salivation, frothing, depression and death. More common than direct toxicity, some lupine alkaloids produce birth defects in cattle when eaten during early gestational. Cows eating lupine during early gestation often give birth to calves with cleft palates, crooked legs and distorted/malformed spines ('crooked calf disease'). Such deformed calves have to be euthanized. Outbreaks of such birth defects can have high morbidity resulting in large economic losses. There are however other causes of crooked calves, including some viral causes; a crooked calf does not establish a firm diagnosis of lupine poisoning. Often it is hard for us to rule lupines out since the exposure takes place early in gestation. Poisonous species of lupine are dangerous from the time they start growth in the spring until seed pods shatter in late summer or fall. Younger plants are more toxic than older plants; however, plants in the seed stage in late summer are especially dangerous because of the high alkaloid content of the seeds and enhanced palatability in preference to dried senescent grasses. Restricted fetal movement due to general or localized uterine contraction is suggested as one reason why the fetal calf develops the skeletal deformities of crooked calf disease.|
|Cocklebur poisons all classes of livestock. The entire plant is considered toxic but young seedlings and seeds contain the largest amounts of toxin. The toxin in seeds causes liver damage. Although livestock generally do not eat the seeds voluntarily, we see problems when cattle are fed cocklebur-contaminated hay. Cattle may be found dead and the liver has evidence of acute necrosis. We had several cases in cattle in December 2008. The toxin remains in seedlings through the cotyledon stage, and the concentration drops rapidly when true leaves appear. A toxic dose of seedlings is about 0.75 to 1.5% of an animalís weight. Seedlings are toxic even when dead and dry.|
||Some crops (e.g., oat hay, sorghum, corn, sudangrass, Johnsongrass, beets) and weeds (e.g., kochia, pigweed, Russian thistle) accumulate nitrate. Plants containing >1.5% nitrate (as KNO3) dry weight may be lethal to livestock. Sublethal effects may occur in livestock from eating feed containing between 0.5 - 1.5 %nitrate. The type of soil, availability and form of nitrogen present in the soil, various environment factors and chemical or physical plant damage influence the amount of nitrate in plants. Drought, frost, or treatment of nitrate-accumulating plants with 2,4-D can cause them to accumulate excessive nitrate. Nitrates are converted to nitrite in the gastrointestinal tract. Nitrite causes the production of methemoglobin, a form of hemoglobin that cannot carry oxygen. Nitrate poisoning causes oxygen starvation - in effect, suffocation. The amount of plant material required to poison an animal depends on the amount of nitrate in the plant and, to a lesser degree, the rate at which the plant is eaten. Many factors affect toxicity, but in general about 0.05 percent of an animal's weight of nitrate is near a minimum lethal dose. Poisoning occurs primarily in ruminants, especially cattle. Acutely poisoned animals are often found dead. Live, severely affected animals have cyanotic (blue) mucous membranes and are short of breath. Lower concentrations of nitrate cause abortion. We routinely check the aqueous humor of aborted calves for nitrate concentrations. It is not a very common cause of abortion, but we see a few cases every year. We've seen several spectacular episodes of nitrate poisoning due to Sudan grass during the current drought. Crops that accumulate nitrate and grow under conditions favoring nitrate accumulation should be tested at a laboratories for nitrate content. High nitrate forage should be diluted with low nitrate forage to decrease nitrate intake. If you think you are seeing nitrate toxicity, get the diagnosis confirmed and in the interim stop feeding nitrate-accumulating forage.|
||Greasewood (Sarcobatus vermiculatus), and halogeton (Halogeton glomeratus) contain soluble potassium and sodium oxalates - both are common in alkaline western soils. Halogeton was introduced from Asia, whereas greasewood is native. Both cause heavy death loss in sheep because of their high oxalate content. Oxalate poisoning occurs when unadapted sheep or, less commonly, cattle graze large amounts of halogeton or greasewood as they pass through rangeland containing heavy stands. Often this occurs in the fall as they are being off summer range. Ruminants can tolerate relatively more oxalate in their diet than other animals because they can detoxify oxalate in the rumen thereby preventing absorption of soluble oxalates. When large quantities of soluble oxalates are eaten, the rumenís ability to metabolize oxalates is overwhelmed and they are absorbed. Insoluble calcium and magnesium oxalate crystals are formed and cause renal failure. Prior adaptation of rumen microflora to oxalates allows animals to consume more oxalate because the increased number of oxalate-degrading bacteria in the rumen effectively metabolize oxalate Ruminants allowed to graze small quantities of oxalate-containing plants can increase tolerance for oxalate 30 %or more over a few days. Once adapted to oxalate, sheep and cattle can make effective use of range forages containing oxalate that are otherwise toxic. Within hours of consuming toxic concentrations of oxalate, sheep and cattle develop muscle tremors and weakness, and die acutely of hypocalcemia and hypomagnesemia. Coma and death may result within 12 hours. Animals surviving acute effects of oxalate poisoning frequently succumb to renal failure. Livestock should not be grazed on rangeland on which oxalate-containing plants predominate without precaution, especially if animals are hungry and are not adapted to oxalate. Livestock should be introduced to oxalate plants for at least 4 days by incrementally increasing the time they are allowed to graze the plants. Overstocking and overgrazing increase the risk of oxalate poisoning if there is no other vegetation for animals to eat. Cattle and sheep driven through or held overnight in pastures rich in oxalate-containing plants are prone to poisoning, and such circumstances should be avoided. Supplementary dicalcium phosphate in the diet before and during high-risk oxalate exposure is effective in reducing losses. High levels of dietary calcium bind oxalate in the rumen as insoluble, nonabsorable calcium oxalate. Calcium may be provided to the animals in a salt mix or in pelleted alfalfa.|
common cause of hepatic failure in horses and to a
lesser extent cattle is due to pyrrolizidine
alkaloids (PAs). There occur in a variety of
plant families. In Wyoming the important ones are
members of the Senecio species (a sunflower-like plant;
upper image), such as Ridell's groundsel, and hound's
tongue (Cynoglossum officinale)(lower image).
The most common presentation is a group of horses on a low plane of nutrition that have been fed hay containing PAs for weeks to months. The amount of PAs varies with the species of plant and its stage of growth. Generally the content is highest in plants just before flowering . They remain stable in hay for months, so when we see this it is generally in horses that are fed poor quality hay. Animals tend to refuse fresh plants containing PAs if other forage is available.
PAs cause liver failure. Typically animals have been on the diet for weeks-months before developing clinical signs (jaundice; weight loss; sunburn of unpigmented skin). The changes in the liver of a chronically poisoned horse or cow are characteristic and make a pathologist's day: there is a combination of giant cell formation in hepatic cells, and bile duct hyperplasia. Less commonly, animals can be acutely poisoned if they eat a large amount of PA-containing plants. I have not yet recognized this.
The effects of the PA are cumulative. Hepatic disease and photosensitization may not appear for months after animals were exposed to toxic quantities of PA. This makes identification of the suspected toxic plants difficult, because they may not be present in the pasture or hay when disease develops. Sheep and goats are resistant to PAs.
||Selenium is accumulated by a number of plants in sufficient amounts to be toxic if consumed by livestock. Plants that accumulate high amounts of selenium and may require selenium for growth are found in selenium-rich soils. Historically these plants have been called indicator plants. The indicator plants include certain species of Astragalus (top), prince's plume (bottom), and some of the woody asters. The indicator plants may accumulate up to 3000 parts per million (ppm) selenium. Plants that accumulate selenium but do not have a requirement for it are called facultative or secondary selenium absorbers. These plants can accumulate up to 50 ppm. The secondary selenium accumulators include native range plants and crop plants such as western wheatgrass, barley, wheat, and alfalfa. Plants containing more than 5 ppm selenium are potentially toxic in cattle. It is these plants that are much more likely to cause problems - the selenium indicator plants are distasteful, not readily eaten, and early accounts attributing all sorts of diseases to them are largely bogus. Selenium is required in the diet of most animals. Concentrations of 0.3 ppm are recommended for most food producing livestock. Acute selenosis has been associated with ingesting large amounts of selenium such as would happen if animals eat indicator plants (>400 ppm), but in Dr. Raisbeck's experience this is rare. Oral selenium doses of between 1 - 5 mg/kg body weight are considered toxic. Lower doses of between 5 and 40 ppm in the diet for several weeks or months result in chronic poisoning (alkali disease, due to a mistaken association with alkali soils). Classical alkali disease occurs in horses and less commonly cattle - sheep are resistant. The lesions are characteristic: all four hooves have circumferential cracks below the coronary band, animals are very lame and in a lot of pain, and there is loss of long hair of the mane and tail. Native species such as pronghorn appear to be less susceptible to selenium intoxication from forage. When very high doses of selenium are given (more commonly by accidental overdose), it causes acute necrosis of heart muscle and death. The issue of selenium in forage, how it cycles and accumulates naturally, and what effects it has on aquatic avian species has been a recurrent issue for the strip-mining industry as it reclaims seleniferous overburden.|
||Bristly or prairie foxtail , needle and thread grass, squirrel tail barley and other traumatic plants rarely get a mention in toxic plant texts because they are nontoxic. But they are common sources of traumatic injury to the mouths of horses and cattle - every year we get biopsies of oral lesions that resemble FMD or VSV. We often find plant fragments which are the presumed culprit. Sometimes it presents when normally docile horses become difficult to bridle. A close examination shows varying levels of injury to the gums (gingivitis) around the upper and lower dental arcade. A separate class of injurious plants are those like buttercups (Ranunculus spp.) and marsh marigold (Caltha spp.) that contain oils which are break down to form volatile, irritating oils.|
important in our area is ponderosa pine and
related evergreens. This was
mentioned briefly in the diseases of reproduction in
cattle lecture. The needles of ponderosa pine cause
abortion when grazed by cattle. Induced abortions
generally occur during the last trimester of pregnancy,
and the placenta is retained - losses can occur earlier
in gestation (early part of third trimester) but tend to
be less. We tend to see it mostly
in NE Wyoming in the Black Hills country. Cattle
generally graze pine needles during storms with
increased snow, wind, cold, changes in feed, or hunger.
The toxin that causes abortion is isocupressic acid.
The ponderosa pine is a hardy tree used
extensively as timber. Both the dry and green needles
from the ponderosa pine tree cause abortion. Abortions
occur between 2 days - 2 weeks after exposure to needles. The abortifacient dose is variable as some cows
are sensitive and small amounts of needles induce an
abortion. Abortion incidence varies from a few to 100
percent of the cows involved. Cows appear to have no
other signs of intoxication other than abortion and
complications (retained placenta and uterine
infections). The aborted calves may survive if the
abortion occurs in late gestation but they are small and
weak, may not suckle, and require extensive
care and treatment to survive. Keep pregnant cows away
from pine trees and fallen needles or slash piles,
especially during the third trimester. Provide
supplemental feed when the weather is cold and/or snow
covers dormant forage.
Broom snakeweed (Gutierrezia sarothrae) is a sporadic cause of abortion in Wyoming. The mechanism involved is unclear. Cattle must eat 20 lb of this plant to develop abortion. An unexplained feature of abortion is that only plants growing on sandy soils (not clay) are associated with problems. Some cattle will develop an enlarged vulva and mammary gland. The only way to control the problem is to fence off heavy stands, graze non-pregnant cattle on the pasture, or knock it back with herbicide. In 2007 and 2008 we had a producer in central Wyoming who, based on exposure history and lack of other findings in a series of submitted fetuses, appeared to have a problem with broom snakeweed on his winter pastures.
1. List four circumstances in which might you expect to see plant poisoning
2. What is the common name for Zygadenus, at what time of the year does poisoning occur, why, and in what species does it occur?
3. Larkspur (poison weed) is important in the Laramie valley as a toxic plant. What clinical signs will you to see?
4. Name a plant containing pyrrolizidine alkaloids. What is the disease that this family of compounds causes?
5. What is the toxic part of ponderosa pines, what disease does it cause, and how is it prevented?
6. Why does greasewood cause low blood calcium? On a practical level, why does this matter?
7. How does moldy sweet clover cause disease? On a practical level, why does this matter?
Dr. Donal O'Toole