Livestock-Poisoning Plants of New Mexico Rangelands
Chris Allison, Extension Range Management Specialist
College of Agricultural, Consumer and Environmental Sciences New Mexico State University. (Print Friendly PDF)
Poisonous plants rank high among the causes of economic loss to the livestock industry in New Mexico. This circular will help ranchers, veterinarians, county Extension agents and all other persons concerned with identifying potentially poisonous range plants. Plants known or suspected to be toxic enough to cause animal disorders are included. Other sources of poisoning such as grass tetany, mold and fungus are also discussed.
A poisonous or toxic plant causes physiological or biochemical changes when eaten by livestock. These changes result in varying degrees of deviation from the normal state of health in animals. The effects of poisonous range plants vary from mild sickness to death, and can produce abortions, birth defects, photosensitization, chronic illness or debilitation. Although livestock deaths attributed to poisonous plants vary with years and location, recent estimates indicate the annual death loss is from 3 to 5% for cattle, sheep and horses. Economic losses probably are more significant and are reflected in lower weaning weights, percent calf or lamb crop, unmarketable animals because of birth deformities, and reduced longevity of the breeding herd. Poisonous plants on rangelands cost producers and consumers more than $250 million annually in the United States. These costs are attributable not only to livestock deaths and diminished productivity related to plant poisoning, but also to the management costs associated with using forage in areas infested with poisonous plants.
The least obvious loss caused by poisonous plants on New Mexico ranges is that the range resource is used at less than its potential. For example, deciding which class of livestock to graze could be based on trying to avoid poisonous plant problems rather than on which class of animal is best suited to use the range on the basis of forage and topography. Poisonous plants also dictate the season of use of ranges, thereby not allowing them to be used as efficiently as they could without this danger. Range management costs are also higher where poisonous plants are a problem. These costs include plant control costs, fencing, and more intensive management associated with the presence of poisonous plants.
There are more than 200 plants in New Mexico that are poisonous or injurious, but only about half of these are dangerous enough to cause severe losses. These plants vary greatly in their toxicities, the classes of animals affected, and the conditions under which poisoning occurs.
Poisonous Plant Substances
A toxic plant may contain one or more compounds of similar or different chemical structure, and the poisoning principle may be organic or inorganic. Toxic compounds associated with poisonous plants include alcohols, alkaloids, glycosides, phytotoxins and salts, or organic and inorganic acids.
Poisonous plants may contain at least one of the following substances: (1) Substances that are, by themselves, toxic such as alkaloids in certain lupine species and oxalates in halogeton, (2) Harmless substances that are changed when eaten by the animal and then become toxic. Normally harmless nitrates in plants such as carelessweed are converted into toxic nitrite in the paunch of ruminant animals. Another example is chokecherry, which contains the non-toxic glycoside amygdalin—amygdalin forms the highly toxic prussic acid in the animal’s rumen, (3) Elements in the soil that are absorbed and accumulated in toxic amounts by the plant. Selenium is a common element that certain milkvetch species tend to accumulate, (4) Compounds that make parts of the animal hypersensitive to sunlight, (5) Miscellaneous substances, including toxic metals such as fluorine, arsenic and lead, which have been concentrated on plants in areas of industrial development.
Factors Influencing Toxicity
The toxicity of plants is modified by various plant and animal attributes.
Palatability—The degree to which animals graze the plant is important; if a plant is not eaten, the toxicity is not important. Plant palatability is extremely variable. Many species are more palatable after herbicide or fertilizer applications. Toxicity and palatability of plants can also vary with stage of development. Generally, plants are most palatable during the early growth stages, and this is often the most dangerous period for poisoning because many poisonous plants start to grow before other forage plants do.
Forage Availability—Generally speaking, most poisonous plants do not taste good, so livestock will usually choose more palatable and desirable species. However, if a range does not provide livestock with enough forage, animals may be forced to eat toxic amounts of poisonous plants. In some cases, poisonous plants may be quite palatable.
Climatic Conditions—Climatic stress, such as drought or freezing, usually increases the toxicity of plants. For example, Johnsongrass is normally a non-harmful forage plant, but under conditions of cool nighttime temperatures and warm daytime temperatures it can accumulate dangerous levels of prussic acid.
Soil Conditions—The mineral composition of soil has a powerful affect on plant toxicity. For example, four-wing saltbush is a valuable browse species under most conditions; however, when growing in areas with a high selenium concentration in the soil, saltbush will accumulate toxic levels of selenium.
Plant Part—Poisonous compounds are often concentrated in different parts of the plant. Western water hemlock accumulates the poison cicutoxin in large amounts in the roots. Sacahuista, on the other hand, causes photosensitization in animals that eat the plant’s flowers or seedheads.
Type of Toxin—Although some toxins, such as cicutoxin in western water hemlock, are lethal in small amounts, most are not. Some toxins, such as those found in tansy mustard, rayless goldenrod and some locos or peavines, have a cumulative effect.
Kind and Class of Animal—Some poisonous plants are more dangerous for one kind of livestock, while others are equally toxic to all classes. Larkspurs are toxic to cattle, but sheep are seldom affected. Some lupines, on the other hand, are poisonous to sheep and only rarely to cattle and horses. Generally, as an animal grows there is usually a corresponding change in the amount of toxin required to be serious. Younger animals are more susceptible to poisoning than are older ones.
Sex of Animal—A few poisonous plants are sex-specific. Pine needles and broom snakeweed appear harmless when consumed by males, but may cause abortion when eaten by females.
Color of Animal—Skin color determines the susceptibility of animals to photosensitization, with light-colored animals affected more.
Condition of Animal—Livestock in poor physical condition, or subjected to stress conditions such as cold temperatures or exertion, are usually more susceptible to poisoning than animals in good condition.
Level of Nutrition of Animal—Most poisonous plants are more toxic when eaten by hungry animals than when eaten by fully-fed animals.
Management to Reduce Livestock Poisoning
The amounts and kinds of poisonous range plants eaten by livestock vary greatly from area to area, and from ranch to ranch, in New Mexico. Management of ranges and livestock is a major determining factor behind these differences.
Proper Use of Ranges—The most common situation where livestock are poisoned by range plants is when ranges are repeatedly overgrazed. As ranges are overgrazed, the more palatable plant species decrease in abundance and the less palatable ones increase. Most poisonous range plants fall into the latter category. As range deterioration continues, animals are forced to eat more and more of the less palatable plants to meet their intake requirements. This relationship between lack of good feed and poisonous-plant-inflicted losses cannot be overemphasized.
Proper numbers of livestock, proper season of use, proper distribution of grazing over the range, and proper kind of grazing animals, considering the type of vegetation, are four practices that will minimize livestock poisoning. Various types of grazing systems allow for occasional rest from grazing, allow the better plants to become established and, over the long run, provide a good feed reserve.
Well-Fed Animals—Animals graze less selectively when they are hungry than when they are full. Hungry animals tend to eat whatever plant is available first. Hungry animals should never be released onto areas containing poisonous plants, or driven through areas containing large numbers of poisonous plants, until they have been well fed.
Proper Turn-In Time—Where certain parts of the ranch are used only during spring and summer, like high mountain pastures, it is necessary to wait until the right time before turning animals onto these areas. If these pastures are grazed before they are ready, the earliest growing species must carry the grazing load. Many poisonous plants are among the first to green up. During this stage, they are most succulent and palatable; livestock can be expected to eat more of the poisonous plants at this time. Livestock should not be placed on seasonal ranges until the desirable forage plants have grown enough to support grazing.
Graze Animals Familiar with the Area—Animals that are new to an area will be less selective in their grazing and eat more undesirable, and possibly poisonous, plants than animals familiar with the range. Exceptions to this rule do occur. For example, animals that have been “locoed” tend to develop an addiction to locoweed. In general, where livestock are grazed in new or unfamiliar pastures, ranchers should watch them carefully.
Proper Herding—Herding or driving animals needs to be done slowly and with little crowding to minimize the amount of poisonous plants eaten. Crowded animals are not able to feed normally and may be forced to eat any vegetation available. When animals are driven or trailed, they often become nervous and will graze less selectively. Hungry animals driven quickly are even more susceptible to poisonous plants.
In the few areas of New Mexico where herders are used, it is good management to select proper bed grounds. Livestock prefer to graze late in the evening while bedding down and in the morning soon after leaving the bed ground. During these periods, animals are less selective and more likely to eat toxic amounts of poisonous plants, if present. This becomes more hazardous when the same bed grounds are used night after night. New trails and bed grounds should be selected if the old ones support large amounts of poisonous plants.
Provide Adequate Nutrients—Animals with severe nutrient deficiencies develop depraved appetites and may eat poisonous plants in trying to satisfy the deficiency. Salt and phosphorus should be supplied year-round to ensure proper mineral nutrition. Salt can also be used effectively to improve livestock distribution, attracting animals away from areas where poisonous plants grow. Salt should be moved regularly to prevent destruction to the native vegetation.
Animals need adequate water all the time. When livestock have been without water for several days, and finally drink, they tend to graze more indiscriminately. Also, without access to water, animals tend to graze succulent plants for the water content, and these may be toxic.
Under many situations, animals eat poisonous plants in early spring before green grass appears, even if enough dry grass exists. Judicious feeding of mineral or protein supplements often solves this problem.
Feed High Quality Hay—Livestock sometimes need to be fed hay to minimize losses from poisonous plants until the better range forage has grown enough. However, if poisonous plants are mixed with the more palatable non-poisonous plants and fed together in hay, livestock are not able to discriminate between plants as readily as they do in the field. Consequently, livestock are more vulnerable to poisoning under these circumstances. Milkweed is one poisonous plant that grows in hayfields and remains highly toxic after haying. Areas containing large amounts of poisonous plants should not be hayed, and hay containing poisonous plants should not be fed.
Know when Plants are Poisonous—Species of poisonous plants vary in their toxicities and palatabilities according to conditions, seasons and years. Tansy mustard, for instance, is not toxic when young, but turns toxic from the time it starts to bloom until the seed pods mature. Areas with stands should be avoided during the danger period.
Graze the Proper Kind of Livestock—Many poisonous plants are only poisonous to certain kinds of livestock. Also, each kind of livestock tends to graze certain types of plants more than others. For example, cattle and horses prefer grasses, while sheep prefer forbs and browse. Ranges should be inspected for the kinds and quantities of poisonous plants before grazing. This information should be used to decide what kind of livestock should be grazed.
Effect of Environmental Conditions
Snowstorms—Early fall and late spring snow may cover up many of the shorter, more desirable species, leaving only the taller plants available to livestock. Under these conditions, livestock should be moved or fed hay.
Winter and Spring Precipitation—In years when ranges get more than normal amounts of precipitation during winter and early spring, there usually will be a flourish of forb growth in spring. Many of New Mexico’s early spring forbs are poisonous, and a number of livestock poisonings result during these years. The problem is compounded because most grasses and other desirable forage species are still dormant, and livestock are craving something green and lush.
Drought—During drought, many palatable range plants mature and dry up early. Consequently, little good forage is produced during the growing season. In contrast, many poisonous plants have the ability to remain green during these periods. As a result, these poisonous plants receive considerable use. Poisonous plants are more abundant after a long drought because the higher successional plants die off. Desirable plants are replaced by poisonous ones because poisonous plants come into a bare area first.
The adverse effects of drought are greatly magnified on overgrazed ranges. In these situations, the more palatable non-poisonous plants are already weakened, and even a slight drought can cause severe problems through high plant mortality. Ranges should be grazed properly, leaving a carryover of forage that can be used in times of drought. In periods of extended drought, livestock numbers may have to be reduced or supplemental feeding initiated.
Control of Poisonous Plants
Control of poisonous plants is the best way to reduce livestock losses. However, it is difficult to control some plants, and several have forage properties that offset their poisonous nature. Generally, removing poisonous plants does not increase forage production to a great extent. So it is the extent of livestock losses that dictates how much money can be used to control toxic plants.
Good grazing management has been effective in poisonous plant control if the plant was not originally present in the native vegetation, and is only abundant in the lower stages of plant succession. Range improvement through grazing management is generally a slow process on New Mexico arid ranges. Therefore, to reduce poisonous plant numbers to a manageable level sooner, some type of control measure may be necessary. Control practices include mechanical and chemical measures, the use of fire and, occasionally, the use of biological agents. Such treatments can be expensive and, in many cases, are not practical except on small areas such as holding pens, calving or lambing pastures, traps and around waterings. Quite often, control of poisonous plants is necessary if a pasture is to be used and it is infested with a large number of poisonous plants. Sometimes it is not a case of whether the rancher can afford to control, but of whether he can afford not to control and stay in the livestock business.
The recommended control treatment for the common poisonous plants of New Mexico are given in Table 1. Chemical applications should be made with the recommended herbicide or one that is labeled for use on the particular poisonous plant. Applications should be made at the most susceptible plant growth stage, and with the recommended form and rate of the herbicide. Spraying poisonous plants may increase the palatability of poisonous plants for a short time after application. Animals should be kept off ranges supporting poisonous plants for at least 2 weeks after herbicides are applied.
Chemical treatments, as well as mechanical treatments such as mowing, grubbing and hand pulling, may be economically feasible around heavily used areas such as bed grounds, corrals and waterholes. Disturbance associated with these areas generally opens up the vegetation and allows invasion of noxious species. Spot treatment of these areas is recommended, even when it is not practical to control the plants in larger pastures.
Seldom is one method completely successful. Often they must be repeated, and in many cases combinations of methods, in conjunction with good range management, are the key to success. Management after control is just as important as the control itself. Good forage species must replace poisonous plants for benefits of poisonous plant control to be lasting.
Care of Poisoned Animals
It is usually easier to prevent poisoning than to cure a poisoned animal. In cases where a poisoned animal is found alive, it should be removed from the problem area, if possible, placed in a cool, shaded area and provided with feed and water. A veterinarian should be contacted as quickly as possible to diagnose and treat the animal. However, treatment of poisoned animals is seldom practical on rangelands. Effects of many poisonous plants have no known treatment, or the poisoning may be too far advanced to treat. Treatments exist for cyanide (prussic acid) poisoning, nitrate poisoning, oxalate poisoning and tansy mustard poisoning. These are effective, but should be tried only when the nature of the poisoning is known, and treatment is administered by a veterinarian.
Key to Principal Stock-Poisoning Plant’s
A key to some principal livestock-poisoning plants was prepared by J. J. Norris and K. A. Valentine in 1957 in New Mexico Extension Circular 274. The key is based on symptoms, class of livestock affected, and the habitat and distribution of the plants in New Mexico. The following is that key:
Chronic; vomiting, greenish frothing at mouth, greenish discharge from nose, heavy breathing, belching, sneezing, coughing; mainly sheep but cattle may be affected:
Borrow ditches, dry intermittent lake and tank bottoms, areas with light perennial vegetative cover; valleys and plains in the central, southern and eastern parts of the state—Bitterweed
Open woodland and forest range on foothills, mesas and mountains of western, central and northern parts of the state—Pingue
Mountain meadows, canyon bottoms, parks and open timber in high mountains throughout the state—Sneezeweed
Chronic; frothy green slobbering, weakness, stiffness, trembling; thumping heartbeat upon exertion, audible several feet distant; sheep; lowland plains, mesas and foothills in southern and central parts of the state—Baileya
Acute; slobbering and vomiting followed by weakness, staggering and convulsions, then coma for several hours or days, followed by death; mainly sheep, but cattle and horses may be affected; open forest and woodland in mountains, foothills and adjacent plains in several parts of the state—Death Cam As
Acute; frothing at mouth, uneasiness followed by violent intermittent convulsions; bellowing and groaning; death occurs in from a few minutes to an hour; mainly cattle, but other Classes of Livestock may be affected; wet meadows, stream bottoms and ditches; mountains in several parts of the state—Water Hemlock
Acute; death from respiratory failure following first appearance of symptoms within a few hours or rapid complete recovery from sub-lethal dosage, even after severe poisoning; breathing first deep, becoming rapid and labored; finally noisy violent gasping, trembling, staggering and convulsions; bloat common in late states of poisoning; all classes of livestock; open foothill and mountain range in western and southwestern part of state—Annual Goldeneye
Fresh or saline marshes and meadows on foothills and mountain ranges in several parts of state—Arrowgrass
Moist canyon bottoms, along streams, moist slopes at middle elevation throughout state—Chokecherry
Foothills; mesa and mountain range throughout the state—Mountain Mahogany
Roadsides, flood areas, field borders and fields; lower elevations throughout state—Johnsongrass, Sorghums
Muddy margins of temporary ponds, tanks, lakes in northeastern quarter of state—Suckleye
Old fields, roadsides, weedy ranges throughout state—Pigweed
Acute; stiff-legged staggering gait; repeated falling, the front legs frequently giving away suddenly; legs stiffly extended, violent kicking in attempt to regain standing position; constipation, bloat, death occurring in short time; inflammation of windpipe, paunch contents in windpipe; kidneys and blood vessels of body surface extremely congested; cattle only; high plains, foothills, forest openings and along streams in mountains throughout state—Larkspurs
Acute; weakness, unsteady gait; rapid breathing, rapid weak pulse, subnormal temperature, convulsions, vomiting; death in fatal poisoning in 12 to 24 hrs after first symptoms; all Classes of Livestock; old fields, intermittent lakes, drainage ways, around stock tanks, lower and middle elevations throughout the state—Cocklebur
Acute; listlessness and depression; staggering and falling or lying down, convulsions at intervals, legs exhibiting running movements when down (in sheep); pulse rapid and weak, breathing a series of grunts and pants, all developing in a few hours; congestion and degeneration of liver, kidneys and spleen; all classes livestock; fields, along roads, borrow ditches and open range; lower and middle elevations throughout the state—Milkweeds
Acute; listlessness, drowsiness, depression and weakness followed by non-violent prostration and difficult breathing, all developing in a few hours; condition lasting several hours before death; sheep and cattle; lowland plains and valleys with alkaline soil, center of state northward and westward—Greasewood
Intermittently flooded bottomlands and clay soil flats south central and southwestern parts of the state—Drymaria
Acute; depression developing over several days into coma, followed by death without struggle; pinpoint hemorrhages on outer lining of digestive tract and on lining of abdominal cavity; cattle and sheep; along streams, gullies and washes in northwest section of the state—Copperweed
Chronic; trembling after exertion, weakness, inactivity, humped-up posture, constipation, breathing becoming labored and gasping just before non-violent death; liver pale, gall bladder distended, bile dark and thick; cattle and horses—Rayless Goldenrod
Chronic; nervous disorder, incoordination, erratic stumbling gait, shying at familiar objects, jumping imaginary hazards, emaciation, coat coarse and roughened; all Classes of Livestock, various habitats throughout the state—Locoweeds
Chronic; muscular trembling and incoordination resembling that of intoxication, varying from unsteady gait to inability to rise; all Classes of Livestock; grassland ranges throughout the state—Ergot
Chronic; depression, incoordination, especially of hind legs, characterized by crossing of hind legs in walking, rapid labored respiration, coughing, rapid loss of condition; cattle, sheep and goats, in various habitats throughout the state except the higher elevations—Red-Stemmed Peavine
Acute; frenzied running and butting into objects and other animals; trembling, labored breathing, and violent spasms, frothing at mouth; sheep only; various habitats in foothills and mountains throughout state—Lupine
Chronic; aimless walking, stumbling into and pushing against solid objects, inability to swallow because of paralysis of tongue or throat; all Classes of Livestock, various habitats throughout the state except at higher elevations—Mustard Weed, Patterson's Loco, Prince's Plume, and other seleniferous plants
Chronic; aimless walking with tendency to stumble into and push into solid objects; sometimes violent, frequent attempts to void scanty yellowish feces; coat rough, nose dry and scaly, liver abnormally hard, gall bladder thick and much enlarged, intestines frequently surrounded by gelatinous fluid; mainly cattle affected; various habitats at lower and middle elevations throughout the state—Groundsel
Acute; excitement, rapid pulse, difficult breathing, trembling and staggering; horses, cattle and sheep; moist habitats throughout the state—Horsetail
Acute; bleeding from nose, bloody feces, high temperature, difficult breathing; cattle; moist sites in forests and meadows at higher elevations—Bracken Fern
Chronic; scanty dry feces, dark, bloody or mucous-coated, later becoming watery but remaining dark; nose dry, scaly; temperature subnormal; depression, emaciation; mainly cattle; shinnery and other oak brush ranges throughout the state—Oak, Shinnery
Acute; unsteady gait, posture with head lowered and ears drooped; dark watery diarrhea, increased urine production, bloat, abdominal pain, temperature rise, pulse rapid, breathing weak and labored; bloody froth in air passages, complete prostration and coma preceding death; widespread damage to internal organs; all Classes of Livestock; various habitats throughout the state—Patterson's Loco, Prince's Plum, and other seleniferous plants
Chronic; listlessness, loss of appetite, arched back and drooping head; urine bloody in severe cases, liver and kidneys severely damaged; mainly cattle; plains and foothills throughout state—Broom Snakeweed
Chronic; listlessness, emaciation; sore feet, lameness, hoof growth excessive with cracking and sloughing; erosion of contact surface of bones; all classes of stock; various habitats throughout the state except higher elevations—Patterson's Loco, Prince's Plum, and other seleniferous plants
Acute; yellowish coloration and intense irritation of light-colored skin areas upon exposure to sunlight; swelling and oozing of serum from affected parts, sloughing of scabby skin, urine dark, liver yellowish brown to green, green plugs in bile ducts, kidneys enlarged greenish to greenish black; all classes of livestock; dry plains and foothills in several parts of the state—Sacahuista, Horsebrush, Lechuguilla
Gangrene, sloughing of ears, tails, teats, hooves, all Classes of Livestock; various habitats throughout the state—Ergot
Abortion; all classes of stock, various habitats throughout the state—Pine, Juniper, Broom Snakeweed, Pigweed, Ergot
Symptoms of Poisoning
The rancher faces confusion and frustration when managing livestock operations and dealing with poisonous plant problems. Poisoning symptoms for many plants were defined in the laboratory under forced feeding conditions. Symptoms may not follow the classic Description under range conditions. Some poisonous plants can be grazed without trouble most of the time, but can be extremely toxic at certain times. Poisoning can occur on lush pastures at one time and under drought at another time. Several poisonous plants may have the same, or a similar, poisonous principle, and cause similar symptoms. A single species can be poisonous in several ways so that the symptoms vary, depending on the toxic ingredient most active at the particular time.
Much poisonous plant research is not reproducible in the field because symptoms and lethal dose were determined mostly by force feeding animals in confinement. It is virtually impossible to duplicate the number of diet combinations possible when a range animal has access to 30 or 40 plant species, which may include two or three kinds of poisonous plants.
Principal Livestock-Poisoning Plants
All problems with poisonous plants cannot be predicted, or effectively prevented or alleviated by management. In some cases, the manager must accept losses in production, or not use the range where poisonous plants occur. However, good range management, understanding of poisonous plants on the range, and common sense animal husbandry can keep losses to a minimum. One of the first steps in preventing livestock losses caused by poisonous plants is to recognize the plants and understand their effects on animals. The plants presented in this section do not include all plants known to be poisonous in New Mexico, but are the major plants that cause the most problems for ranchers.
Description—A bright green, succulent bush forb about 1 ft tall when fully grown. Leaves alternate and pinnately or twice pinnately divided. Flowers are white and showy with five petals. The fruit is a 2- to 4-cavitied, many-seeded leathery capsule about 3/8 inch in diameter.
Distribution and Habitat—This plant is native to the deserts of Africa and southern Asia. It was first reported in the United States near Deming, New Mexico in 1935 and has since spread across southern New Mexico, Arizona and western Texas.
Classes of Livestock Affected—Cattle and sheep. It is uncertain whether horses are affected.
Poisonous Principle and Toxicity—Alkaloids extracted from African rue have proven toxic to laboratory animals, producing the same symptoms as observed when the whole seed was fed. The seeds contain at least four alkaloids, of which three have the indole configuration.
Conditions of Poisoning—African rue is highly unpalatable to livestock, and the few cases of poisoning were reported on denuded ranges.
Annual Goldeneye, Resinweed
Description—An erect, branching forb 1 to 2 ft in height with yellow sunflower-like heads 1 inch in diameter and 1- to 1.5-inch leaves, narrow, opposite, entire.
Distribution and Habitat—Annual goldeneye is a weed on ranges at elevations up to 7,000 ft. It grows on hills, plains and river bottoms in southwest to west central New Mexico. It flowers from May to October and often colors the landscape with a brilliant yellow.
Classes of Livestock Affected—Cattle are the only livestock known to be poisoned.
Poisonous Principle and Toxicity—The poisonous nature of the plant is unknown; symptoms suggest prussic acid.
Signs of Poisoning—The first symptoms are deep, rapid breathing which progresses from labored to violent gasping. The animals tremble, stagger and fall in convulsions. Animals that show symptoms should not be disturbed unnecessarily nor watered. In borderline cases, the animal may recover in an hour or so if not excited. A glucose drench may be beneficial.
Conditions of Poisoning—Annual goldeneye is reported to make good forage for cattle and sheep and, in general, large quantities must be eaten to cause losses, but under some conditions, small amounts may be lethal. Poisoning occurs mainly in fall when growth is abundant, or when other feed is scarce.
Seaside arrowgrass (Triglochin maritima)
Marsh arrowgrass (T. palustris)
Description—Perennial, unbranched, grasslike plants 1 to 3 ft tall. Leaves basal: 6 to 18 inches long, linear, unjointed, somewhat fleshy. Flowers small, 1/8 inch long, greenish, inconspicuous individually, bunched together on the upper portion of the main flowering stem. Seedpods 3-seeded, about 1/4 inch long, lobed and oblong. Arrowgrass leaves are unlike grass leaves, in that they are more fleshy and flat on one side and round on the other.
Distribution and Habitat—Both species are scattered throughout New Mexico in damp, wet, marshy areas. They are most abundant on saline and alkaline soils, and may be underwater, or partially underwater, for all or part of the growing season. Arrowgrass is commonly found growing abundantly with sedges, rushes and slough grasses.
Classes of Livestock Affected—All classes are somewhat susceptible, but sheep and cattle are the most commonly poisoned.
Poisonous Principle and Toxicity—Hydrocyanic acid contained in both fresh and dried leaves. Consumption of from 0.1 to 0.5% of the animal’s weight (1–5 lb for a 1,000-lb animal) can be lethal.
Signs of Poisoning—Uneasiness; abnormal breathing, either rapid or slow; muscle weakness, staggering and falling; possible dilation of eyes; bloating; convulsions; coma followed by death. Poisoning by lethal amounts is followed so rapidly by death that animals are not commonly found in time to administer an antidote.
Conditions of Poisoning—Poisoning is most common in spring on ranges where hungry livestock have little green forage to choose from. Poisoning from hay containing arrowgrass is also quite common. If allowed to complete its life cycle with adequate moisture, arrowgrass accumulates little potential toxic material. Arrowgrass growing under drought conditions has been found to be 5 to 10 times as toxic as those plants that have been partially submerged throughout the entire growing season.
Plants are apparently poisonous at all times of the year, and both the leaves and the flowering structures contain the poison. Hydrocyanic acid is not cumulative, and for it to be fatal, the animal must consume a lethal dose in a relatively short period (1/2 to 1 hour). Cases have been reported where cows lacking salt have consumed greater than normal amounts of arrowgrass because of its high salt content.
Description—An erect annual; grows up to 2 ft in height. Stems are purplish near the base; leaves are alternate, entire to pinnately divided, glandular and usually woolly on the underside. The bright flower heads occur at the tips of the long stems. Fruit is a one-seeded, dry capsule (achene) with a crown of scales.
Distribution and Habitat—Bitterweed occurs in the southern half of the state and is more predominant in the southeastern quadrant.
Classes of Livestock Affected—Sheep are poisoned by bitterweed more often than are other livestock.
Poisonous Principle and Toxicity—Sesquiterpene lactones are the toxic constituents in bitterweed, and cause severe irritation of nasal and intestinal membranes. As little as 1% of an animal’s weight of green plant material is lethal, whether ingested at one time or over a period of several months. Rapid consumption produces chronic symptoms and eventually death. Toxicity increases with maturity and under drought conditions.
Signs of Poisoning—Symptoms include depression, vomiting, salivation and general weakness. A green salivary discharge is a typical range symptom. Affected animals should be removed from infected areas and given good quality feed and clean water. They likely will make a slow recovery with such treatment . There is no treatment for poisoned animals. Symptoms usually appear after a month or so of access to the plant.
Conditions of Poisoning—Since 1925, bitterweed has increased because of overstocking accompanied by destruction of perennial grasses and forbs. Bitterweed is distasteful to range livestock. Probably for this reason, it has not been known to produce natural cases of poisoning in cattle, horses or goats, although these animals can be poisoned experimentally. Under conditions of starvation, sheep will eat bitterweed and may develop a liking for it. If removed at the onset of symptoms, sheep may be expected to make an uneventful, though slow, recovery.
Description—Large, coarse, perennial herb; originating from stout, black horizontal rootstalks often more than a yard long. Leaves scattered, 1 to 4 ft long, 1/2 to 2 ft wide; terminating erect, rigid, straw-colored stalks, 1 to 3 ft tall; broadly triangular in outline; divided in three main parts, each part subdivided, the ultimate segments oblong, the upper undivided, and the lower lobed. Fruiting bodies appear as small circular dots on the underside of mature leaves.
Distribution and Habitat—Scattered throughout New Mexico mountains on burned areas, woodlands and shaded areas. Most abundant on dry, sandy or gravelly soils.
Classes of Livestock Affected—All classes, but sheep are most resistant.
Poisonous Principle and Toxicity—Thiaminase in horses, unknown in cattle and sheep. The poisonous principle is cumulative in all Classes of Livestock. In general, feeding hay containing more than 20% bracken fern produces signs in horses in about a month. Cattle eating an amount of bracken fern roughly equivalent to their body weight over a period of 1 to 4 months will end the period with Signs of Poisoning, followed shortly by death.
Signs of Poisoning
Monogastric Animals (Horses). Loss of weight and condition, progressive incoordination. Animals become drowsy, depressed and will stand in a crouching position with legs apart and back arched. Muscles begin to twitch, ending in severe tremors, pulse becomes weak and fast, convulsions or spasms set in and death soon follows. Inspection of poisoned animals reveals no characteristic gross lesions.
Ruminant Animals (Cattle and Sheep). Rough coat, high temperature, difficulty breathing, loss of appetite, increased salivation, depression, nasal and rectal bleeding, blood in urine, and hemorrhages of mucous membranes. The disease is of short duration, and poisoned cattle usually die.
Conditions of Poisoning—Losses can occur either by feeding hay containing high amounts of bracken fern, or when livestock are grazed on ranges where the more desirable species are scarce. This is especially true in late summer to fall when most range grasses are dried up and have become less palatable. Both the dried and green leaves of bracken fern are poisonous. Livestock have been poisoned by eating rhizomes of bracken fern. These rhizomes are about five times as toxic as the leaves.
(Gutierrezia sarothrae, G. microcephala)
Description—Snakeweeds are low, perennial half-shrubs growing 1 to 2 feet tall. They are many branched and quite resinous. The leaves are linear, entire and alternately arranged. The yellow flowers occur in small composite heads. The heads usually occur in small clusters at the tips of the numerous branches.
Distribution and Habitat—The two species occur over most of the state from 3,000 to 8,000 feet.
Classes of Livestock Affected—Cattle, sheep and goats have all been reported to have been poisoned.
Poisonous Principle and Toxicity—The poisonous principle is apparently a saponin. It is most toxic at the earlier stages of growth during early leaf development and when growing on sandy soils. Broom snakeweed is also a secondary or facultative selenium absorber.
Signs of Poisoning—Effects of snakeweeds include death, abortion, weak or light-weight calves and retained placentas. As little as 20 lb of fresh plant material consumed in 7 days will cause cows to abort. Consuming 10 to 20% of the body weight in 2 weeks has caused death in sheep, cattle and goats.
Symptoms include listlessness, loss of appetite, loss of weight, nasal discharge, fecal mucous, bloody urine and vaginal discharge. A dry and peeling muzzle with nasal discharge has also been noted in cattle. Post-mortem lesions include severe damage to kidneys and liver. The spleen is congested and the intestinal tract inflamed. The most common symptom is a retained placenta.
Conditions of Poisoning—Drought conditions or times when no other green forage is available aggravate the problem, as livestock begin to search for fresh green material.
Burroweed, Jimmyweed, Rayless Goldenrod
(Haplopappus heterophyllus, H. tenuisectus)
Description—These plants are semi-woody half shrubs growing 1 to 2 ft tall. Jimmyweed and rayless goldenrod will grow up to 4 ft tall. Leaves are alternate, narrow and divided into linear lobes. Leaves are resinous and sticky. The yellow flowers are borne in flat-topped clusters. The mature flowers produce a crop of seeds with numerous short bristles.
Distribution and Habitat—Burroweed is found mainly in southwestern New Mexico in Grant, Luna and Hidalgo counties. It grows on plains, mesas and hillsides at elevations of 2,000 to 6,000 feet, and is most abundant on depleted ranges. Jimmyweed or rayless goldenrod is common throughout the state, particularly along roadsides and in areas such as river drainages and irrigation canals. It has been a particular problem along the Pecos Valley drainage in southeastern New Mexico.
Classes of Livestock—All Classes of Livestock are subject to poisoning, and calves and lambs may be poisoned from the milk of poisoned dams. In some instances, calves may die from the milk of the poisoned dam before she shows symptoms. The poison can be transmitted to humans through the milk of the cow, causing milk sickness in man.
Poisonous Principle and Toxicity—The alcohol tremetol is the toxic principle. Tremetol is present in both the green and dry leaves, making these plants poisonous at all times. The poison is cumulative, with toxic doses in the neighborhood of 1 1/2% of the body weight of an animal accumulated over a 2 or 3 week period.
Signs of Poisoning—Burroweed and rayless goldenrod or jimmyweed produce the disease known as trembles in livestock, the name being derived from violent trembling of afflicted animals. Muscular trembling is particularly noticeable around the nose, hips and over the shoulders. It is particularly noticeable after exercise. The animal will stand in a humped-up position and move with a stiff gait. Stiffness and weakness are most emphasized in forelegs. As poisoning progresses animals become weaker, inactive, lie down and eventually are unable to rise. Other symptoms are constipation, vomiting, quickened and labored breathing, and dribbling of urine.
Conditions of Poisoning—Burroweed is generally low in palatability, but is eaten in quite large amounts when better forage is not available. Precautions must be taken in winter when snowfall covers better forage plants and burroweed is the only plant available. Native livestock apparently become sickened from eating the plant and tend to avoid it. An adequate supply of good feed during harsh times when livestock are more prone to consume burroweed may reduce its consumption. There is no definite medicinal treatment for poisoned animals. They should be removed from the area and fed good quality hay and given clean water. Veterinarians have found the intravenous administration of glucose and calcium gluconate helpful. The use of purgatives, stimulants and laxative feeds may help the animal recover. Oral administration of activated charcoal, at 1 gram per kilogram of body weight, shows promise as a treatment. Calves and lambs should be taken off poisoned dams, the mothers milked out and the milk thrown away.
Description—A large, erect shrub or tree, up to 30 ft tall. Young twigs red to brown, covered with light colored dots (lenticels). Leaves dark green, 2 to 4 inches long and 1 to 2 inches wide, usually appearing oval with a pointed tip, rounded base and saw-toothed margins. Flowers small, yellow-white, in dense clusters. Fruit dark red to black, about 3/8 inch in diameter.
Distribution and Habitat—Found throughout the state on moist soils of river banks, valleys and hills.
Classes of Livestock Affected—Potentially poisonous to all Classes of Livestock, but sheep and cattle are most often affected.
Poisonous Principle and Toxicity—Hydrocyanic or prussic acid. Consumption of 0.25% of the animal’s weight (2 1/2 lb for a 1,000-lb animal) of fresh green leaves is usually fatal to cattle. Sheep often die from eating as little as 1/4 lb of fresh green leaves.
Signs of Poisoning—Uneasiness, abnormal breathing, either rapid or slow, muscle weakness, staggering and falling, possible dilation of eyes, bloating, convulsions, coma followed by death. Lethal dosage is followed so rapidly by death that animals are not commonly found alive or in time to administer an antidote.
Conditions of Poisoning—Although this plant is poisonous in some cases, it is generally considered to be a good forage for both livestock and wildlife. Problems from poisoning arise in early spring. At this time, the more preferred species are still scarce, especially on overgrazed ranges, and the concentrations of hydrocyanic acid are highest.
Hydrocyanic acid is not cumulative and, for it to be fatal, the animal must consume a lethal dose in a relatively short period (1/2 to 1 hour). Poisoning can be intensified when animals consume water soon after eating chokecherry.
By the end of summer, chokecherry leaves have lost their toxicity. The fleshy fruit of chokecherry is not poisonous, although eating pits has been reported to cause death, and should be a concern from the standpoint of human health.
(Xanthium saccharatum, X. spinosum)
Description—Coarse annuals with alternate, rough and broad triangular leaves. Cocklebur has separate male and female flowers on the same plant. The male flowers are in dense clusters at the ends of the stems and the female flowers occur in clusters in the leaf axils. The fruit is a hard two-celled, two-beaked bur covered with stiff hooked barbs, containing two seeds.
Distribution and Habitat—Cockleburs are common annual weeds occurring throughout the state. They are more common in disturbed areas along roadsides and around water holes.
Classes of Livestock Affected—All Classes of Livestock are susceptible.
Poisonous Principle and Toxicity—For many years, the toxic agent in cocklebur was thought to be hydroquinone. The actual toxic agent is carboxyatractyloside, a glycoside shown to be hypoglycemic.
The seeds contain the toxic substance, but are rarely eaten. Upon germination, the toxic principle is distributed to the seedling and remains through the cotyledon stage. The concentration drops quickly as the first true leaves develop. A toxic dose of seedlings equals 0.75 to 1.5% of the animal’s body weight. Poisoning is apparent within 12 to 48 hours. After onset of symptoms, death can occur within a few hours to several days. Toxicity is not lost through drying.
Signs of Poisoning—Animal symptoms include weakness, depression and an unsteady gait when moving. There is rapid, labored breathing and a weak, rapid pulse. Body temperature is subnormal. There is nausea and vomiting. Prostrated animals go into convulsions, making running motions with their legs, or show a marked backward curvature of the neck. Postmortem findings include degenerative changes in liver and kidney, hemorrhages on the heart and elsewhere, and moderate irritation of the stomach and intestines.
Conditions of Poisoning—Cocklebur often grows in areas that are underwater for long periods of time but that dry out during the summer. These conditions are found along streams or around farm ponds. Giving animals fatty substances such as cream, lard or linseed oil may prevent poisoning after animals have eaten cockleburs. Linseed oil should be administered through a stomach tube to avoid producing inhalation pneumonia.
Rocky Mountain death camas (Zygadenus intermedius)
Foothill death camas (Z. paniculatus)
Meadow death camas (Z. veneosus)
Description—Slender, perennial herbs 8 to 24 inches tall, growing from an onion-like bulb 1 to 1 1/2 inch long, 4 to 6 inches below the ground. Stems single, unbranched and produced at time of flowering. Leaves basal, grasslike, smooth, 8 to 26 inches long, 1/6 to 1/2 inch wide, V-shaped in cross section. Flowers whitish to yellow, borne along the main stem.
Death camas is often confused with the nonpoisonous wild onion, but can easily be distinguished by its lack of the characteristic onion odor.
Distribution and Habitat—Found throughout the state in moist meadows, pastures at elevations over 7,000 feet.
Classes of Livestock Affected—Sheep, although all classes are somewhat susceptible.
Poisonous Principle and Toxicity—Zygadenine and several other complex alkaloids. Toxic levels for sheep are between 2 and 2 1/2 lb (green weight basis) per 100 lb of body weight. One-tenth pound of death camas seeds can kill a mature cow.
Signs of Poisoning—Increased salivation, nausea followed by vomiting, increased rate of breathing; initial rise in body temperature, but soon falling below normal; weakness and staggering; coma frequently followed by death.
Conditions of Poisoning—Death camas is the most important of all poisonous plants in spring. It begins to grow early, and if there is a lack of other better forage, animals will eat death camas. At this time there may be high losses. The bulbs of death camas are extremely poisonous, but are rarely pulled up by grazing animals. All parts of the plant are poisonous at all times, but after the plant blooms, it soon withers and sheep seldom eat it.
Humans are sometimes poisoned by eating the bulbs of this plant, mistaking them for wild onions.
Description—Filaree is an introduced, low-growing annual forb usually less than 6 inches tall. Leaves are somewhat hairy, alternate and pinnately divided. Flowers are in clusters on slender stalks arising from leaf axils. Flowers are lavender and bloom from February to July. The fruit is a spindle-shaped capsule with a sharp, pointed base and a tail that coils at maturity.
Distribution and Habitat—Plants grow on the plains and mesas throughout the state, generally at elevations below 7,000 ft. Some growth occurs in fall and winter, but most occurs in the spring.
Classes of Livestock Affected—Primarily cattle.
Poisonous Principle and Toxicity—Filaree is normally a valuable forage plant, furnishing good forage in both green and dry states. However, plants occasionally develop high concentrations of nitrate that may cause loss of livestock. Several instances of heavy death loss of cattle in New Mexico have occurred.
Signs of Poisoning—Symptoms of filaree-poisoned animals are typical of nitrate poisoning. Nitrate content has run as high as 4.25%. Danger is highest during the flush period of growth.
Conditions of Poisoning—Filaree poisoning is usually a problem in early spring in New Mexico before other forage plants have greened up. The combination of cold nights and warm days increases the nitrate concentration in the plant.
Description—Highly branched woody shrub, 6 to 36 inches tall. Leaves and twigs covered with a fine mat of white hairs. Leaves linear, narrow, 1/2 to 1 inch long. Flowers yellow, four in a head; heads in small clusters terminating in short supporting stalks.
Distribution and Habitat—Scattered throughout the state on dry open areas in foothills and plains.
Classes of Livestock Affected—The only susceptible class is sheep.
Poisonous Principle and Toxicity—Unknown, but thought to be a resin-like organic substance. Consumption of 1 1/4 lb of leaves and stems will cause bighead, a condition involving sensitization of the skin to sunlight (photosensitization). This condition is characterized by swelling of the head, neck, ears, eyelids and nose. These signs appear within 24 hrs after ingestion. Many ewes abort and become sterile after eating a sublethal dose.
Conditions of Poisoning—Photosensitization is more severe in light-skinned animals. This condition is greatly intensified when the affected animal has been exposed to direct sunlight.
Because gray horsebrush is an unpalatable species, sheep consume it at toxic levels only when forced to eat it. This usually happens on overgrazed ranges lacking in more desirable species, or when animals are trailed and not allowed to practice selective grazing. Gray horsebrush produces new growth in early spring when most of the better range plants are still scarce. Its toxicity is also greatest at this time, makes spring the most dangerous season.
Description—Erect, woody, highly branched shrub 3 to 5 ft tall. Stems smooth, bark whitish; smaller twigs tapering to a spine-like point. Leaves originating singly or in pairs, fleshy, almost round in cross section, long and narrow, 1/4 to 1 1/4 inch long; bright green when young, becoming rusty with age. Flowers of two kinds: pollen-producing—small, borne in dense cylindrical, cone-like clusters at end of short branches; and seed-producing—small, inconspicuous, greenish, on short branches in leaf axils. Fruit small, encircled by a thin, ruffle-like wing around the middle.
Distribution and Habitat—Scattered throughout New Mexico on saline and saline-alkali soils. Especially common on clayey soils and in small basins with high water tables.
Classes of Livestock Affected—Sheep and occasionally cattle.
Poisonous Principle and Toxicity—Soluble sodium and potassium oxalates. Consumption of between 1 1/2 and 3% of an animal’s weight (1 1/2 to 3 lb for a 100-lb animal) of green leaves is generally lethal if eaten in a short period.
Signs of Poisoning—Dullness, depression, loss of appetite, lowering of head, reluctance to follow band, weakness, irregular gait, prostration, weak respiration and heartbeat, and coma followed by death. Signs appear within 3 to 5 hrs after consumption of a lethal dose, followed by death within 12 to 20 hrs after consumption.
Conditions of Poisoning—Greatest losses occur in spring when hungry sheep are turned onto dense stands of greasewood and fill themselves in a short time. Heavy losses are also common when sheep are trailed through stands and are not allowed time to practice selective grazing. Spring is usually dangerous because the leaves are succulent and palatable, while other forage is often scarce. In a wet spring, plants are low in poison or devoid of it, but poison becomes more concentrated during dry periods. Oxalate content is greatest in the leaves and increases with maturity, reaching maximum levels in August and September.
Greasewood is usually considered a good forage and valuable to sheep and cattle for winter and spring grazing on New Mexico’s ranges. A moderate amount of other forage in the diet will prevent poisoning by greasewood. Other beneficial management practices include preventing hungry animals from filling up on greasewood exclusively, spreading consumption of greasewood out over a period of time, and allowing animals free access to salt supplements, because salt-hungry animals may sometimes consume excessive amount of greasewood.
Description—Annual herb with thick, juicy stems; branching from the base, at first spreading, then usually becoming erect. Stems measuring a few inches to more than a foot long, generally with numerous short lateral branches. Leaves thick, succulent, 1/4 to 1/2 inch long, nearly tubular, tipped with a weak spine. Flowers greenish, inconspicuous, of two kinds. Fruits winged, conspicuous, often mistaken for flowers, basally enclosing single seed. Seeds small, of two types: black, winged, immediately germinating; brown, wingless, delayed-germinating. Plants dark red to light purple in early spring, become pale yellow to light tan in late summer.
This plant looks like Russian thistle or tumbleweed (Salsola kah), but the leaves of halogeton are rounded and tipped with a delicate spine, whereas the leaves of Russian thistle taper to a rigid spine.
Distribution and Habitat—Introduced from Eurasia, with only scattered stands now present in the state, but it appears to be spreading. Halogeton thrives in the salty soils of semi-arid regions, especially in those areas where heavy grazing and other disturbances have removed the native vegetation.
Classes of Livestock Affected—Sheep, and less frequently cattle.
Poisonous Principle and Toxicity—Soluble sodium and potassium oxalates. Eating as little as 1/3 to 1 1/2% of its body weight (1/3 to 1 1/2 lb for a 200-lb animal) can kill a fully fed sheep. The lethal dose for a fasted sheep is between 1/4 to 1/3 as much. Although figures are few, toxicity to cattle appears to be about the same.
Signs of Poisoning—Highest livestock losses occur in late fall and early winter when hungry animals are driven along trails, or bedded down in areas infested with halogeton. If other more desirable forage is available and animals are allowed to select their own feed, they seldom consume lethal amounts of halogeton. Livestock are affected only after a lethal dose is eaten. Lesser amounts apparently cause no ill effects.
Halogeton is dangerous at all times, but becomes more toxic as the growing season advances, reaching a peak of toxicity at maturity. All above-ground parts are toxic, but the greatest concentration is in the leaves and fruiting structures.
Description—Biennial to perennial (on more favorable sites) erect herb, 2 to 10 ft tall. Stems highly branched, hollow, purple-spotted. Leaves twice divided, deeply cut, similar to parsley; when crushed fresh leaves have a strong parsnip odor and nauseating taste. Flowers small, white and grouped together in umbrella-like clusters.
Poison hemlock is often confused with water hemlock (Cicuta douglasii), but while the former is found on moist areas, the latter is usually semi-aquatic. The leaves of poison hemlock are much more finely divided than those of water hemlock, and the leaf veins terminate at the tips of the teeth, while those on water hemlock terminate between leaf teeth.
Distribution and Habitat—Introduced from Europe and now scattered throughout most of the state. Although poison hemlock is widespread on some ranges, generally it is most abundant in moist meadow sites above 6,000 ft elevation.
Classes of Livestock Affected—All classes are susceptible.
Poisonous Principle and Toxicity—Poison hemlock contains at least five distinct, yet closely related, alkaloids. The best known of these alkaloids is coniine. Toxic levels for cattle are between 0.1 and 0.5% (green-weight basis) of the animal’s weight (1–5 lb for a 1,000-lb animal). Reported levels for sheep are similar.
Signs of Poisoning—Nervousness, trembling, loss of coordination, dilation of the pupils, weakened pulse, coma and eventual death through respiratory failure. Signs usually appear soon after ingestion and are similar to those by water hemlock, but without convulsions.
Conditions of Poisoning—Livestock poisoning is most common in spring when the tender, succulent, highly toxic new leaves appear. Poison hemlock leaves have a nauseating taste. Livestock seldom eat it, and usually do so only when forced by lack of preferred forage.
Several cases of human poisoning have resulted from eating hemlock after mistaking the roots for wild parsnip (Pastinaca sativa) and the leaves for parsley. All parts of the plant—fruits, flowers, leaves, stem and roots—are extremely poisonous.
Horsetail, Scouring Rush, Jointfir
Common horsetail (Equisetum arvense)
Marsh horsetail (E. palustre)
Description—Erect, herbaceous perennials, 8 to 24 inches tall. Aerial stems either perennial or annual, rushlike, straight, jointed, hollow, originating from deeply buried underground stems (rhizomes). Stems maybe unbranched or may bear whorls of small, jointed branches. Leaves small, reduced to scales, borne in rings at the nodes. Fruiting bodies dark-colored, cone-like structures terminating ordinary green stems or special fertile stems.
Distribution and Habitat—Species of this genus are scattered throughout the state in meadows, swales, flood plains or wherever the water table is high. They are a common component of some irrigated haylands.
Classes of Animals Affected—Although all Classes of Livestock are affected, horses are most commonly poisoned.
Poisonous Principle and Toxicity—Thiaminase and other unknown substances. The poisonous principle is cumulative in all Classes of Livestock. Hay containing at least 1/5 Equisetum arvense fed to horses will produce Signs of Poisoning in 2 to 5 weeks.
Signs of Poisoning—Monogastric Animals (Horses). Loss of condition; muscular exhaustion, especially in the hindquarter; staggering gait; difficult breathing; rapid and weak pulse; convulsions; coma followed by death.
Ruminant Animals (Cattle and Sheep). Loss of condition, excitement, muscular weakness, trembling, staggering and diarrhea.
Conditions of Poisoning—Although most poisoning comes from feeding hay containing large amounts of horsetail, animals grazing ranges short on good, more preferred species have also been poisoned. The latter case is most likely in spring. Young green growth appears to be more poisonous than older growth. Young animals are more susceptible to poisoning than older animals.
Description—Inkweed is a succulent, grayish-green annual forb that lies prostrate against the ground, radiating from a single root and rebranching, forming a plant up to 1 ft in diameter. The leaves are paired opposite, ovate, less than 1/2 inch long by 1/4 inch wide, obtuse tipped. Flowers are small, white, solitary, inconspicuous, borne singly in leaf axils, with five sepals and five petals. Fruit is a small capsule with many small seeds. A purplish juice can be squeezed from the immature capsules (hence the common name, inkweed).
Distribution and Habitat—Alkaline clay soils in southern and south-central parts of the state. The seeds germinate only when moist. Inkweed is killed by the first frost
Classes of Livestock Affected—All kinds and Classes of Livestock are susceptible. Goats appear somewhat more resistant.
Poisonous Principle and Toxicity—Inkweed is highly toxic and unpalatable to all Classes of Livestock. About 0.5% of body weight is uniformly lethal to cattle and sheep. The toxic compound in inkweed is unknown.
Signs of Poisoning—Symptoms appear 18 to 24 hrs after ingesting a toxic dose. The period between the onset of symptoms and death is brief and characteristic of drymary poisoning. It can be less than 2 hours. In cattle, symptoms include loss of appetite, diarrhea, restlessness, arched back or tucked up appearance, depression, and frequently coma and death.
Conditions of Poisoning—Inkweed is exceedingly distasteful; however, in drought years when other forage is not available, enough can be consumed to cause death. The plant lies prostrate on the ground during the day and is relatively unavailable for grazing. During the night, however, it becomes turgid so the branches are elevated a few inches, and is more easily consumed. Losses are most common during late summer.
Jimson Weed, Sacred Datura
(Datura meteloides, D. stramonium)
Description—Jimson weed is a coarse weed with stout stems and malodorous herbage. Leaves are large and oval with wavy to pinnately lobed margins. Flowers are large, showy, tubular, white to purple, and fragrant. The fruit is an oval or round, nodding or erect, prickly capsule.
Distribution and Habitat—Jimson weeds occur throughout New Mexico. These plants are particularly abundant along roadsides and ditches and other disturbed areas.
Classes of Livestock Affected—All Classes of Livestock and humans can be poisoned by jimson weeds.
Poisonous Principle and Toxicity—Species of jimson weeds contain several solenacious alkaloids. Poisoning of both livestock and humans occurs from eating any part of the plant, including the seeds. As little as 10 to 14 oz of the plant, or less than 0.1% of the body weight of the animal, has been proven fatal to cattle. Numerous incidents of human poisoning have resulted from eating the seeds and unripened seed pods. On occasion, plants have been eaten for their hallucinogenic effects.
Signs of Poisoning—Symptoms of poisoning are similar among humans and livestock. They include intense thirst, distorted vision, uncoordinated movement, high temperature, a rapid and weakened heart beat, convulsions, coma and death. There is no specific medicinal treatment recommended for livestock.
Conditions of Poisoning—Livestock rarely eat jimson weeds. The ill-scented herbage makes the plants highly distasteful, and livestock literally have to be forced to eat it because of lack of other forage.
Description—Johnsongrass is a coarse perennial with scaly root stalks. It has broad leaves and grows 3 to 6 ft tall. The numerous seeds are yellow to purplish and occur in large, many branched clusters.
Distribution and Habitat—Johnsongrass is an introduced grass found throughout the state. It is considered a weed in cultivated fields, waste places, and along irrigation ditches and stream bottoms.
Classes of Livestock Affected—Most mortality occurs in cattle, but sheep and horses have also been poisoned.
Poisonous Principle and Toxicity—Most losses from johnsongrass are from prussic acid or hydrocyanic acid poisoning, but plants also accumulate dangerous levels of nitrate.
Signs of Poisoning—Symptoms are typical of prussic acid poisoning. The reliable diagnostic sign of bright red venous blood will help identify prussic acid as the poison. However, dark brown arterial and venous blood would indicate poisoning by nitrate.
Conditions of Poisoning—Danger from prussic acid poisoning is greatest when soils are high in available nitrogen and low in phosphorus, when plants have been exposed to drought or disease that slows or stunts growth, and when plants are making rapid regrowth or have been frosted. Leaves are more toxic than stems, and young plants are more toxic than mature ones.
Description—Kochia is an annual forb. Stems are erect and branches are erect or ascending. Kochia grows from 1 to 3 ft tall and is leafy; leaves turn bright red in fall. Leaves are alternate and linear; flowers are clustered in the axils of the leaf-like bracts.
Distribution and Habitat—Kochia is common in New Mexico in cultivated fields, go-back lands and other waste areas.
Classes of Livestock Affected—All classes are affected, but kochia toxicity afflicts cattle and sheep predominantly.
Poisonous Principle and Toxicity—There has been interest in using kochia as a weed or feed plant due to the fact that protein and fiber contents of kochia are similar to alfalfa and kochia can produce the same amount of forage per acre as alfalfa with one-half the water. Kochia will poison livestock occasionally, and high levels of oxalates were implicated because of the elevated blood urea nitrogen levels that indicated kidney damage. However, recent information has suggested that alkaloids are the primary toxin in kochia. Nitrates are also involved at times.
Signs of Poisoning—Jaundice and photosensitization, progressive central nervous system disfunction, cirrhosis of the liver, gastrointestinal tract inflammation, and polioencephalomalacia, the last of which suggests involvement of a thiaminase or liver toxin that may lead to impaired thiamine utilization.
Conditions of Poisoning—Kochia is most toxic during drought and at seed maturation.
Locoweeds, Point Locos, Peavines
(Astragalus spp. , Oxytropis spp.)
Description—Low-growing, perennial herbs, with erect to spreading stems, originating from woody taproots. Leaves pinnately compound into numerous linear to oval leaflets. Flowers white to purple, with a rounded keel petal (the lowermost petal), generally borne on leafy stems. Fruit a pealike pod, few- to many-seeded.
The Astragalus genus is often confused with the genus Oxytropis. While the former has rounded keel petals and generally leafy flowering stems, the latter has keel petals abruptly narrowed to beak-like points, and leafless flowering stems.
There are three distinct groups of toxic species within the Astragalus genus. Because they differ markedly in nearly all aspects of poisoning, they are discussed separately:
I. Selenium—The following four species are able to take up selenium from the soil and concentrate it at levels toxic to animals:
Two-grooved milkvetch (A. bisulcatus)
Narrowleaf poisonvetch (A. pectinatus)
Gray’s milkvetch (A. grayi)
Stinking vetch (A. praelongus)
Distribution and Habitat—These four species are common on selenium-rich soils.
Classes of Livestock Affected—All classes.
Poisonous Principle and Toxicity—Selenium concentrated within the tissues of the plant, although there are still questions as to whether there may be other toxic compounds involved. As little as 5/8 lb of the two-grooved milkvetch has been fatal to sheep within 30 minutes.
Signs of Poisoning—Three basic syndromes can develop from eating toxic quantities of selenium. These syndromes are determined by the level of selenium concentration of the plant, the amount ingested, and the time over which the poisoning takes place. The first type of poisoning is acute, while the latter two are more or less chronic.
Acute selenium poisoning appears to be caused by eating a large single dose. Animals suffering from this type of poisoning can be recognized by their uncertain gait, lowered head and drooped ears, diarrhea, increased urination, bloating accompanied by abdominal pain, rise in temperature, rapid weak pulse, labored breathing and dilated pupils. Death from respiratory failure occurs after complete prostration and apparent unconsciousness. These signs generally appear within a few hours to a couple of days after ingestion. Widespread damage (hemorrhage, congestion, tissue degeneration and necrosis) to the heart, lungs, kidneys, liver, spleen and digestive tract also result from this type of poisoning.
Chronic poisoning occurs in two forms. The more pronounced case, commonly referred to as blind staggers, results from livestock grazing plants with moderate selenium concentrations (up to 200 parts per million) for 1 to 2 weeks. It is characterized by excitement; animals wandering aimlessly, failing to distinguish fences or other immobile objects; and inactivation of the digestive tract, giving animals a depraved appetite and causing them to chew on fence rails, pieces of bone or metallic objects. These signs may be followed by paralysis, weakness, difficult breathing and death through respiratory failure.
The second, and most chronic, situation results from livestock grazing plants with lower selenium concentrations (5 to 40 parts per million) ingested over a period of a month or more. This case is sometimes, inappropriately, referred to as alkali disease. It is characterized by dullness, emaciation, deformed hooves and severe lameness. Hooves may become so severely deformed and bent forward that affected animals are unable to obtain adequate food or water. Death from starvation or thirst is not uncommon.
Internal lesions are similar in both the chronic syndromes. They are characterized by marked degeneration of the body organs and erosion of the contact surfaces of the long bones. In severe cases, bone marrow becomes gelatinous.
Conditions of Poisoning—Species within this group are always found growing on soils containing selenium, so they are considered indicator plants of these soils. Livestock generally find these plants quite unpalatable, and will eat them only when forced to by the lack of more preferred forage. Selenium, when incorporated into these plants, gives them a garlic odor and is directly responsible for their lack of palatability.
In the process of incorporating selenium into plant tissues, the selenium-accumulating Astragalus species change selenium to an organic compound that is more readily absorbed by other toxic and non-toxic species. When these converter plants drop their leaves, or die and decay, there is a build-up of readily absorbable selenium in the area around these plants. Many normally good forage species like western wheatgrass (Agropyron smithii), blue grama (Bouteloua gracilis), and winter fat (Ceratoides lanata), when growing in conjunction with these converters, may also contain toxic quantities of selenium. Consequently, these latter species may also become a major concern of the livestock operator.
II. Loco—The following species of Astragalus are known to cause locoism in livestock:
Specklepod loco (A. lentiginosus)
White point (Oxytropis sericea)
Purple point loco (O. lambertii)
Two-grooved milkvetch (A. bisulcatus)
Earle’s loco (A. earlei)
Woolly loco (A. mollissimus)
Sheep loco (A. Nothoxys)
Wooton loco (A. wootonii)
Silverline loco (A. tephrodes)
Distribution and Habitat—These species are most common on plains and foothills.
Classes of Livestock Affected—All classes, especially horses.
Poisonous Principle and Toxicity—The indolizidine alkaloids swainsonine and swainsonine N-oxide have been identified in Astragalus lentiginosus, and cause locoism in animals.
The indolizidine alkaloid swainsonine inhibits the lysosomal enzyme α-mannosidase, which is an essential enzyme in the cellular metabolism of oligosaccharides. With the inhibition of α-mannosidase, mannose-rich oligosaccharides begin to accumulate in lysosomes and cause increasing disruption of cellular function. This cellular damage impairs function of the brain, liver, digestive organs, placenta, and the testicles and accounts for the various clinical signs evident in animals poisoned with locoweed. In the early stages of locoism, cell damage is reversible, but permanent cellular damage occurs as animals eat locoweeds for long periods.
A factor that enhances permanence of lesions is that animals appear to become addicted to locoweeds, selectively seeking the plants when grazing.
Signs of Poisoning—Classic neurologic signs appear in animals that have consumed locoweeds for several weeks to months. Locoism in horses, sheep and cattle is variable in onset and severity but is often characterized by incoordination, visual impairment, depression, unpredictable behavior, emaciation and eventual death. Horses in particular appear to become addicted to the plant; the addiction extends to subsequent growing seasons, so clinical signs often progressively worsen in successive years. Impaired function of the liver, the pancreas and the thyroid and parathyroid glands contributes to weight loss of so-called locoed animals. Decreased tear secretion and damage of retinal cells accounts for the impaired vision evident in some affected animals. Horses with chronic locoism rarely recover sufficiently to be used for riding.
Abortions and congenital deformities of the limbs occur in sheep poisoned with locoweed. Further reproductive failure occurs as a result of rams having damaged testicular cells. Limb deformities in foals born to mares eating locoweed also have been reported.
Experimental feeding of locoweed to sheep produces immunosuppression, which might account for the increased incidence of such infections as pneumonia, foot rot and keratoconjunctivitis in animals exposed to locoweed.
Locoweed poisoning also is associated with an increased incidence of failure of the right side of the heart in cattle grazing Oxytropis sericea at high altitudes. Damage to pulmonary tissue might predispose cattle to this failure (high mountain disease). Indolizidine alkaloids of locoweeds are passed in the milk of cows and will induce cytoplasmic vacuolation in calves; this may account for unthriftiness of calves suckling cows that are grazing locoweed.
Various hematologic changes occur in locoweed poisoning that reflect generalized cellular damage. Liver enzymes are often elevated because of hepatocellular damage.
Conditions of Poisoning—Livestock that have never grazed locoweed find it unpalatable and will avoid it if other more palatable forage is available. However, once livestock have grazed locoweed, they often become addicted to it and will seek it out. Unless these animals are moved to areas that do not support locoweed, or to holding pens, they will continue to graze it until they become locoed and die. Animals are more susceptible to loco poisoning after they have once been addicted.
Locoweed is poisonous at all stages of growth and throughout the entire year, even after it has matured and dried. All plant parts are toxic. Greatest losses generally occur in spring when little other succulent forage is available. The poisoning hazard is less in late spring through fall because other more palatable forage is present. Because loco plants remain green through late fall into winter, they again may receive considerable use, especially by horses. Locoweed poisoning is one of the most common types of poisoning in the state.
Loco is Spanish for crazy, and as can be noted from the Signs of Poisoning, locoism adversely affects the animal’s judgment, vision and nerves. It is common for a locoed horse to jump a small crack and then step into a large ditch.
Treatment—Successful recovery from locoweed poisoning depends on recognizing the disease early and preventing animals from eating more of the plants. Mild cases generally resolve in 1 to 2 weeks. Animals with chronic locoism, in which clinical signs are present for some time, do not recover. There is some indication that reserpine might be helpful in relieving the clinical signs of locoism in horses; however, severely locoed horses remain a liability because of behavioral changes that tend to be permanent.
Animals will generally not eat toxic quantities of locoweeds if other good forages are available. Because locoweeds emerge early in the spring when other plants might be scarce, however, the animals’ feed should be supplemented until normal forages are available.
III. Nitro Compound—Astragalus species in this category include:
Timber milkvetch (A. miser, A. convallarius, A. campestris)
Red-stemmed peavine (A. emoryanus)
Distribution and Habitat—Scattered throughout the state on dry hillsides to moist timbered slopes and well-drained alpine meadows.
Classes of Livestock Affected—Although all classes are somewhat susceptible, cattle, especially lactating females, are most vulnerable.
Poisonous Principle and Toxicity—Recent research has isolated 3-nitro propanol (miserotoxin) as the acute toxic material. Two pounds of green timber milkvetch may kill a 1,000-lb cow. In acute cases of poisoning, the cow generally dies within 1 to 4 hrs after ingestion of the plant.
Signs of Poisoning—This disease may either be chronic, lasting from several months to several years, or it may be acute, with death following ingestion within a few hours. Common Signs of Poisoning include nervousness, emaciation, weakness, a depraved appetite, impaired vision, frequent urination, and incoordination of the hind legs causing cattle to knock their heels together in walking (cracker-heel disease). In fatal cases, cause of death is usually heart failure or respiratory paralysis. Sheep and horses exhibit signs similar to cattle, but their reactions are more acute. Common lesions include an enlarged and flabby heart with thin walls, and congestion of the liver, spleen, lungs and various parts of the digestive tract.
Conditions of Poisoning—Most losses from timber milkvetch occur near mid-summer at about its late-flowering stage. This corresponds to the season when many of the better range plants have dried up and become less palatable. Conversely, red-stemmed peavine causes poisoning during spring before other plants have greened up. The toxicity drops rapidly after seed scatter and following this period it is unlikely animals will be poisoned. While the leaves are the most concentrated area of poison, lesser quantities are also present in the roots, flowers and seeds.
In the case of cattle and sheep, lactating females are by far the group most susceptible to poisoning. Although the death rate in horses is low, recovery allows only minimal usage. Livestock unfamiliar with these plants are more susceptible to poisoning than are animals that have previously grazed them. Poisoned stock tends to build up a partial immunity.
Anderson’s larkspur (Delphinium andersonii)
Low larkspur (D. bicolor)
Nelson’s larkspur (D. nelsoni, D. nutallianum)
Description—Low-growing, perennial forbs, stems 6 to 24 inches tall, somewhat fine-hairy. Leaves few, mostly basal, originating from a cluster of roots; up to 2 inches in diameter, round in outline, deeply divided into a number of linear segments. Flowers showy, up to 1 inch across, blue to purple, with a long (1/2 to 3/4 inch) spur at the bottom; few to 15 on short stalks along the main flowering stem.
Distribution and Habitat—Common throughout the state’s mountain meadows and valleys that are dry to moderately moist, at elevations to 10,500 ft. Low larkspurs are often found growing abundantly in the same areas with death camas.
Classes of Livestock Affected—Cattle, horses and sheep, listed in order of decreasing susceptibility. Although sheep are not commonly poisoned, they are somewhat susceptible.
Poisonous Principle and Toxicity—Delphinine and other closely related alkaloids are the source of toxicity. Although the toxicity under natural conditions depends on several factors, the lethal dosage ranges between 0.5 and 3% of the animal’s body weight (5–30 lb for a 1,000-lb animal).
Signs of Poisoning—Nervousness, stiffness, staggering and falling. The front legs frequently give way and the animal falls and may kick convulsively in attempts to rise. Nausea, excessive salivation, and frequent swallowing. Bloating is common but not always present. Death results from respiratory failure, and the heart continues to beat for a short time after breathing stops.
Conditions of Poisoning—Low larkspur grows in early spring, and its youngest growth is most poisonous; therefore, spring is the season of greatest danger from poisoning. Because cattle will feed on larkspur even when good forage is available, losses in heavily infested areas can be reduced by keeping cattle off these ranges until after plants have flowered.
It is doubtful whether all larkspur species are poisonous under range conditions. However, it is wise to treat them all with caution.
Description—Large, erect, perennial forb, 3 to 7 ft tall. Stems straw-colored, darkening near the base; originating from a deep woody rootstock. Leaves broad, divided into deep lobes. Flowers whitish to blue, densely bunched together on the upper part of the stems.
Sticky geranium (Geranium viscosissinium) and tall larkspur may be confused in their early growth. The stems of tall larkspur are hollow, while those of geranium are solid. Also, geranium’s leaves are shallow lobed and have sticky hairs covering the leaves and stems, while tall larkspur has deeper lobed leaves and smooth stems and leaves. In flower, Columbia monkshood (Aconitum columbianum) looks like tall larkspur, but lacks a spur on the flower and has a solid stem.
Distribution and Habitat—Widely distributed around the state in rich, moderately moist soils in half-shaded localities, especially on slopes of foothills and mountains and among underbrush of streams. It is found in valleys and at elevations to 9,000 ft.
Classes of Livestock Affected—Cattle are most susceptible, horses are occasionally poisoned, and sheep are seldom affected by this plant.
Poisonous Principle and Toxicity—Delphinine and other closely related alkaloids. The lethal dosage ranges between 0.5 and 3% of body weight (5–30 lb for a 1,000-lb animal).
Signs of Poisoning—Nervousness, stiffness, staggering and falling. The front legs frequently give way and the animal falls and may kick convulsively in attempts to rise. Nausea, excessive salivation and frequent swallowing. Bloating is common but not always present. Death results from respiratory failure, and the heart continues to beat for a short time after breathing stops.
Conditions of Poisoning—Poisoning from tall larkspur is most prevalent in its flowering stage. Although overall toxicity decreases with maturity, the seeds remain toxic. The occurrence of late spring and early fall snow storms covering up more desirable associated species increases the chances of tall larkspur poisoning. While cattle are susceptible to larkspur poisoning, sheep and horses are only occasionally poisoned from larkspur, and may safely graze infested ranges. Cattle often will feed on tall larkspur, even when grazing ranges that offer plenty of good forage.
Silvery lupine (Lupinus argenteus)
Velvet lupine (L. leucophylius)
Silky lupine (L. sericeus)
Description—Perennial herbs, 1/2 to 3 ft tall, originating from a taproot. Leaves palmately compound, divided into five to seven finger-like leaflets. Flowers blue, occasionally white, pink, yellow or blue-and-white, found in loose clusters around the upper stalks. Fruit a pea-like pod, 2- to 12-seeded.
Distribution and Habitat—Abundant throughout New Mexico on mountain slopes, valleys and plains.
Classes of Animals Affected—Sheep, and only rarely cattle and horses.
Poisonous Principle and Toxicity—Lupinine and several other alkaloids. Sheep have died from eating as few seed pods and seeds as 1/2 to 1 1/2 percent of their body weight (1/2 to 1 1/2 lb for a 100-lb sheep). It takes 7 to 24 lb of lupine per 100 lb of body weight to poison horses. Cattle fed 1 1/2 lb of lupine per day during the breeding season have given birth to calves with crooked legs and with other congenital deformities.
Signs of Poisoning—Consuming lethal quantities results in loss of condition, a rough dry coat, excitement, animals running about and butting into other animals and objects, difficult breathing, trembling, frothing at the mouth, depression, convulsions, and coma followed by death. Ingestion of sublethal quantities by pregnant cows may result in the birth of calves having marked congenital deformities. This syndrome, known as crooked calf disease, is characterized by malformation of the forelimbs, neck and back, and in some instances a cleft palate.
Conditions of Poisoning—Almost all losses occur when animals consume large quantities of mature (podded) lupine over a short time. Common cases include moving hungry animals through areas supporting dense stands of lupine, and not allowing them time to practice selective grazing; unloading or bedding animals down in lupine-infested areas; grazing animals on areas where other, more palatable species are grazed out and lupine is the only green vegetation available; feeding hay that contains podded lupine; and grazing animals on areas where early snow has covered most of the shorter vegetation, leaving lupine pods projecting above the snow. Most cases of serious losses occur in fall when these conditions are most probable
Incidence of newborn calves suffering from crooked calf disease is spotty geographically and from year to year, within a given herd, varying from less than 1 up to 100% of the calf crop. It is not correlated with heredity or breeds, but in some areas it is always associated with early calves and may be controlled by delaying breeding. The most dangerous period for malformation occurs between the 40th and 70th day of gestation, although slight to moderate malformation may occur when lupine is fed to cows before and after this period.
Description—Mesquite is a deciduous shrub or tree, usually with several trunks. The branches are arching and irregularly bent, with paired large woody spines at the leaf axils. Leaves are bipinnate and linear. Leaflets are linear, about 1 inch long. Inflorescence is a catkin-like spike,
1 1/2 to 2 1/2 inch long. Flowers are small, numerous and leguminous. Fruit is a leathery legume pod or bean, 2 to 6 inches long. Seeds are brown or reddish brown.
Distribution and Habitat—Mesquite is common throughout the southern half of New Mexico. It is a predominate plant on many dry southern ranges, and is a serious competitor with forage plants.
Classes of Livestock Affected—Cattle are the primary livestock affected by mesquite.
Poisonous Principle and Toxicity—Ingestion of large amounts of mesquite by cattle over an extended period of time results in rumen stasis and impaction with associated symptoms and eventually death. The biochemical pathology is not fully understood. Animals develop a liking or craving for mesquite beans, and will consume nothing but mesquite beans when so addicted.
Signs of Poisoning—Symptoms appear only after several months on a mesquite diet, during which the animal may gain weight. Symptoms consist of profuse, foamy salivation, continuous chewing, eventual rumen stasis and emaciation. The disease is characterized in many animals by abnormalities in the use of jaw and tongue and stance, the tongue protruding between the lips. As animals become increasingly poisoned, frequency of eructation is decreased and eventually it ceases. Terminal stages may be characterized by nervousness and muscular tremors, especially about the head.
Conditions of Poisoning—Losses occur in areas where large bean crops are produced each year and other forages are relatively sparse. Thus, ingestion of relatively large amounts of mesquite beans can occur over a period of many months.
Plains milkweed (Asclepias pundla)
Showy milkweed (A. speciosa)
Whorled milkweed (A. verticillata)
Description—Erect, perennial, highly variable herbs, up to 4 ft tall, usually with milky juice. Leaves few to many, narrow (1/8 inch wide) to broad (greater than 2 inches wide); arising along the stem singly, in pairs, or in groups of up to six. Flowers whitish to purple, grouped together in dense, many-flowered umbrella-like heads at the top of the stem or leaf axils.
Distribution and Habitat—Scattered throughout the state in dry to moist soils, along stream banks and in moist meadows to dry plains.
Classes of Livestock Affected—All classes susceptible, but most frequently affecting sheep.
Poisonous Principle and Toxicity—A resinoid compound (most important), several glycosides and an alkaloid. Lethal levels for milkweed range from 0.2 to 2% of an animal’s body weight (0.2–2 lb for a 100-lb sheep) of green plant tissue.
Signs of Poisoning—Depression, muscular weakness, disturbed equilibrium, increased salivation, bloating, difficult breathing, dilated pupils, rapid and weak pulse, and coma followed by death from respiratory failure. Signs appear within a few hours after ingestion of a toxic dose, and death generally follows within one to a few days.
Conditions of Poisoning—Milkweed is unpalatable to all Classes of Livestock. Losses occur only when animals are forced to eat these plants because better feed is not available, or when mixed in hay. Many losses result from hungry animals being concentrated around milkweed-infested corrals, bed-grounds and driveways. Although milkweed is potentially poisonous at all seasons, it is most dangerous during the active growth season. It is likely that all members of the genus Asclepias have some degree of toxicity.
Description—Pigweed is a herbaceous summer annual varying in height from 1 to 6 ft, depending upon growing conditions. The leaves are alternate and somewhat diamond-shaped in outline. The flowers are small and separated into male and female flowers. They form long clusters in the axils between the leaves and the main stems and at the ends of the stems.
Distribution and Habitat—Pigweed is common throughout the state and is particularly abundant along river bottoms, drainage ways and in irrigated fields. Plants flower throughout the summer months and are a main cause of hay fever in humans.
Classes of Livestock Affected—Cattle and sheep are more affected by pigweed toxicity than are horses.
Poisonous Principle and Toxicity—The poisonous principle is nitrate. Pigweed, under favorable growth conditions, will store high concentrations of nitrate.
Signs of Poisoning—Nitrate poisoning symptoms produced by pigweed are typical, but frequently complicated by the concurrent development of bloat. Care of poisoned animals should include treatment for bloat as well as for nitrate toxicity.
Conditions of Poisoning—Pigweed is relished by livestock, particularly during early growth stages. It is most dangerous immediately following significant environmental changes, but poisonings have occurred during all growth stages under a variety of conditions. The nitrate content of pigweed usually is significantly higher in a sample collected in the morning compared to afternoon samples. Known areas of pigweed should be avoided by livestock during the early growth stages, and following periods of sudden temperature changes as occur in fall in New Mexico. Pigweed may remain dangerous in hay and in silage.
Description—Pingue is a small perennial half shrub growing up to 1 ft high from a thick woody taproot. Numerous stems arise from the woody base, which is covered with tufts of white cottony hair. Pingue has bright yellow flowers in flat-topped clusters. The leaves are divided into three to five narrow lobes and are dotted with glands.
Distribution and Habitat—Pingue is found primarily in the piñon–juniper and ponderosa pine zones of northern and western New Mexico.
Classes of Livestock Affected—Pingue is most poisonous to sheep, although cattle and goats also are affected.
Poisonous Principle and Toxicity—The toxic principle of pingue has recently been determined to be a sesquiturpine lactone. These lactones are highly irritating to the nose, eyes and gastrointestinal tract.
Signs of Poisoning—Symptoms include a loss of appetite, abdominal pain, cessation of rumination, depression, bloating, frothing at the mouth, and a greenish discharge from the nose. Poisoned animals often lag behind the flock and may stand with an arched back. Post-mortem lesions include congestion of lungs and intestinal tract, hemorrhages of the heart, and fatty degeneration of the liver.
Conditions of Poisoning—The plant is more often a problem in spring and fall, and all parts of the plant are poisonous. There is no specific treatment for pingue-poisoned animals, therefore, prevention through range management and livestock husbandry is the best approach. Livestock should be kept away from pingue-infested areas.
Ponderosa Pine, Western Yellow Pine
Description—Large erect tree 50 to 150 ft tall, up to 6 ft in diameter. Bark on young trees brown to black, deeply furrowed, on older trees yellow-brown to cinnamon red, 2 to 4 inches thick, broken into large flat plates. Needles grouped together in bunches of three (sometimes two), 2 1/2 to 8 inches long, in tufts at ends of branches. Cones bright green, becoming reddish brown when older, 2 to 4 inches long, 1 to 2 inches thick before opening.
Distribution and Habitat—Widespread throughout the mountains of New Mexico at elevations between 7,000 and 9,000 ft.
Classes of Livestock Affected—Cattle, and possibly all other classes.
Signs of Poisoning—Cows consuming toxic quantities of pine needles appear normal up to the time of the abortion, which is characterized by weak parturition contractions, excessive uterine hemorrhage, incomplete dilation of the cervix and a nauseating odor. A retained placenta usually requires manual removal and is characteristic of those cows affected. The mortality rate of these cattle is high if they do not receive supportive treatment. Most deaths are probably by secondary complications. In several instances, where cows have been examined after aborting, severe liver damage has been found. Calves born alive from poisoned cows are often weak and soon die.
Conditions of Poisoning—Abortions resulting from eating pine needles occur in the latter part of pregnancy. The most common seasons include late fall, winter and early spring when animals may be deficient in vitamin A and desirous of green plant material. Because of the resinous taste, animals seldom eat toxic quantities unless forced to do so through a lack of other more preferred forage. Severe losses (abortions) have occurred after winter storms that leave fallen ponderosa pine trees available to hungry cattle.
Description—Coarse, herbaceous perennial originating from a stout woody taproot. Stems erect, thick, woody towards the base, 1 1/2 to 5 ft tall. Leaves variable, pale green, somewhat thickened and fleshy, lower usually pinnately compound, 2 to 8 inches long, upper becoming smaller, attached directly to the stem. Flowers numerous, yellow, attached directly onto the upper 1/2 to 1 1/2 ft of stem, conspicuous above the foliage part of the plant. Fruit is slender pod, 1/16 to 1/8 inch diameter, 1 to 3 inches long.
Distribution and Habitat—Sparsely scattered around the state on dry grasslands or shrublands with soils high in selenium.
Classes of Livestock Affected—All classes.
Poisonous Principle and Toxicity—Selenium, which may be in high or low concentrations. Actual concentration determines the toxicity of the plant.
Signs of Poisoning—Refer to the selenium toxicity section for locoweeds.
Conditions of Poisoning—Prince’s plume grows only on soils high in selenium, and is often used as an indicator of high selenium bearing soils. The plant absorbs small amounts of selenium from the soil and accumulates it in sufficient amounts to kill livestock feeding on the plant material. Often several nonpoisonous plants, such as western wheatgrass (Agropyron smithii), winterfat, (Ceratoides lanata) and Nuttall saltbush (Atriplex nuttallii), when growing in association with prince’s plume, also contain toxic levels of selenium.
Although prince’s plume is poisonous at all times, and only small amounts are required to cause poisoning, animals will usually find it so unpalatable that they will only eat it when forced to by near starvation conditions. On good condition range where more palatable species are abundant, there is little danger of losses by this species.
(Nolina microcarpa, N. texana)
Description—Sachahuista or beargrasses are perennials with thick woody basal stems. The numerous long, narrow leaves with finely toothed margins arise from a short basal stem giving the plant the appearance of a course bunch grass 2 to 3 ft tall. The small white to greenish flowers appear in May and June and are in dense, elongated clusters on stalks extending above the leaves. The fruit is a dry, three-part capsule containing plump seeds in separate cells.
Distribution and Habitat—The beargrasses are largely restricted to the southern one-third of the state, and found on hills and mountainsides at elevations from 3,000 to 7,000 ft.
Classes of Livestock Affected—Cattle, sheep and goats may be poisoned, but goats and sheep are most susceptible.
Poisonous Principle and Toxicity—The poisonous principle is sapogenin; it is found mainly in the flower buds, flowers and fruits. The evergreen leaves are usually grazed without ill effects, and are even considered desirable forage for cattle in times of drought. However, excessive grazing of the plant can cause photosensitization. The minimum toxic dose for sheep is about 1.1% of the animal’s weight of buds or blooms.
Signs of Poisoning—Symptoms appear several days after the first feeding. Poisoned animals show signs of jaundice, loss of appetite and progressive weakness. Animals that develop severe jaundice usually die. Less severely poisoned animals, and those in the early stages of poisoning, usually recover if they are removed from the pasture and given feed and water. Other symptoms include a yellow nasal discharge, yellow or red urine, yellow-brown liver with greenish plugs in the ducts, greenish kidneys, appearance of a purplish band above the hoof, and photosensitization evidenced by itching skin and swollen face and ears.
Conditions of Poisoning—Animals relish the flower stalks in spring when other forage plants are lacking. The best control is to remove the animals from the heavily infested pastures for a short period during the flowering and early fruiting stake when the stalks are succulent and palatable.
Shinnery Oak, Gambel Oak
(Quercus harvardii, Quercus gambelii)
Description—Gambel oak and shinnery oak are deciduous shrubs or small trees of the beech family. The 3- to 6-inch leaves of gambel oak are deeply cut into long lobes. Shinnery oak leaves are not deeply cut into lobes. Male flowers hang in clusters; female flowers are solitary. Fruit is an acorn.
Distribution and Habitat—Gambel oak plants are found throughout the mountainous regions of New Mexico at elevations from 5,000 to 8,000 ft, often in thickets. Shinnery oak is found predominantly in the eastern one-third of New Mexico and is most prevalent in sandy areas.
Classes of Livestock Affected—Oaks have caused extensive losses of cattle, horses, sheep and goats.
Poisonous Principle and Toxicity—Oaks contain tannic acid and possibly other toxins. Toxicity of oak is low and losses usually occur only when oak is eaten almost exclusively. Where oak consumption makes up less than 50% of the diet, it is usually harmless.
Signs of Poisoning—Symptoms include impaction of the rumen, constipation, gaunt appearance, rough coat, dry muzzle, abdominal pain, excessive thirst and frequent urination. At first, cattle pass small amount of hard, brownish black, pelleted feces, which later changes to diarrhea containing blood and mucous. Watery swellings may occur in the upper side of the body. Pulse becomes rapid, but fever is absent. Symptoms usually last 3 to 10 days, but death may occur within 24 hours. Death occurs in more than 85% of the cases, if effective treatment is not given. Poisoned animals should be removed from the oaks, given a laxative, and fed alfalfa hay or similar forage.
Conditions of Poisoning—Occasional poisoning can occur anytime, but most losses occur during a 30-day spring period when buds and immature leaves are relished by livestock, and other feed is scarce. Freezing of young leaves in this period may increase their normal toxicity. Poisoning from acorns is common in Europe, but not in America. Several oak species cause poisoning, but in New Mexico, shinnery oak is the most serious threat, mainly in areas where stands become dense. Losses can be prevented by deferring oak ranges during the period of high palatability in spring until other feed becomes plentiful, or by supplemental feeding of at least 3 lb of alfalfa hay per day during the danger period. A high-protein feed containing hydrated lime can prevent or minimize tannic acid poisoning. The treatment is a preventive and not an antidote, and it is critical that livestock be on the feed before heavy consumption of oak. Once tannic acid has damaged their organs, it is too late. A ration formula calling for 1,040 lb of cottonseed meal, 600 lb of dehydrated alfalfa, 160 lb of vegetable oil and 200 lb of hydrated lime has proven effective in preventing oak leaf poisoning.
Skunk Cabbage, False Hellebore
California false hellebore (Veratrum californicum)
Green false hellebore (V. viride)
Description—Large, coarse, erect, perennial herb, 2 to 6 ft tall. Stems stout, hairy; arising from thick, short rootstalks. Leaves broad, prominently veined, 4 to 12 inches long and 3 to 8 inches wide; basal leaves oval, becoming lance-shaped above. Flowers numerous, white to greenish, loosely to densely bunched along the main stem.
Distribution and Habitat—Western part of the state on wet ground at moderate altitudes. Commonly found on stock driveways in the foothills and mountains as a result of disturbance.
Classes of Livestock Affected—Primarily sheep, although other classes sometimes are affected.
Poisonous Principle and Toxicity—Numerous complex alkaloids. Sheep have shown Signs of Poisoning after eating 6 to 12 oz of green stems or leaves.
Signs of Poisoning—Excessive salivation, vomiting, muscular weakness resulting in general paralysis, muscular tremors and spasms; fast, irregular heart beat; slow, shallow breathing; convulsions; coma followed by asphyxia. A lethal dose will cause death in 3 to 10 hrs after eating the plant.
Pregnant ewes that eat false hellebore during the second or third week after conception may produce lambs with a congenital malformation referred to as monkey face. Many lambs are born with only one central eye. In severe cases, the eyes and nose are entirely lacking, and the upper division of the brain is imperfectly formed.
Monkey-face lambs carried the full term are usually born alive, but soon die because they cannot breath and feed properly. Ewes carrying severely deformed fetuses may fail to lamb at the end of the normal term In these cases, the fetus either continues to grow to an abnormal size or dies within the uterus. In either case, the fetus must be removed to save the ewe.
Conditions of Poisoning—Because of its sharp, burning taste false hellebore is not eaten in normal grazing situations. Most losses occur when animals are forced to eat it, either by being held on a range lacking more preferred species, or by not being allowed to practice selective grazing while being herded through dense stands. Human poisoning has resulted from using the leaves of false hellebore for plates while camping and picnicking, and eating them along with the food.
Description—Sleepygrass is a stout perennial grass forming erect clumps mostly 2 to 4 ft tall. Leaves are flat, 5/16 inches wide, up to 2 ft long. Inflorescence is a green or greenish yellow terminal panicle, up to 1 ft long; spikelets are narrow, about 1/2 inch long, tipped by a long, dry, twisted awn about 1 inch long.
Distribution and Habitat—Sleepygrass grows primarily in the ponderosa pine zones in the mountains of the state.
Classes of Livestock Affected—In the past, horses were the class of livestock of greatest concern; sleepygrass in now mainly a problem of cattle. Sheep are not affected as severely as are cattle and horses.
Poisonous Principle and Toxicity—The narcotic-like substance is diacetone alcohol. The soporific effects may be caused by acetone, a known depressant, released in the digestive tract. Cows fed sleepygrass have been observed in a position similar to that seen in ketosis or acetonemia. The least toxic dose for a horse is 0.6% of the animal’s weight; 1% of the body weight is the average effective single dose.
Signs of Poisoning—Symptoms appear within 6 to 24 hrs and last 24 to 48 hours. Sleepygrass has an interesting effect on animals. Ingestion of a moderate, but nonlethal, amount of the grass induces a profound stuporous condition that can last several days. When the horse was the principle means of travel, considerable inconvenience and sometimes danger occurred when animals ate the plant. Horse traders sometimes fed sleepygrass to wild horses and sold them as halter broken. Mildly poisoned animals are dejected, inactive and withdrawn. With a large dose, they become sleepy, with a drooping head, closed eyes, and irregularity of gait if forced to move. They slobber copiously and may urinate frequently, even while lying down. Severely poisoned animals lie flat on their side with their head on the ground. They are in profound slumber and can be wakened only momentarily. Animals may freeze in one position with a hoof raised and remain absolutely motionless, oblivious to pestering flies, for as long as 45 minutes.
Conditions of Poisoning—Sleepygrass is not palatable and is eaten only when other forage is lacking. In general, livestock will not eat the plant again after a bout of sleepygrass poisoning.
White Sweetclover (Melilotus alba)
Yellow sweetclover (M. officinalis)
Description—Highly branched herb, 2 to 6 ft tall. Stems robust, erect, sparsely hairy. Leaves divided into three finely toothed ovoid leaflets. Flowers white or yellow, about 1/4 inch long, pea-like, borne in slender clusters arising from the axils of the leaves. Fruit a pod, egg-shaped, one—(usually) to four-seeded.
Distribution and Habitat—Introduced from Eurasia, but now abundant throughout the state in fields, roadsides and waste places; found in a wide range of soil and moisture conditions.
Classes of Livestock Affected—Cattle, although other Classes of Livestock are mildly susceptible.
Poisonous Principle and Toxicity—Dicoumarin, a toxic product synthesized from coumarin in molded hay or silage. Large amounts of molded sweetclover are required to produce Signs of Poisoning. Moderately toxic sweetclover hay will produce signs in from 3 to 8 weeks, the average being about a month.
Signs of Poisoning—Common signs include marked swellings on any part of the body, although most common on either side of the vertebral column, shoulders, thighs, neck and chest areas. These swellings may reach several feet in circumference, protruding as much as 10 to 12 inches. The visible membranes may turn pale, while the animal becomes dull and stiff. The pulse becomes fast and weak just before death without struggle.
Examination of the dead animal reveals hemorrhages in almost all tissues within the body. Animals suffering from the disease may bleed to death from small wounds or minor operations such as dehorning and castration.
Conditions of Poisoning—Losses from sweetclover poisoning generally occur in the winter, after being eaten for at least 2 weeks. Only damaged or spoiled sweetclover hay or silage is toxic. The damaged hay is generally moldy, although not all moldy hay is toxic. The mold may not be readily visible because the fungus is in the stalk cavities.
Upon molding, the normally harmless substance coumarin is synthesized to form the toxic product dicoumarin. This latter substance interferes with blood clotting by depressing the prothrombin level, which is essential for coagulation. Although all Classes of Livestock are mildly susceptible, sweetclover poisoning is restricted almost exclusively to cattle. Young animals are more susceptible to poisoning than older ones.
There is no evidence that green sweetclover growing on the range, or properly cured sweetclover hay, is ever toxic. Under these conditions, it provides good forage for all Classes of Livestock. Any questionable hay should be inspected by a qualified individual before feeding. Moldy sweetclover can be safely fed by either alternating (at less than 2 week intervals) or mixing with good quality hay.
Description—Tansy mustard is an annual forb growing up to 2 ft tall. It is usually single-stemmed, leafy throughout, and covered with fine gray hairs. Leaves are alternate and pinnately divided into numerous small segments. Flowers are small, yellow and occur in long clusters at the ends of the stem. Fruits are long, round, slender, two-celled capsules filled with numerous small, waxy seeds.
Distribution and Habitat—Tansy mustard is widely distributed throughout the state up to 7,000 ft in elevation. This annual forb appears to prefer sandy range sites.
Classes of Livestock Affected—Cattle are the only kind of livestock reported to be poisoned by tansy mustard.
Poisonous Principle and Toxicity—The toxin is unknown. Despite similarity of the symptoms to those produced in one type of selenium poisoning, tansy mustard does not contain enough selenium to produce the disease.
Signs of Poisoning—In cattle, the first symptom is a partial or complete blindness. This is followed by an inability to use the tongue or to swallow. The disease is popularly termed paralyzed tongue or wooden tongue. Because of blindness, animals may wander aimlessly until exhausted, or stand pushing against a solid object in their path for hours. Because of the inability to swallow, animals may be observed standing at water unable to drink, or unsuccessfully grazing forage. Animals become thinner and weaker, and will die if not treated.
Treatment is simple and effective. Administer 2 to 3 gallons of water/cottonseed meal slurry twice daily by stomach tube. This gets the digestive system functioning and symptoms gradually disappear.
Conditions of Poisoning—A diet almost entirely of tansy mustard is required before poisoning is evident. The appearance of stands of tansy mustard thick enough to enable such a diet is erratic from year to year. If rainfall during the early winter months is adequate, the plant becomes well established and flowers during February, March or April. It is dangerous during the bloom period and until the pods have matured, when the plants become tough and fibrous. If other feed is scarce, tansy mustard is readily consumed.
Description—Tarbush is a perennial branched leafy shrub, growing from 1 to 6 ft in height. Leaves are alternate, entire, ovate, approximately 1 inch long. Composite flower heads are small, yellow, rayless and inconspicuously borne in the angles of reduced leaves along long terminal inflorescent axes.
Distribution and Habitat—Tarbush is common in southeastern to south-central New Mexico, forming thickets on dry plains, hills and mesas.
Classes of Livestock Affected—Cattle, sheep and goats, as well as pronghorn, have been reported to be poisoned by tarbush.
Poisonous Principle and Toxicity—Experimental forced feeding has indicated the tarbush fruits are toxic, but the foliage in moderate amounts is not poisonous. About 1% of the animal’s body weight in tarbush fruits is toxic. There is considerable variation in individual susceptibility and only a small margin exists between toxic and lethal doses.
Signs of Poisoning—Under range conditions, symptoms appear a day or less after eating a toxic amount of the plant material. Depending on the acuteness of poisoning, death can occur within 24 to 72 hours, or rapid recovery is also possible after an animal has shown symptoms for several days to a week. Symptoms are somewhat modified by the severity of poisoning, but in general are loss of appetite, abdominal pain, reluctance to move and, occasionally, some respiratory distress. In acute cases, salivation may be observed. Animals remain on their feet until shortly before death, which occurs usually without struggle.
Conditions of Poisoning—Tarbush is distasteful and will not be browsed unless livestock are unusually hungry. Range cases are usually traced to conditions of improper management. Tarbush is useful in providing shade for animals on the range in summer and possibly has forage value. Poisonings occur mostly in January, February and March after the fruit has matured (green fruit is not eaten), but before it falls from the plants.
Threadleaf Groundsel, Woolly Groundsel
Riddell’s Groundsel, Broom Groundsel
Description—Woolly groundsel is an erect, branched, woolly white shrubby perennial common on ranges throughout the state. It is leafy throughout and 1–2 ft tall. Leaves are narrow and linear, thick white and occasionally lobed, up to 4 inches long. It has composite heads in numerous terminal clusters and 13 ray flowers approximately 3/8 inch long.
Riddell’s groundsel is a bright green herbaceous perennial, approximately 1 1/2 ft tall. Stems are smooth and leafy above; leaves are thread-like; composite heads are numerous in flat-topped terminal cluster. It has six to eight yellow, 1/2-inch rays per flower.
Distribution and Habitat—Woolly or threadleaf groundsel occurs throughout the state on a variety of soil types and range sites. Riddell’s groundsel occurs primarily in the eastern third of the state and is found predominantly on sandy range sites.
Poisonous Principle and Toxicity—Both groundsel species contain pyrrolizidine alkaloids, which provoke liver lesions. Acute poisoning can result from doses of 1–5% of an animal’s weight, fed at one time or over a few days; this is rare but not unknown under natural conditions. Chronic cases are brought on by smaller daily, but larger total, doses obtained over the course of several weeks or months. In most cases, the amount consumed by cattle and horses before chronic symptoms appear varies between 12% and 15% of animal’s weight, with symptoms appearing in less than a month or not until after 5 months. Variation depends in part on species of Senecio, species of animal, and growth stage of the plant. Cattle and horses are about equally sensitive to the toxic effects. Sheep and goats are more resistant, but have been poisoned experimentally. A dose of 1–4% per day provokes symptoms only after a month. Roughly twice as much is required to poison sheep and goats as cattle and horses.
Signs of Poisoning—In chronic poisoning of horses, symptoms often appear abruptly. The affected animal stands apart, appearing depressed or sluggish and without appetite. Death usually occurs within a week, although some animals linger longer. The animal becomes rapidly worse. Yellow or muddy discoloration of the mucous membranes is observed, and a peculiar sweetish and unpleasant odor emanates from the skin. Weakness, uneasiness, abdominal pain and reduced sensibility occur. Some animals chew fences, mangers and dirt. In some instances, weakness and depression increase and the animal dies quietly; in others, restlessness increases and the animal starts walking aimlessly, not avoiding objects in its path. Animals will lean or push against fences or buildings, and sometimes become frenzied. Chronic poisoning in cattle is similar in most respects. The same peculiar odor has been noted in the milk and from the skin. Poisoned cattle generally display roughened coat and dry, scaly muzzle. Cattle may remain quiet or become agitated or even dangerously aggressive, even attacking automobiles.
Conditions of Poisoning—No Senecio species is palatable to livestock. Woolly groundsel stays green longer and is succulent in winter. Young stages are consumed unselectively with grasses in spring by raising cattle. There is some evidence that young stages of groundsel, particularly young leaves, are the most highly toxic. Poisoning incidence is seasonal, with the most cases occurring in the summer, but individual cases may be found in almost any month.
Description—A stout, erect, branched leafy herb, 2 to 7 ft tall, arising from tuberous, thickened roots. Leaves 4 to 16 inches long, two or three times divided; the final divisions (leaflets) 1 to 4 inches long with saw-toothed edges. Flowers are white, grouped in numerous umbrella-like clusters 2 to 5 inches wide.
Poison hemlock (Conium maculatum) is often confused with water hemlock, but while the former is found on moist areas, the latter is usually semi-aquatic. The leaves of poison hemlock are more finely divided than those of water hemlock, and the leaf veins terminate at the tips of the teeth, while those of water hemlock terminate between the leaf of the teeth. If the base of the stem of water hemlock is cut lengthwise just above the root, many small chambers are visible. This characteristic is not shared by other members of the carrot family.
Distribution and Habitat—Introduced from Europe, and now widely distributed throughout the state. Found in wet meadows, pastures, along streams and ditches.
Classes of Livestock Affected—Principal loss is from cattle, but all classes are susceptible.
Poisonous Principle and Toxicity—Cicutoxin, an extremely poisonous unsaturated alcohol. As little as 2 oz of the young leaves, stems or tubers has killed sheep; 8 to 10 oz will kill cows and horses.
Signs of Poisoning—Excessive salivation, muscular twitching, frothing at the mouth, uneasiness; violent convulsions, involving clamping of jaws and grinding of teeth; evidence of abdominal pain; elevated body temperature; dilation of the pupils; coma; death caused by respiratory paralysis and asphyxia.
Conditions of Poisoning—Most losses occur in early spring before more preferred forage is available. At this time of the year, new growth is highly toxic. Also, the ground is often soft and loose, permitting the roots to be pulled up and eaten along with the tops. The highest concentration of cicutoxin is found in the roots, but it is also present in the leaves and stems during early growth. Leaves and stems lose most of their toxicity as they mature. People are sometimes poisoned by eating water hemlock roots, mistaking the plant for wild parsnip (Pastinaca sativa). Children have been poisoned by simply blowing through the hollow chambers of the base of the plant as they would a reed.
Losses From Causes Other Than Poisonous Plants
Poisonous plants are not the only cause of death and sickness in range livestock. Accidents, killing by predators, lambing and calving losses, and hollow belly syndrome can usually be distinguished from losses caused by poisonous plants. Other losses may be confused with those caused by plant poisoning. Among these are diseases, nutritional disorders, bloat caused by non-poisonous plants, water-borne poisons, poison in feeds, and poisons in things such as paint, oil, herbicides and insecticides. The rancher should investigate all conditions associated with sickness and death of animals so that he can identify the true cause of the trouble.
A veterinarian should be contacted when any type of disease is suspected in the herd. Some diseases may be confused with poisoning by range plants.
Acute Bovine Pulmonary Emphysema—ABPE is a disease of cattle characterized by a sudden onset of acute respiratory distress, shortly after a change in feed or forage. Local terms sometimes used include cow asthma, green grass sickness, summer pneumonia, lungers, grunters, panters and others.
Its occurrence is unpredictable, but occurs most commonly in late summer or early fall, apparently from transferring cattle from dry summer range to lush, improved pastures. Generally speaking, the incidence is increased following exceptionally dry summers.
The disease is more prevalent in cattle over 2 years of age. Symptoms of ABPE become apparent between 2 and 10 days after a change in feed or forage. The most obvious sign is an increased rate of respiration accompanied by severe dyspnea. An audible grunt is commonly observed. Affected cattle stand with the head lowered. As the disease progresses, cattle breathe through the mouth and the tongue protrudes. The animals will generally remain standing because it is easier for them to breathe in that position. It is difficult to predict which animals in an affected herd will die, but large-scale death losses have been reported.
The specific cause of ABPE is the amino acid trytophan and indole acetic acid precursors found in large quantities in lush plants, converted in the rumen to 3-methylindole (3 MI). The 3 MI is rapidly absorbed and converted by the pulmonary cytochrome P-450 enzyme, creating a toxic compound that damages the lung tissue and results in emphysema.
High-Mountain (Brisket) Disease—The term brisket disease is, in many ways, confusing, because it is not a disease of the brisket but one of the circulatory system. Specifically, it is a syndrome of congestive right heart failure. High mountain disease affects animals at 7,000 ft or more elevation. The incidence of the disease in any one herd ranges from zero to 5%, and usually less than 2%. Newly introduced cattle reportedly have a greater incidence than native cattle. The disease occurs primarily in fall, and affects all ages, breeds and sexes of cattle.
The disease is caused by the lowered available oxygen at high elevations, which causes the blood pressure to rise. Brisket disease usually develops slowly. The affected animal is first noted to be depressed and remains apart from the herd. As the disease progresses, edema develops in the brisket region. Marked distention and pulsing of the jugular vein is usually present. Breathing is labored and the animal may appear cyanotic. Animals are reluctant to move, lie down and, when exerted, may collapse and die.
It is essential that affected animals be moved to a lower elevation with minimal stress and excitement, where some will recover spontaneously. Because the disease may recur, recovered animals should not be returned to high altitudes. Because the disease susceptibility is inherited, affected cattle should not be kept for breeding. Bulls should be tested for high blood pressure if they will be used on cows in high elevation ranges. There is a high correlation and incidence of brisket disease on locoweed-infested ranges, which indicates brisket disease may not be totally genetic in origin.
Polioencephalomalacia—Polio or PEM is a non-infectious neurologic disease, primarily of young ruminants. Animals with polio are in a state of thiamine (vitamin B1) depletion. The disease occurs mostly in young cattle on high energy diets, but can occur on native ranges.
Animals with PEM usually have a sudden onset of dullness and lack of appetite, but may not have an elevated temperature. They become blind, wander aimlessly, stand pressing their heads against objects. They may grind their teeth, become dehydrated, lose coordination of their muscles, and twitch various parts such as skin, ears and eyelids. They eventually lie down and can’t get up, with muscle convulsions, become comatose and die within a few hours to days. If down cattle are not treated, the death rate is nearly 100% within 3–4 days. Normally, the number affected in a herd is not high. The symptoms are similar to tansy mustard poisoning, so PEM may not be diagnosed in time to get proper treatment.
The cause of the disease is well known. It is actually a severe deficiency of thiamine (a B vitamin). This is brought about because the thiamine normally produced in the digestive tract has been destroyed by thiaminase. What causes some bacteria that produce thiaminase in large quantities to suddenly proliferate is not fully understood. Generally, in feedlots, the sudden change to a rapidly fermentable carbohydrate diet leads to a change in the rumen population. The disease occurs when high numbers of the bacteria that produce thiaminase (Clostridium sporogenes or Bacillus spp.) proliferate. The excess thiaminase destroys all thiamine before it can be absorbed into the body. The animal is soon deficient in thiamine, which is crucial to energy metabolism. Brain cells are the first to be impacted by the lack of energy and begin to die. Along with the necrosis, there is some swelling in the brain.
PEM on pasture is usually associated with lush pastures, although it has occurred when a change in protein supplement was made. Moldy feed can cause PEM because some types of mold will produce thiaminase. Also, there are some plants with a high level of thiaminase. Bracken fern is one of these. Grazing turnips has been shown to predispose PEM in some cases. Other contributing factors are use of a high sulfate fertilizer or a high content of sulfates in the drinking water. Besides tansy mustard poisoning, there are some chemical poisonings that will give similar symptoms. A veterinarian should be consulted for positive diagnosis.
PEM is a serious emergency because neurons are dying by the millions. To be successful, therapy should begin immediately after the onset of signs. Thiamine hydrochloride, given intravenous and intramuscular at 2-4 mg/kg (cattle) by each route, ensures rapid reactivation of the deficient enzyme complexes. Along with this, there should be a change in diet for all of the animals to prevent further cases. How fast the animals recover depends on how fast the disease was recognized and treatment initiated. Recovery of vision and growth often is possible, but may take 2 to 3 weeks convalescence. Additional thiamine in the diet does not seem to help because it is destroyed almost immediately in the rumen. The main point is to get rapid diagnosis and treatment for affected animals, and change the diet for remaining ones. This may mean switching supplements, changing pastures, adding hay or decreasing the amount of grain.
Pregnancy Toxemia—Also referred to as pregnancy disease, ketosis, acetoanemia or twinning disease because it is most common among ewes carrying twins or triplets. The disease is caused by inadequate energy intake during the last 4 weeks of pregnancy when nearly 2/3 of fetal growth occurs. Symptoms are similar to those of many toxic plant poisons. Ewes begin showing dullness and lagging behind the flock. Animals become unsteady and urinate frequently. There may be a grinding of teeth, and breathing is labored. Vision is impaired and blindness may result. Animals tend to walk in circles or push against solid objects. Finally, the ability to stand is lost and the ewe frequently lies down on her chest with her head turned to one side. Occasionally, the lambs are delivered, in which case the recovery is prompt. Otherwise, the disease is fatal in 1 to 7 days.
Pregnancy toxemia is easier to prevent than to treat. Providing more concentrated sources of nutrients in late gestation is quite helpful. Glycerol or large doses of long-acting glucocorticoids are usual treatments administered by a veterinarian.
Enterotoxemia—Various forms of overeating disease are in the same category. These may occur when sheep are shifted from poor forage to rich feed, and are caused by toxins produced by intestinal bacteria as a response to the rich feed. Affected animals lag behind, stagger, knuckle over on the front legs, and show a depraved appetite. They fall and make futile attempts to rise. Respiration becomes rapid and labored. Salivation and champing of the jaws are common, and bloat may develop. Animals may die in convulsions or enter a coma and die quickly. Vaccination with enterotoxemia vaccine usually prevents losses from this cause.
White Muscle Disease—This disease is caused by an interference with selenium metabolism, or an actual deficiency of selenium or vitamin E in the diet. Affected sheep have usually been grazing on irrigated pastures, and the incidence is much higher on legume pastures.
Symptoms include an arched back and incoordination of the rear legs. The disease is most common in lambs 3 to 8 weeks old. There is a progressive paralysis of the muscles, heart, diaphragm, tongue and esophagus.
A common treatment is an injection of selenium and vitamin E, available only from a veterinarian or by feeding a mineral mix with added selenium. Care should be observed when treating for selenium deficiency because selenium toxicity is just as detrimental as selenium deficiency.
Salt Toxicity—The exact conditions necessary for salt poisoning in livestock are rather obscure. However, it is generally agreed the availability, or lack of, good quality water is the controlling factor.
Salt poisoning occurs when animals are starved for salt, have a restricted water supply, and suddenly have access to loose salt or brine solutions. Cases of salt poisoning have occurred in New Mexico during wet periods when normally dry playa lakes have standing water in them. These waters are often salty and livestock must have other water available. Caution is also advised when feeding salt-limiting protein supplements.
Affected animals show signs of abdominal pain and diarrhea. The oral mucosa is dry and bloody. There is great thirst and dehydration. Frequent urination, paralysis of the hind limbs, general paralysis, and death occur in 6 to 24 hours after ingestion of the salt.
Blue-Green Algae—Blue-green algae of a number of species have caused livestock death in many countries when animals drank algae-infected water. Algae blooms occur in summer and autumn when stock watering ponds are low. Anaerobic bacteria in the bottom mud raise the soluble phosphorus and nitrogen levels, and increase the availability of carbon dioxide. These factors, combined with long days, bright sunlight and warm water, favor proliferation of algae. The algal cells develop gas bubbles, causing the algae colonies to rise to the surface, after which they are blown by wind into dense algal blooms. Among the toxic blue-green algae are Microcystis aeruginosa, Anabaena circinalis and Nodularia spumingena. The toxic principles of blue-green algae are cyclopeptides.
Removal of animals from the toxic water supply is essential. Algal growth may be suppressed with copper sulfate or other algicide, but this does not remove the toxin already in the water. If no other water supply is available, animals should be allowed to drink from the clearest water on the upwind side. Animals dying from algal poisoning must not be used for food because the toxic principle is stable and can be passed on to the consumer.
Moldy Hay or Grain—Moldy hay or grain can produce aflatoxicosis if certain species of molds are involved. In all animals, the first symptoms are loss of appetite, reduced growth rate or loss of condition. Other signs of aflatoxin poisoning are usually not seen until a week or two before death. Advanced stages of aflatoxicosis include jaundice and apathy.
Urea Poisoning—Urea poisoning almost always is a result of improperly mixed feed. Ruminant animals use urea nitrogen to form microbial protein if there is enough energy in the diet for rumen microbes to form proteins. If there is not enough energy, or if the urea feed is not mixed properly, the animal suffers from ammonia toxicity. If diet energy sources are not available in sufficient amounts, or if the animal eats too much urea at once, the excess ammonia generated by breakdown of urea is absorbed by the blood.
Urea poisoning is almost always acute, with symptoms appearing within 30 to 60 minutes. The syndrome is marked by excessive salivation with frothing ataxia, weakness, trembling of muscles, occasional paralysis of the forelegs, bloat, and sometimes severe tetany or strychnine-like convulsions. Breathing is slow, difficult and deep. Gasping is often seen, and grinding of the teeth is almost always noted. Death usually occurs within a matter of hours. Early signs of urea poisoning also include staggering, stretching, frequent urination, and knuckling of the rear fetlocks.
Special Problems and Associated Plants
Ergotism—Ergot poisoning on rangelands is relatively rare in New Mexico. Poisoning results from continued ingestion of a parasitic fungus that infests the seedheads of grains and some range grasses. Several species of range grasses can be infected with ergot, but it is most commonly seen in galleta (Hilatia jamesii) and tobosa (Hilaria mutica) in New Mexico.
Two syndromes are produced in cattle, the gangrenous and convulsive. Relatively large amounts of ergotized feed are involved in each, although daily intake of ergot sclerotia can be small in gangrenous ergotism. Eating as little as 0.02% of the animal’s weight for 11 days has produced gangrenous ergotism in cattle.
Ergot alkaloids constrict the vascular system and reduce circulation in the extremities. Most cases involve one or both hind feet. Symptoms begin with lameness, followed by coldness and insensitivity of the affected area. In more severe cases, tips of tails, ears and tongue can become gangrenous. Typically, a distinct band circles the affected limb between gangrenous and healthy tissues. A crack forms in this area, and continuing constriction causes disjunction of gangrenous from healthy tissue. Often, the horns or switch of the tail will come off if pulled.
Convulsive ergotism in cattle and humans appears to result from ingesting larger amounts of ergot per day. Symptoms appear within 48 hours to a week after animals have access to a heavy infestation. Hyperexcitability is the first sign of convulsive ergotism. This is sometimes accompanied by belligerency and followed by prominent trembling and incoordination. Exaggerated flexure of the forelegs may be observed when the animals are made to run.
Seedheads of range grasses are more apt to become infected with ergot during humid summers. It is worth mentioning that undergrazing, a practice opposite to that usually resulting in plant poisoning of animals, in this instance has the opposite effect. It allows pasture grasses to develop inflorescences and become potentially dangerous.
Prussic Acid—There are a number of plants that, under the proper conditions, produce an excess of the glycoside of hydrocyanic (prussic) acid. Worldwide, about 1,000 plant species in 250 genera are known to release prussic acid (HCN). Many plants that are valuable forage most of the year can accumulate high levels of HCN under specific conditions. Important prussic-acid-producing plants in New Mexico include johnsongrass, sudangrass, mountain mahogany, chokecherry, arrowgrass, milo, cocklebur, and annual goldeneye.
The poisonous properties of these plants depend on what condition they are in. Mature cyanogenic plants are thought to contain less potential HCN than younger plants. Cyanogenic plants made into hay produce less prussic acid than they do as fresh forage. Wilted plants are considered more dangerous than fresh plants because of their high content of preformed prussic acid. Any interference with the normal plant growth, such as frost, drought or trampling, tends to increase the amount of free prussic acid in the plant.
Ruminant animals seem to be more susceptible than nonruminants to HCN poisoning from plants because the rumen microflora and pH encourage greater glycoside breakdown than occurs in nonruminants. Degradative enzymes need not be present in the consumed plant for HCN to be released in the animal. Prussic acid is absorbed directly from the rumen. HCN is a small molecule, and is rapidly absorbed and excreted by several routes. Much is eliminated simply in breathing.
Prussic acid inhibits the action of the enzyme that links atmospheric oxygen with metabolic respiration. Body cells cease to function because they are deprived of oxygen. HCN poisoning causes asphyxiation (oxygen starvation) at the cellular level. In a poisoned animal, venous blood is bright red, like arterial blood, because the oxygen of the arterial blood has not been utilized.
Prussic acid is one of the fastest acting poisons. There is little difference between toxic and lethal HCN levels in the blood. It takes only about 2 milligrams per pound of body weight per hour to kill an animal. Plants containing more than 20 mg per 100 g (0.02%) are considered dangerous.
Animals that have ingested a toxic amount of prussic acid quickly exhibit an increase in the depth and rapidity of breathing. Weakness, tail twitching, and staggering are followed by inability to stand. They may assume a position characteristic of milk fever, that is, lying on the sternum with the neck turned backward and the head resting on a shoulder. In the final stages, the animal usually lies on one side and breathes heavily through an open mouth, and often has respiratory convulsions. Death is usually preceded by a characteristic bellow. Bright red venous blood differentiates this condition from other types of poisoning with similar symptoms.
Sodium nitrate and sodium thiosulfate are specific antidotes for hydrocyanic poisoning. An intravenous injection of 1.2% sodium nitrite and 7.4% sodium thiosulfate solution in a dose of 125 to 250 cc is the best treatment for prussic acid poisoning. If the solution is injected before the heart stops beating, the animal may be saved. Care must be taken to distinguish between nitrate and HCN poisoning because this treatment would cause death if the animal suffered from nitrate poisoning.
Nitrate Poisoning—Although poisoning from the various forms of nitrate is referred to as nitrate poisoning, the nitrate ion itself is relatively nontoxic. In the ruminant, ingested nitrate is broken down to nitrite then undergoes further degradation to ammonia, which is used to form microbial protein. The reduction of nitrate to nitrite occurs much more rapidly in the rumen than the reduction of nitrite to ammonia. Consequently, when ruminants consume plants high in nitrate, excess nitrite formed in the rumen enters the bloodstream where it converts blood hemoglobin to methemoglobin. This greatly reduces the oxygen-carrying capacity of blood, and the animal suffers from starvation of the tissues. Prussic acid also produces death by tissue asphyxiation, but by an entirely different process.
The methemoglobin content of the blood of cattle succumbing to nitrate poisoning may be as high as 80%. Conversion of one-third of the hemoglobin to methemoglobin produces only slight symptoms. Life is still possible when 60% of the hemoglobin has been converted, but death is a certainty when hemoglobin has fallen to one-third normal levels.
Plants containing more than 1.5% nitrate (KN03) are dangerous, and nitrate consumption in amounts of as little as 0.05% of the animal’s weight can be lethal. Losses are most frequently associated with cool temperatures and cloudy days, drought, heavy applications of nitrate fertilizers, and soils characteristically high in nitrogen.
The rate of nitrate formation is slow at soil temperatures below 50° F, but conversion rates increase in direct proportion to increased soil temperatures up to 80–90° F. Nitrate concentration in forages increases greatly during drought conditions.
Low light, such as a cloudy day, causes nitrate accumulation in plants because nitrates accumulated during the night are not dispersed until sunlight hits the plants.
Some plants contain a substance that, under proper conditions, can reduce nitrates to nitrites. This is thought to be the mechanism whereby nitrate poisoning has occurred on previously harmless pastures and hays. Controlled experiments, as well as carefully investigated field cases, have shown that oat hay moistened with water and exposed to air may contain toxic amounts of nitrites in a relatively short time. The reduction of nitrates to nitrites reaches a peak in 18 to 22 hours after the hay or plant material has been moistened. During this time, about 40% of the nitrate is converted to nitrite. This makes toxic amounts of nitrites present where harmless amounts of nitrates previously existed.
Nitrate poisoning acts quickly; therefore, symptoms may not be observed before animals are found dead. Poisoned animals may stand apart from the herd, then collapse, or they may fall in their tracks if driven. Signs of Poisoning, in the usual order of appearance, are weakness and unsteady gait, collapse, shallow and rapid breathing, rapid pulse coma and death the latter accompanied by the usual terminal muscular reflex movements.
Respiratory distress is not as obvious as when associated with choking or pneumonia. The unpigmented parts of the body, such as the white of the eye, the tongue and lips, have a blue-brown discoloration from the onset as a result of methemoglobin circulating in the superficial vessels.
Blood in which at least 10% of the hemoglobin has been converted to methemoglobin is chocolate brown in color. Fatal methemoglobin levels range above 70% of the total hemoglobin, so the color of the blood of a dead animal may indicate poisoning. Even if plant nitrate poisoning is suspected as a cause of death, be cautious in accepting the color of the blood of the dead animal as confirmatory evidence if some time has passed since death. A chemical analysis to determine the presence of methemoglobin, nitrate or nitrite in a blood sample is the most reliable method to determine nitrate poisoning.
Few tissue changes are evident at autopsy after nitrate poisoning. Some inflammation of the respiratory and gastrointestinal tract may be noted, and there may be a few small hemorrhages, particularly in the heart.
Following an abnormal exposure to nitrates or nitrites, a cow may abort a fetus that died because of oxygen starvation. Grazing plants containing borderline levels of nitrate has also been associated with abortion, reduced milk flow, lower weight gains and signs of vitamin A deficiency. (Nitrate is thought to interfere with the conversion of plant carotene to vitamin A.)
Death usually occurs so suddenly that treatment is not possible, and few treated animals recover.
Treatment used to include a methylene blue solution intravenous injection. However, methylene blue is no longer available.
Grass Tetany—Grass tetany, sometimes called grass staggers, wheat-pasture poisoning, lactation tetany and hypomagnesemia, is a metabolic disorder of livestock. It occurs primarily in ruminants, and lactating cows are most susceptible. Older, high-producing cows are more susceptible than younger ones, and cows that are worked or herded may be more susceptible to tetany.
Grass tetany is common during cool, cloudy and rainy weather, and often occurs when cool weather is followed by a warm period. Animals get grass tetany most often while grazing cool-season grasses or small-grain pastures in spring or fall. Rapidly growing, lush grasses are the most dangerous. Grass tetany has occurred on orchardgrass, perennial ryegrass, timothy, tall fescue, crested wheatgrass, bromegrass and winter annuals such as cheatgrass. The small-grain pastures include wheat, oats, barley and rye. Grass tetany also occurs when livestock are wintered on low magnesium grass hay or corn stover. It is not usually a problem on legume pastures or in animals wintered on legume hay.
High rates of nitrogen and potassium fertilizer are sometimes associated with increased grass tetany. Forages should be analyzed when a grass-tetany hazard is suspected. Forage containing less than 0.2% magnesium and more than 3% potassium and 4% nitrogen (25% crude protein) are especially likely to cause tetany. Forage high in potassium and nitrogen should also have at least 0.25% magnesium. When an animal is on high-nitrogen forage, the rumen produces a large amount of ammonia. Under these conditions, dietary magnesium may be converted to the relatively insoluble hydroxide, lowering availability to the animal’s tissues.
The exact mechanism of poisoning is not well understood. A deficiency of serum magnesium is generally associated with tetany, frequently accompanied by a less-marked decrease in serum calcium. Normal levels of blood magnesium are around 2 mg per 100 ml of plasma. If the level drops to around 1 mg per 100 ml, it is referred to as hypomagnesemia; if it drops below 1, tetany can be expected to occur. However, a test for serum magnesium level is not a good indicator of grass tetany.
Immediately preceding the occurrence of visual symptoms, plasma magnesium is low, but as tetany begins, plasma magnesium usually increases to a near-normal level and is no longer a diagnostic symptom. Because the kidneys apparently start conserving magnesium when the serum level reaches about 1.8 mg per 100 ml, one of the better aids in diagnosing hypomagnesemia is low urinary magnesium (less than 20 parts per million of magnesium).
Quite often, clinical signs are not observed, and the only evidence is a dead cow. In mild cases, milk yield is decreased, and the animal is nervous. These signs may indicate the need for preventive measures.
Animals affected by acute grass tetany may suddenly stop grazing, appear discomforted and show unusual alertness, such as staring and keeping their heads and ears in an erect position. Also, they may stagger; have twitching skin, especially on the face, ears, and flanks; and lie down and get up frequently. At this stage, they are easily disturbed, and any stimulation may lead to startling reactions, such as continuous bellowing or running. Sooner or later, a staggering gait develops, followed by collapse, stiffening of muscles and violent jerking convulsions with the head pulled back. Animals lie flat on one side, the forelegs pedal periodically, the eyes and ears twitch, and chewing motions produce froth around the mouth.
Between convulsions, the animals appear relaxed. During this period, a noise or touching the animal, as when administering treatment, may result in violent reactions. These produce an increase in body temperature and respiratory rate. Heart sounds become audible. Animals usually die during or after a convulsion unless treatment is given.
Subacute and chronic grass tetany are generally slower to develop and muscular affection may be limited to twitching, a clumsy walk or exaggerated motions. Convulsions may occur if animals are driven or handled roughly. Both are characterized by loss of appetite, suppressed milk flow and dullness.
Symptoms of milk fever in lactating cows are similar to grass tetany, except animals become paralyzed rather than show violent muscular response. Serum calcium is low in animals with milk fever, which it may or may not be with grass tetany. Calcium deficiency may cause sluggishness in animals instead of the nervousness they have with magnesium deficiency.
Nitrate toxicity and grass tetany may occur at the same time on some pastures. In cases of nitrate toxicity, the blood is usually a chocolate-brown color. Also, there is a grayish to brownish discoloration of white areas on the skin and on non-pigmented mucous membranes of the mouth, nose, eyes and vulva.
Stockmen who have not seen animals with grass tetany should consult a veterinarian, county agricultural agent, or other person who has had experience with the problem. Where grass tetany has been a problem, one or more of the following practices may be useful.
Application of magnesium fertilizer and dolomitic limestone to the soil can increase the magnesium concentration in plants. The effect of magnesium fertilizer or dolomitic limestone is generally greatest on coarse-textured acid soils that are low in potassium. Local recommendations should be obtained before fertilization.
Dusting pastures with magnesium oxide (MgO) as finely powdered calcined magnesite helps increase the magnesium intake by cattle. Rates of 15 to 30 pounds of MgO per acre are recommended, with the lower rates for pastures where cattle are moved every 2 or 3 days.
To keep rain from washing the MgO off the plants, a water slurry containing 10% MgO and 1.5% bentonite can be applied with a suspension fertilizer applicator. Where forage yields are low, as in many arid regions, dusting or spraying pastures with MgO is not practical.
Animals can be fed a supplement of special high magnesium mineral blocks or mineral salt mixtures. Also, magnesium may be added to a protein supplement, silage or liquid supplements. Assuming a 20% availability, the cow’s magnesium requirement for maintenance and lactation would be from 13 to 15 grams per day. However, situations may require at least 36 grams to prevent development of tetany in herds. Lactating ewes should receive about 3 grams of magnesium (5 grams MgO) per day.
Magnesium supplements include good legume hay and mineral mixtures, such as:
- Mixture of 30% salt (with iodine and cobalt), 30% bone meal or dicalcium-phosphate, 30% magnesium oxide and 10% dried molasses. This mixture provides about 18% magnesium.
- Mixture of 75% salt and 25% magnesium oxide. Concentrate mixtures, such as:
- For self-feeding (with adequate available water and forage containing 10% protein), 65% ground grain (corn, oats, milo), 20% magnesium oxide and 15% salt.
- For self-feeding (with adequate available water and low protein forages), 65% cottonseed meal and 35% MgO.
- For hand feeding of supplements, use mixture 1 or 2, but with more salt.
Use grass-tetany hazard pastures for steers and dry stock, and use legume hay or high-legume pastures for lactating cows. A 1,000 pound lactating cow should consume approximately 30 pounds of dry matter per day. If the forage is lush and contains only 20% dry matter, the animal must eat 150 pounds of feed per day to meet these requirements. Under these conditions, it may be profitable to feed hay, especially to cows who have previously had grass tetany.
Early treatment is important. Cattle down for more than 12 hours are prone to suffer enough muscle damage to make them unable to rise and support themselves. These downer animals rarely recover.
Cows in the early stages of grass tetany should be handled gently, producing the least stress and exertion possible. Driving, roping or anything producing excitement can cause sudden death.
Injected under the skin, 200 cubic centimeters (cc) of a saturated solution (50%) of magnesium sulfate (epsom salts) gives a high level of magnesium in the blood in 15 minutes. This can be administered by ranchers under range conditions.
Any solution injected into an animal should be sterile; otherwise an infection may be introduced. Therefore, cattlemen interested in using magnesium sulfate solutions should contact a veterinarian.
Some veterinarians use intravenous injections of chloral hydrate or magnesium sulfate to calm excited animals, then follow with a calcium-magnesium gluconate solution. Intravenous injections should be administered slowly by a trained person, because there is danger of heart failure if they are given too rapidly.
As a followup treatment, the animal should be removed from the tetany-producing pasture and fed hay and concentrates. Also, 30 grams of magnesium sulfate should be given daily. Force feeding of magnesium may be necessary, but after a week the amount can be greatly reduced.
Cows that have tetany are likely to get it again later in the season or in later years. Yet these animals may continue to be high producers.
Selenium—Plants contain selenium in widely varying amounts depending upon the species of plant, plant part and soil selenium content. Certain plants are restricted to seleniferous soils. These are called primary selenium indicators and include various species of Astragalus, Machaeranthera, Haplopappus and Stanleya. Some of these plants have offensive odors.
Other plants are not restricted to seleniferous soils but can accumulate toxic levels of selenium if growing on those soils. These plants are referred to as secondary selenium absorbers and include some species of Aster, Atriplex and Grindelia. Also, crop plants, grasses and a number of weeds can absorb lesser amounts of selenium, usually not more than 50 ppm.
Two types of chronic selenosis have been described. These are the blind staggers and the alkali disease types. Blind staggers appears in cattle and sheep that consume primary selenium indicator or secondary selenium absorber plants of moderate (less than 200 ppm) selenium content over a week or more.
The blind staggers syndrome expresses itself in three stages. In the first stage, inappetence and some impairment of vision have been noted. Animals may wander in circles and disregard objects in their paths. In the second stage, the severity of the above signs increases. The front legs become weak and cannot support the animal. In the third stage, the tongue and swallowing mechanisms become paralyzed, respiration is labored and quickened, there are obvious signs of abdominal pain, the animal grates its teeth, and there is excessive salivation. The body temperature is below normal, the cornea becomes cloudy, the eyelids are swollen, and the mucous membranes of the mouth are pale. The third stage usually appears suddenly, and death often follows within a few hours, apparently as the result of respiratory failure. Gradual weight loss is common.
Recovery from the syndrome is often incomplete; mature animals lack vigor and young animals are stunted. A delayed action of the poison has been noted; clinical signs can appear up to several months after animals are removed from seleniferous feeds. The disease is not as easily diagnosed in sheep as it is in cattle because the three stages are not as clearly differentiated.
The second chronic syndrome, alkali disease, usually appears in animals on forage or grain crops grown on seleniferous soils. Corn, wheat, oats, barley, grass and hay containing 5 to 40 ppm selenium, ingested over a period of a week to a month or more, produce the symptoms of the syndrome.
Symptoms are loss of long hair from the mane and tail of horses and from the the switch of cattle; loss of body hair from swine; and sore feet with inflammation at the coronary band in horses, cattle and swine, followed by lateral cracking and other deformities of the hoof. Dullness and emaciation are also pronounced. Lesions at the horn bases in cattle are similar to those of the hoof, but less pronounced. Anemia, cirrhosis of the liver, atrophy of the heart, erosion of the joints of the long bones, deterioration of the bone marrow, and some kidney lesions are prevalent in horses and cattle. Sheep apparently are not affected in the manner of cattle and horses. In fact, no chronic effects of selenium on sheep have been reported, except for severely reduced reproduction rates when the animals graze pastures that produce the typical syndrome in cattle.
Diagnosis of the alkali disease type of selenosis is usually based on the clinical signs described previously. The South Dakota Agricultural Experiment Station used blood and hair analysis in diagnosis. Blood analysis indicates what the present level of selenium intake is. Hair analysis indicates what the long-term ingestion has been. The guidelines in Table 1 have been developed in South Dakota.
The only practical control measures have been based on management. These include avoidance or limitation of seleniferous feeds. With range animals, this demands a mapping program based on knowledge of the geology of the area and on plant analysis. Proper protein nutrition somewhat reduces the effects of excessive selenium intake.
Table 1. Expectation of selenosis according to levels of selenium (parts per million) in blood and hair.
|Blood (ppm)||Hair (ppm)|
|under 1.0||under 5.0||Chronic selenosis not expected|
|over 2.0||over 10.0||Excessive selenium intake;
selenosis can be expected
Acute selenium poisoning is produced by a single massive dose of primary indicator or other plants containing several hundred ppm or more of selenium. As many as 340 sheep have died within 24 hours after consuming Astragalus bisulcatus plants. This type of poisoning is uncommon.
Symptoms appear in a few hours to a day or two, and consist of loss of appetite, depression, frequent urination, difficulty in breathing, coma, and death through respiratory and myocardial failure. Death usually occurs before the disease can be diagnosed, and there is no known treatment.
Photosensitization—Certain plants make animals highly sensitive to sunlight and cause watery swellings under the skin and eventual death of skin in affected parts. Photosensitization is produced by plant pigments or other light-reacting substances in the bloodstream and usually occurs in white or light-colored areas of the skin not covered with a dense coat of hair. The disease is called bighead in sheep because swellings are prominent about the head.
Photosensitivities are of two types: primary photosensitivity, produced by substances coming directly from ingested plants, and hepatogenic photosensitivity, produced by toxic accumulations of a normal digestive product of chlorophyll which, because of liver damage, is sensitive to light. Also, certain breeds of cattle and sheep are more susceptible to photosensitization because of heritable defects in pigment metabolism.
Liver damage usually is caused by toxic plant substances and precedes onset of hepatogenic photosensitization. Jaundice is a prominent sign associated with photosensitization and indicates liver damage.
Plants capable of causing photosensitivity include buckwheat (Fagopyrum spp.), horsebrush (Tetradymia spp.), puncturevine (Tribulus spp.), molds (Aspergillus spp.), sacahuista (Nolina spp.), lechuguilla (Agave lecheguilla) and kleingrass (Panicum coloratum). Kleingrass does not seem to affect cattle as severely as sheep. Severe cases of bighead have been reported from sheep grazing seeded kleingrass pastures in Texas.
Photosensitization effects can be reduced by pasture rotation or supplemental feeding during the danger season. Animals should be moved to a new pasture as soon as symptoms appear. Sick animals should be placed in the shade or in the dark with feed and water, and protected from flies.
Common Poisonous Plants in New Mexico and Their Control
|Name||Season of Application||Control|
|African rue||Any time of year, except when ground is frozen or snow covered||1.5 lb/ac tebuthiuron, 0.5 oz per plant tebuthiuron, 4–8 ml per plant hexazinone, grubbing, mowing, cultivation plow and reseed|
|Arrowgrass||Anytime during growing season||1–3 lb glyphosphate per acre 2% solution glyphosphate, spray to wet|
|Spring when weeds are 1-6 inches tall, before blooming, good growing conditions||0.5 to 2 lb 2,4-D amine or ester per acre. 0.5 to 1 lb dicamba: 2,4-D (1:3 mixture) per 0.125 to 0.25 lb dicamba + 0.375 to 0.75 lb 2,4-D per 0.3 to 0.9 lb piclor— am 2,4-D (1:4 mixture) per acre; 0.125 to 0.25 lb picloram + 0.375to 0.75 lb per acre.|
|Spring—spray before frond emerges||4 to 8 lb dicamba per acre. 1 to 2 lb piclorarn per acre; cultivation or mowing|
|Broom snakeweed||Fall, after bloom to mid-December||0.25 lb picloram per acre, 0.75 lb dicamba per acre|
|Chokecherry||Anytime, except when ground is frozen or snow covered||Spot treatment 0.25 to 0.5 oz tebuthiuron per 3 feet canopy diameter. 4 to 6 ml hexazinone per 3 ft canopy diameter. 1% solution imazapyr, spray to wet|
|When plants are actively growing and before bloom||2 to 4 lb 2,4-D per acre. 1 to 2 lb dicamba: 2,4-D (1:3 mixture) per acre; 0.25–0.5 lb dicamba + 0.75 to 1 lb 2,4-D per acre; 0.5 to 0.75 lb dicamba per acre; 0.25–0.5 lb picloram per acre; 0.3 + 0 1.0 lb picloram: 2,4-D (1:4 mixture) per acre; 0.25 to 0.5 lb piclorarn + 0.75 to 1.0 lb 2,4-D per acre|
|False hellebore||Spring, from early growth to bud stage, repeat as necessary||4 lb trichlopyr per acre 1 lb picloram per acre|
|Greasewood||Anytime, except when ground is frozen or snow covered||Cultivation and reseed, mowing. Spot treatment 0.5 oz tebuthiuron per 6 ft canopy diameter; 6-8 ml hexazinone per 3 ft canopy diameter|
|Horsetail||Summer, when plant is fully emerged||Spot treatment with 1 lb amitrol per acre; 1 to 1.5 lb imazapyr per acre; 2% solution imazapyr, spray to wet.|
|Inkweed||Anytime of the year except when ground is frozen or snow covered||Cultivating, mowing grubbing; 4-6 ml hexazinone per plant 0.25 + 0.5 oz tebuthiuron per plant|
|Johsongrass||Any time during growing season||1 to 3 lb glyphosphate per acre; 2% solution glyphosphate, spray to wet; 0.5 to 0.75 lb imazapyr per acre; 1% solution imaza pyr, spray to wet.|
|Larkspur—low and tall||Spring and summer||1 to 2 lb dicamba per acre; 0.5 to 1 lb picloram per acre; repeat as necessary.|
|Mesquite||45 to 90 days after bud break||0.25 to 0.5 lb trichlopyr per acre; 0.5 lb clopyralid per acre; 0.125 or 0.25 l trichlopyr + 0.125 or 0.25 lb picloram per acre (1:1 mixture); 0.125 or 0.25 lb clopyralid + 0.125 or 0.25 lb picloram per acre (1:1 mix ture); 0.5 to 1.0 lb dicamba per acre.|
|Oak—shinnery and gambel||Anytime ground is not frozen or snow-covered. Spring,when leaves fully emerged||0.5–1.0 lb tebuth—iuron per acre; 0.5 to 1.0 lb 2,4D per acre; repeat as necessary.|
|Rayless goldenrod, burroweed||Fall, after bloom and before frost
Anytime, except when ground is frozen or snow covered
0.5 lb picloram per acre 1% solution picloram.
|Sacahuista||Anytime, except when ground is frozen or snow covered||1 to 2 lb tebuthiuron per acre. Spot treat, 4–6 ml hexazinone per 3 ft canopy diameter; 0.5–1 oz tebuthiuron per plant|
|Sleepygrass||Anytime during growing season||1 to 3 lb glyphosphate per acre; 2% solution glyphosphate, spray to wet. 0.5 to 1 lb imazapyr per acre; 1% solution imazapyr, spray to wet.|
|Tarbush||Anytime, except when ground is frozen or snow covered||0.5 to 1 lb tebuthiuron per acre; spot treatment: 0.25 to 0.5 oz tebuthiuron per acre or 4–6 ml hexazinone per 3 ft canopy diameter.|
|Chemical Name||Product Name||Active Ingred.
or Acid Equiv.
|2,4-D||(2,4- dichlorophenoxy) acetic acid||Several manufacturers||Amino salts and esters, 4 lb/gal|
|dicamba||3,6-dichloro-o-anisic acid||Banvel||4 lb/gal|
|Dicamba: 2,4-D (1:3)||see dicamba and 2,4-D||Weedmaster||4 lb/gal|
|Glyphosphate||N-(phosphonomethyl) acid||Roundup||4 lb/gal|
1,3,5, triazine 2,4 (lH,3H) dione
|Velpar RP||2 lb/gal|
|Imazapyr||2-[4,5- dihydro-4-methyl-4- (1-methylethyl -5-oxo-1H-imidazol-2-yl]-3-pyridinecarb oxalic acid with 2-propanamine (1:1) salt||Arsenal||2 lb/gal|
|Picloram||4-amino-3,5,6-trichloropicolinic acid||Grazon PC||2 lb/gal|
|Picloram 2,4-D (1:4)||See picloram and 2,4-D||Grazon P+D||2 1/2 lb/gal|
|Tebuthiuron||N-[5-(I,I-dimethylethyl) 1,3,4 thiadiazol 2-yl)-N,N dimethylurea||Spike 20P||20%|
A Glossary of Toxicology Terms
acute – having a rapid onset, a short course, and pronounced signs
alkali soil – a soil that has either so high a degree of alkalinity (pH 8.5 or higher) or so high a percentage of exchangeable sodium (15% or higher) or both that the growth of most plants is limited
anorexia – loss of appetite, esp. prolonged
anoxemia – a condition of subnormal oxygenation of the arterial blood
anoxia – inadequate oxygenation of the blood, to the extent that permanent damage is done to the affected part results
ascites – the abnormal accumulation of serous fluid in the abdominal cavity
ataxia – an inability to coordinate voluntary muscular movements
carcinogenic – causes cancer
chronic – of long duration; continuing; constant
cirrhosis – a liver disease--excessive formation of connective tissue, followed by hardening and contraction
conjunctivitis – inflammation of the mucous membranes that line the inner surface of the eyelids
cyanosis – a dusky bluish or purplish discoloration of skin or mucous membrane caused by deficient oxygenation of the blood
demyelinate – remove or destroy the myelin--the soft, somewhat fatty substance that forms a thick sheath in nerve fibers
dyspnea – difficult or labored respiration-
edema – an abnormal accumulation of serous fluid in connective tissue causing puffy swelling, (or in a serous cavity causing distention and compression of the contents)
edematous suffusionis – puffy swellings
emaciation – the process of losing flesh gradually; making thin; wasting away
enteritis – inflarnation of the intestines
etythenza – reddening of skin
escutcheon – an area just above the rear part of the udder of many quadrupeds, extending upward and outward to the flanks, distinguished by the hair that turns upward rather than downward
gastroenteritis – inflammation of the membrane lining the stomach and intestines
hypoglycemia – abnormal decrease of sugar in the blood
icterus jaundice – yellowish pigmentations of the skin, tissue and certain body fluids caused by deposition of bile pigments following interference with normal production and discharge of bile
intestinal mucosa – mucous membrane of the intestines
lesion – injury, impairment or flaw. An abnormal change in structure of an organ or part
lethargy – sleepiness, drowsy, dull, listless
lysis – the gradual decline of a disease or lowering of temperature
mutagenic – causes mutations
necropsy – perform a postportern examination upon
nephritis – inflammation of the kidney
paresis – paralysis, action of letting go or slackening
petechia (l) – a minute hemorrhage that appears on the skin or mucous and serous membranes, or within an organ
polyuria – excessive secretion of urine
pruritis – localized or generalized itching caused by irritation of sensory nerve endings
rumen stasis – slowing or stopping of the normal fluid flow in the rumen
serous – of or relating to blood serum
tetatogenic (icity) – causes deformed fetuses
Cheeke, P.R. and L.R. Shull. 1985. Natural Toxicants in Feeds and Poisonous Plants. The Avi Publishing Co., Inc. Westport, Conn. 492 pp.
James, L.F., M.H. Ralphs and D.B. Nielsen (eds.) 1988. The Ecology and Economic Impact of Poisonous Plants and Livestock Production. Westview Press, Boulder, Colorado. 428 pp.
Keeler, R.F., K.R. Vankampen, and L.F. James (eds.) 1978. Effects of Poisonous Plants on Livestock. Academic Press, New York. 600 PP.
Kingsbury, J.M. 1964. Poisonous Plants of the United States and Canada. Prentice-Hall, Inc., Englewood Cliffs, N.J. 626 p.
Norris, J.J. and K.A. Valentine. 1954. Principal Livestock-Poisoning Plants of New Mexico Ranges. New Mexico Exp. Sta. Bull. 390. 78 p.
Seawright, A.A., M.P. Hegarty, L.F. James and R.F. Keeler (eds.) 1985. Plant Toxicology. Queensland Poisonous Plant Committee, Yeerongpilly. 625 pp.
Schmutz, E.M., Freeman, B.N. and Reed, R.E. 1968. Livestock Poisoning Plants of Arizona. Tucson Univ. Arizona Press.
U.S.D.A. 1968. 22 Plants Poisonous to Livestock in the Western States. U.S.D.A. Agr. Info. Bull. 327. 64 pp.
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Printed and electronically distributed February 1991, Las Cruces, NM.