United States 

Department of 

Agriculture

Agricultural 

Research 

Service

Agriculture 

Information

Bulletin Number 415

Revised April 2011

Plants Poisonous 

to Livestock in the 

Western States

United States 

Department of 

Agriculture

Agricultural 

Research 

Service

Agriculture 

Information 

Bulletin Number 415

Revised April 2011

Plants Poisonous 

to Livestock in the 

Western States

Prepared by K.E. Panter, M.H. Ralphs, J.A. Pfister, D.R. Gardner, 

B.L. Stegelmeier, S.T. Lee, K.D. Welch, B.T. Green, T.Z. Davis, 

and D. Cook, U.S. Department of Agriculture, Agricultural 

Research Service, Poisonous Plant Research Laboratory, Logan, 

Utah.
ii

Abstract

Panter, K.E., M.H. Ralphs, J.A. 

Pfister, D.R. Gardner, B.L. Stegelmeier, S.T. Lee, K.D. Welch, B.T. 

Green, T.Z. Davis, and D. Cook. 

2011. Plants Poisonous to Livestock in the Western States. U.S. 

Department of Agriculture, Agriculture Bulletin No. 415.

Poisonous plants are a major cause 

of economic loss to the livestock 

industry. Each year these plants adversely affect 3 to 5 percent of the 

cattle, sheep, and horses that graze 

western ranges. These losses result 

from death of livestock, abortions, 

photosensitization, decreased 

production, emaciation, and birth 

defects. In addition to these losses 

are those of increased management 

costs associated with such things 

as fencing, altered grazing programs, and loss of forage. This bulletin describes more than 30 of the 

principal poisonous plants growing 

on western ranges and the signs of 

poisoning in livestock. Suggestions 

are included for the prevention of 

livestock poisoning by plants.

Keywords: abortion, arrowgrass, 

birth defects, bitterweed, bracken 

fern, chokecherry, copperweed, 

death camas, emaciation, false 

hellebore, greasewood, groundsel, 

halogeton, hemp dogbane, horsebrush, kochia, larkspur, locoweed, 

lupine, milkvetch, milkweed, 

nightshade, nitrate, oak, photosensitization, pingue, poison hemlock, 

poisonous plants, ponderosa pine, 

rayless goldenrod, rubberweed, 

Russian knapweed, selenium, 

snakeweed, sneezeweed, spring 

parsley, St. Johnswort, sweet 

clover, tansy ragwort, veratrum, 

waterhemlock, yellow star thistle, 

yew

The Agricultural Research Service 

conducts research to develop and 

transfer solutions to agricultural 

problems of high national priority 

and provides information access 

and dissemination to—

•	 ensure high-quality, safe food 

and other agricultural products;

•	 assess the nutritional needs of 

Americans;

•	 sustain a competitive agricultural economy;

•	 enhance the natural resource 

base and the environment; and

•	 provide economic opportunities for rural citizens, communities, and society as a whole.

Mention of trade names, commercial products, or companies 

in this publication is solely for 

the purpose of providing specific 

information and does not imply 

recommendation or endorsement 

by the U.S. Department of Agriculture over others not recommended.
iii

Caution: Pesticides used improperly can harm humans, domestic 

animals, beneficial insects, desirable plants, and fish or other wildlife. Follow the directions and heed 

all precautions on labels. Store 

pesticides in original containers 

under lock and key—out of the 

reach of children and animals—

and away from food and feed.

Apply pesticides so that they do 

not endanger humans, livestock, 

crops, beneficial insects, fish, and 

wildlife. Do not apply pesticides 

where there is danger of drift when 

honey bees or other pollinating 

insects are visiting plants or in 

ways that may contaminate water 

or leave illegal residues.

Avoid prolonged inhalation of 

pesticide sprays or dusts; wear 

protective clothing and equipment, 

if specified on the label.

If your hands become contaminated with a pesticide, do not eat 

or drink until you have washed. In 

case a pesticide is swallowed or 

gets in the eyes, follow the first aid 

treatment given on the label and 

get prompt medical attention. If a 

pesticide is spilled on your skin or 

clothing, remove clothing immediately and wash skin thoroughly.

Note: Some States have restrictions on the use of certain pesticides. Check your State and local 

regulations. Also, because registrations of pesticides are under constant review by the U.S. Environmental Protection Agency, consult 

your local county agriculture agent 

or State extension specialist to 

be sure the intended use is still 

registered.

Use only pesticides that bear the 

EPA registration number and carry 

appropriate directions.

While supplies last, single copies 

of this publication can be obtained 

at no cost from USDA-ARS-NPAPPRL, 1150 East 1400 North, 

Logan, UT 84341.

Copies of this publication may 

be purchased in various formats 

(microfiche, photocopy, CD, print 

on demand) from the National 

Technical Information Service, 

5285 Port Royal Road, Springfield, 

VA 22161, (800) 553-6847, www.

ntis.gov.

This publication in its entirety also 

is freely accessible on the Internet 

at http://www.ars.usda.gov/is/np/

indexpubs.html

All photographs in this volume 

were taken by USDA employees 

except “Spineless Horsebrush,” 

page 43, U.S. National Park Service; and “Rayless Goldenrod,” 

page 77, Dr. Samantha Uhrig, 

Desert Willow Veterinary Services, 

Carlsbad, NM.
iv

The U.S. Department of Agriculture (USDA) prohibits discrimination in all its programs and activities on the basis of race, color, 

national origin, age, disability, 

and where applicable, sex, marital 

status, familial status, parental 

status, religion, sexual orientation, genetic information, political 

beliefs, reprisal, or because all or 

part of an individual’s income is 

derived from any public assistance 

program. (Not all prohibited bases 

apply to all programs.) Persons 

with disabilities who require alternative means for communication 

of program information (Braille, 

large print, audiotape, etc.) should 

contact USDA’s TARGET Center at (202) 720-2600 (voice and 

TDD). To file a complaint of 

discrimination, write to USDA, 

Director, Office of Civil Rights, 

1400 Independence Avenue SW, 

Washington, DC, 20250-9410, 

or call (800) 795-3272 (voice) or 

(202) 720-6382 (TDD). USDA is 

an equal opportunity provider and 

employer. 

Revised April 2011
v

Acknowledgments

The authors dedicate this latest revision of Plants 

Poisonous to Livestock in the Western States to Lynn 

F. James, Research Leader of the ARS Poisonous Plant 

Research Laboratory (PPRL) from 1972 to 2007. Under 

his guidance, PPRL gained a national and international 

reputation in the field of poisonous plants. He was the 

guiding force behind the original publication of this 

bulletin in 1980, and in 2005 he began the process of 

updating and revising the work. Dr. James retired from 

ARS in 2008 after over 50 years of service. He is a 

collaborator with PPRL and continues to share his insight 

and experience with the current staff.

The authors acknowledge Terrie Wierenga, PPRL, for 

her editorial and photographic suggestions; the ARS 

Information Staff for their assistance; Wilbert Blackburn, 

Area Director, ARS Northern Plains Area; and Evert 

Byington, ARS National Program Leader. This publication 

was prepared under the direction of L.F. James and edited 

by T.L. Wierenga.
vi

Contents

Poisonous Plants and Livestock................................................1

Economic Impact of Poisonous Plants on Livestock................4

Precautions for Using Herbicides .............................................5

Poisonous Plants of the Western States

Arrowgrass................................................................................8

Bitterweed...............................................................................10

Bracken Fern (Western Bracken)............................................13

Chokecherry............................................................................16

Colorado Rubberweed (Pingue)..............................................19

Copperweed ............................................................................22

Death Camas...........................................................................24

False Hellebore (Veratrum).....................................................27

Greasewood.............................................................................30

Groundsel (Threadleaf and Riddell) and Houndstongue ........32

Halogeton................................................................................36

Hemp Dogbane .......................................................................40

Horsebrush ..............................................................................42

Kochia .....................................................................................45

Larkspur..................................................................................47

Locoweed................................................................................51

Lupines....................................................................................54

Milkvetches.............................................................................58

Milkweed ................................................................................61

Nightshades.............................................................................64

Nitrate-accumulating Plants....................................................66

Oak..........................................................................................68

Poison Hemlock......................................................................71

Ponderosa Pine Needles..........................................................74
vii

Rayless Goldenrod..................................................................76

Selenium-accumulating Plants................................................79

Snakeweed (Broom and Threadleaf).......................................82

Sneezeweed.............................................................................85

Spring Parsley .........................................................................87

St. Johnswort...........................................................................90

Sweet Clover...........................................................................93

Tansy Ragwort ........................................................................95

Waterhemlock .........................................................................98

Yellow Star Thistle and Russian Knapweed .........................101

Yew (Taxus)...........................................................................103

Other Poisonous Plants.........................................................105

Noxious Weeds .....................................................................107

1

Poisonous Plants and 

Livestock 

Poisonous plants are a major cause 

of economic loss to the livestock 

industry. Each year these plants adversely affect 3 to 5 percent of the 

cattle, sheep, goats, and horses that 

graze western ranges. All too often 

the losses to individual livestock 

operations are large enough to 

threaten the viability of that ranch.

Livestock losses can be heavy if 

animals—

•	 graze ranges infested with 

poisonous plants when plants 

are most toxic.

•	 are driven, trailed through, 

or unloaded from trucks onto 

range or pasture areas infested 

with poisonous plants. Animals 

are less selective in their grazing at these times of stress.

•	 are not watered regularly. 

•	 are allowed to become hungry. 

Such animals are more likely 

to eat lethal quantities of poisonous plants.

•	 are grazed on rangelands early 

in spring when there is no 

other green vegetation except 

poisonous plants.

•	 are stressed, such as when 

they are trucked, penned, or 

handled (branding, vaccination, etc.).

•	 are not limited on how much 

and how fast they consume the 

plants.

There are no known treatments for 

animals poisoned by most poisonous plants. Where a treatment is 

available, affected animals are 

usually in remote places and cannot be reached until it is too late 

to provide treatment. Furthermore, 

the stress of handling poisoned 

animals may increase the probability of death. If the animals recover 

enough to be handled, treatment 

should consist primarily of symptomatic treatment except where a 

specific treatment is known.

Prevention of loss from poisonous 

plants in general is a problem of 

range and livestock management. 

Under normal conditions, some 

poisonous plants form an important part of livestock diets without 

negative effects on the animals. 

Poisoning occurs only when these 

animals are enticed by hunger or 

other stress conditions to eat too 

much too fast.

Many of the death losses of 

livestock from grazing poisonous plants are due to management error. This includes failure 

to examine a pasture or range 

prior to use because the growth of 

some of these plants varies from 

year to year. Failure to know and 

understand plants in an area that 

are toxic to livestock can lead to 

catastrophic losses.

Hundreds of plants are poisonous 

to livestock. Many are toxic at all 
2

times, whereas others are toxic 

only under certain conditions. 

Livestock producers are urged to 

become familiar with the plants 

on their ranges and pastures that 

are potentially dangerous to their 

livestock. Help in identifying these 

plants can usually be obtained 

from the local county agricultural 

agent or by mailing a sample to 

the USDA-ARS Poisonous Plant 

Research Laboratory (PPRL) for 

identification. (See PPRL contact 

information at the end of this section.) Help with poisonous plant 

problems can also be obtained 

from local veterinarians. 

Proper diagnosis of livestock poisoning is essential. However, under 

range conditions, diagnosis can be 

difficult. 

Symptoms listed for each plant are 

those most likely to be observed. 

Not all symptoms will be seen in 

all toxicities and signs of poisoning may vary greatly, depending 

on dosage and the time taken to 

consume the dose. Also, individual 

animals respond differently to 

specific poisons.

To protect your animals from 

poisoning, do the following:

•	 Learn to identify the poisonous 

plants that grow on your range.

•	 Learn the conditions under 

which these plants can be dangerous to your livestock.

•	 Develop a grazing plan to improve your range and prevent 

poisoning. These plans should 

take into account the poisonous plants on the range, allowing animals to graze them at 

the most appropriate time or to 

avoid them.

•	 Do not allow animals that have 

been under stress or that are 

overly hungry to graze in areas 

infested with poisonous plants.

•	 Provide adequate water for 

your livestock.

•	 Be especially careful when 

grazing newly acquired livestock on your range.

•	 Provide adequate salt and other 

supplements as needed, but do 

not put them in an area where 

poisonous plants are growing.

•	 Control poisonous plants 

where feasible.

•	 If your animals get sick, consult your local veterinarian to 

ensure proper diagnosis and 

treatment. If a poisonous plant 

is involved, identification of 

the plant by an experienced 

botanist or poisonous plant 

expert is essential for any corrective action.

•	 Many poisonous plants can 

function as useful forage. Poisoning occurs when conditions 

develop that allow, or cause, 

the animal to eat too much too 

fast.

•	 Plants such as poison hemlock, 

water hemlock, arrowgrass, 
3

kochia, hounds tongue, and 

lupine may be growing on land 

from which hay is harvested. 

This is especially true on native pastures. Care must be 

taken when feeding this hay.

For additional information on 

poisonous plants, contact—

USDA-ARS Poisonous Plant 

 Research Laboratory

1150 East 1400 North

Logan, Utah 84341

phone: 435-752-2941

http://www.ars.usda.gov/npa/ 

logan/pprl
4

Economic Impact of 

Poisonous Plants on 

Livestock

Direct losses (effects on animals) 

include the following:

•	 Deaths of livestock

•	 Abortions

•	 Birth defects

•	 Weight loss (due to illness or 

decreased feed intake)

•	 Lengthened calving interval

•	 Decreased fertility

•	 Decreased immune response

•	 Decreased function (due to 

damage to organs such as the 

nervous system, lungs, liver, 

etc.)

•	 Loss of breeding stock 

(due to deaths, functional 

inefficiency, etc.)

Indirect losses (management costs)

include the following:

•	 Building and maintaining 

fences

•	 Increased feed requirements

•	 Increased medical treatments

•	 Altered grazing programs

•	 Decreased forage availability

•	 Decreased land values

•	 Opportunity costs

•	 Lost time to management

•	 Stress to management
5

Precautions for Using 

Herbicides

Herbicide rates in this publication refer to the acid equivalent 

(ae) or active ingredient (ai) 

of the active compound in the 

herbicide, except for metsulfuron 

(Escort), which is a dry flowable 

formulation (60 percent ai) and 

is expressed as ounces of product 

per acre.

Caution: Pesticides used improperly can harm humans, domestic 

animals, beneficial insects, desirable plants, and fish or other 

wildlife. Follow the directions and 

heed all precautions on labels. 

Store pesticides in original containers under lock and key, out of 

the reach of children and animals, 

and away from food and feed.

Note: Some States have restrictions on the use of certain pesticides. Check your state and local 

regulations. Also, because registrations of pesticides are under constant review by the U.S. Environmental Protection Agency, consult 

your local county agriculture agent 

or State extension specialist to 

be sure the intended use is still 

registered.

Always read the label carefully before using any herbicide. Remember that some chemicals, such as 

picloram, may have restricted use. 

Before using any herbicide, check 

first with your county agricultural 

agent or weed specialist. They can 

suggest the most suitable chemical 

for a specific problem and recommend an optimum time and rate of 

application.

Use only pesticides that bear the 

EPA registration number and carry 

appropriate directions.

Herbicides are safe when stored, 

handled, mixed, and used in accordance with label instructions 

and sound agricultural practices. 

Most herbicides are low in toxicity; however, some are poisonous 

to humans, domestic animals, fish, 

and wildlife. Most herbicides are 

toxic to broadleaf crops.

Label all herbicide containers 

clearly and appropriately.

Keep herbicides away from children, livestock, and pets. Store 

containers in a secured place where 

they are not available to children 

or anyone not authorized to use 

them. Store herbicides in closed, 

well-labeled containers in a dry 

place where they cannot contaminate food, feed, or water.

When handling herbicides, wear 

clean, dry clothing. Launder clothing after each spraying operation 

before wearing again. Wear protective clothing and equipment if 

specified on the label.
6

Apply pesticides so that they do 

not endanger humans, livestock, 

crops, beneficial insects, fish, and 

wildlife. Do not apply pesticides 

where there is danger of drift when 

honey bees or other pollinating 

insects are visiting plants or in 

ways that may contaminate water 

or leave illegal residues. Avoid 

spraying in windy conditions.

Do not inhale herbicides and avoid 

contact with spray mist and drift. 

Avoid repeated or prolonged contact of herbicides with your skin. 

Keep herbicides out of your eyes, 

nose, and mouth. Consult the label 

for treatment recommendations.

If your hands become contaminated with a pesticide, do not eat 

or drink until you have washed. 

In case a pesticide is swallowed or 

gets in the eyes, follow the first aid 

treatment given on the label and 

get prompt medical attention. If 

a pesticide is spilled on your skin 

or clothing, remove contaminated 

clothing immediately and wash 

skin thoroughly with soap and 

water.

To protect fish, wildlife, and 

livestock, do not clean spraying 

equipment or dump excess spray 

material in or near lakes, streams, 

or ponds.

Empty herbicide containers may 

be hazardous. Dispose of them in 

accordance with label instructions 

or recommendations of your State 

extension weed science specialist. 

Do not burn herbicide containers.
7

Poisonous Plants of the Western States
8

Arrowgrass

Distribution of Arrowgrass 

Signs and Lesions of Arrowgrass 

Poisoning

•	 Distress

•	 Dyspnea; rapid breathing and 

gasping

•	 Cyanosis (blue coloring of 

the lining of the mouth)

•	 Increased salivation

•	 Muscular twitching, staggering, and convulsions

•	 Bloat may occur; rumen contents may smell like almonds

•	 Convulsions

•	 Coma

•	 Death (animals consuming 

large amounts of the plant 

may die in 1 to 60 minutes 

and show only convulsions 

and death as signs of poisoning)

•	 Blood and tissues a bright 

cherry red (hyperoxygenation)

•	 Tracheal and pulmonary 

congestion

•	 Cattle and sheep may be 

severely affected if they eat 

large amounts of arrowgrass 

leaves or stalks in a short 

time. The leaves contain 

substances that produce the 

poison hydrogen cyanide on 

ingestion.

Arrowgrass (Triglochin maritima

and T. palustris) that is growing 

with adequate moisture does not 

cause poisoning. When growth is 

stressed or stunted from lack of 

moisture or frost, plants quickly 

become toxic. Regrowth foliage 

following harvest is also toxic. The 

toxin in arrowgrass is the same as 

that in chokecherry.

Where and When Arrowgrass 

Grows

Species of arrowgrass are widely 

distributed in marshy areas and wet 

meadows throughout the United 

States. Arrowgrass grows on wet, 

alkaline soils and may be found 

growing over large areas or small 

patches near springs. Arrowgrass 

starts growing in early spring. It 

is often found growing in native 

meadows that are cut for hay. Arrowgrass cut for hay may be toxic.

How Arrowgrass Affects 

Livestock

The amount of arrowgrass required 

to poison sheep or cattle depends 

on the amount of poison in the 

plants and the rate at which the 

plants are eaten. There is enough 

hydrogen cyanide, also known as 
9

hydrocyanic acid or prussic acid, 

found in 1⁄4 to 3 lb of stunted arrowgrass to kill a 600-lb animal. 

The toxic dose must be eaten at 

one time to cause death because 

the poison is not cumulative. Death 

results from respiratory failure.

How to Reduce Losses

Keep animals off areas where the 

growth of arrowgrass has been 

retarded by drought or frost or 

regrowth following harvest.

The action of hydrocyanic acid is 

so rapid that it is usually too late 

to treat an affected animal after the 

signs of poisoning are recognized.

Some poisoned animals may be 

saved by immediate treatment with 

an intraperitoneal injection of a 

mixture of 20 ml of a 10-percent 

solution of sodium thiosulfate 

and 10 ml of a 10-percent solution of sodium nitrite. For animals 

in advanced stages of poisoning, 

give an intravenous injection of 

the sodium thiosulfate and sodium 

nitrite solution. Consult your local 

veterinarian regarding treatment.

Arrowgrass can be controlled by 

metsulfuron (0.5 oz product/acre) 

when applied during seed stalk 

elongation. 

Arrowgrass is a perennial that has 

fleshy, dark-green, half-rounded, 

grasslike leaves that grow from the 

base of the plant. Although clumps 

of leaves are only 6 to 18 inches tall, 

slender flower stalks may reach a 

height of 5 feet. Small, green flowers 

appear close together along the 

upper part of the stalk early in the 

season. Later, the flowers develop 

into golden-brown fruits.
10

Bitterweed

Distribution of Bitterweed 

Signs and Lesions of Bitterweed 

Poisoning

•	 Loss of appetite and weight

•	 Depression

•	 Weakness and irregular gait

•	 Vomiting and coughing 

(lips and muzzle are usually 

stained green with vomitus)

•	 Wasting and eventual death

•	 Head may be elevated

•	 Bloat

•	 Congestion of liver, lungs, 

and abomasum

•	 Inflammation and hemorrhage 

of abomasum and duodenum 

and sometimes the rest of the 

gastrointestinal (GI) tract; 

arched back is indicative of 

abdominal pain

•	 Affected animals may lag 

behind the herd

•	 Lambs may move with a stiff 

gait

Bitterweed (Hymenoxys odorata)

poisoning is a major problem of 

sheep in the Southwest; cattle are 

occasionally poisoned. Bitterweed 

is a member of the sunflower family and is closely related to Colorado rubberweed (pingue) both 

in appearance and in its effects 

Bitterweed is a yellow-flowered annual weed varying in height 

from a few inches to 2 feet. It is erect and branches from the 

base. It is a bitter-tasting plant found mainly in the semiarid 

rangelands of the Southwest.
11

on sheep. Pingue is a perennial, 

whereas bitterweed is an annual. 

Bitterweed has an extremely bitter 

taste and is unpalatable to livestock; thus it is generally a problem only when there is a shortage 

of other green forage. Toxicity 

increases with plant maturity. The 

toxin is a sesquiterpene lactone.

Where and When Bitterweed 

Grows

Though bitterweed occurs from 

southern Kansas to Mexico and 

from central Texas to California, it 

is a problem of magnitude principally in Texas. The critical time for 

livestock is generally in winter and 

early spring when animals may 

graze the plant because of a shortage of other green forage. Maximum plant growth occurs in spring 

and early summer, but seedlings 

may be found at any time of the 

year, depending on moisture and 

temperature conditions.

How Bitterweed Affects 

Livestock

As with many other poisonous 

plants, the tolerance of animals to 

bitterweed depends on many factors. Acute poisonings may result 

in death if large amounts are eaten 

rapidly. Under normal conditions, 

this will not occur. Chronic poisoning is common, with sheep developing a wasting disease. Under 

natural grazing conditions, signs of 

poisoning occur 2 to 4 weeks after 

the sheep start grazing the plant. 

The animal will recover if removed 

from access to the plant at the 

first signs of poisoning. Generally 

speaking, about 1 percent of the 

animal’s body weight of consumed 

plant can be lethal.

Bitterweed is a powerful irritant to 

the digestive tract; thus, poisoned 

animals may lose their appetite, 

the rumen may stop functioning, 

and animals may show signs of 

pain. They lose weight rapidly and 

may lag behind the flock. Animals 

may not die until some time after 

removal from the plant. Post-mortem examinations of animals show 

lung, heart, and kidney changes 

and irritation of the GI tract.

How to Reduce Losses

There is no treatment for bitterweed poisoning. Recent research 

has shown that sheep fed an activated charcoal/protein supplement 

were less affected by bitterweed 

than unsupplemented sheep. Animals not severely poisoned may 

be taken from infested pastures, 

and they may recover within a few 

days if given good feed and water. 

Ranchers with bitterweed-infested 

pastures should be especially 

aware of what their sheep are 

eating, particularly in winter and 

spring months, and should observe 

the flock frequently for early signs 

of poisoning.
12

Bitterweed poisoning has been 

prevented by moderate stocking 

in a four-pasture deferred rotation 

grazing system or light continuous 

stocking with sheep, cattle, and 

goats.

Seasonal control can be obtained 

from 2,4-D (1 lb ae/acre), picloram 

(0.5 lb ai/acre), clopyralid (0.25 lb 

ai/acre), or metsulfuron (1.25 oz 

product/acre) applied from autumn 

to early spring before flowering 

when the plant is actively growing.
13

Bracken Fern (Western 

Bracken)

Distribution of Bracken Fern

Signs and Lesions of Bracken 

Fern Poisoning

In cattle and sheep:

•	 High fever

•	 Loss of appetite

•	 Depression

•	 Difficulty in breathing

•	 Excessive salivation

•	 Nasal and rectal bleeding; 

bloody urine and feces

•	 Anemia, leukopenia, thrombocytopenia, and hemorrhagic syndrome

•	 Hemorrhages on mucous 

membranes

•	 Aplastic bone marrow

•	 Bladder tumors in cattle

In horses:

•	 Loss of weight and condition; 

emaciation

•	 Progressive incoordination

•	 Marked depression

•	 Crouching stance, back 

arched with legs apart

•	 Twitching muscles

•	 General body weakness

•	 Weak, fast pulse

•	 Inability to stand

•	 Convulsions or spasms

•	 Pericardial and epicardial 

hemorrhage

Bracken fern (Pteridium aquilinum var. pubescens) is poisonous to cattle, sheep, and horses; 

sheep, however, are more resistant. 

Bracken contains a thiaminase 

inhibitor that leads to the development of thiamine deficiency in 

horses that can be remedied by 

giving thiamine. Research has 

indicated that bracken fern is also 

carcinogenic. Milk from cows that 

graze bracken fern may be hazardous to humans.

Bracken fern has broad, 

triangular leaves, or fronds. 

The plant reaches a height of 2 

to 4 feet. It grows directly from 

stout, black, horizontal root 

stalks.
14

Livestock losses have been high 

in the Pacific Coast States, as well 

as in the Eastern and Midwestern 

States and some areas of the Intermountain West.

All portions of the fern—both 

green and in harvested hay—are 

poisonous to livestock. The toxin 

is ptaquiloside, a nor-sesquiterpene 

glucoside.

Where and When Bracken Fern 

Grows

Bracken fern is widely distributed 

in many places around the world. 

Bracken fern grows on burnedover areas, in woodlands and other 

shaded places, and on hillsides, 

open pastures, and ranges in sandy 

or gravelly soils.

The plant starts growth in the early 

spring and usually remains green 

until the leaves are killed by frost.

How Bracken Fern Affects 

Livestock

Bracken fern produces different 

signs of poisoning in cattle and 

sheep than it does in horses. Cattle 

poisoning often occurs during late 

summer when other feed is scarce, 

or when animals are fed hay containing bracken fern. The disease 

occurs after cows have consumed 

large amounts of the plant and is 

manifested in an acute, usually 

fatal, form. The disease is more 

chronic in horses.

The poison in bracken fern has a 

cumulative effect. Livestock are 

affected only after they have eaten 

considerable amounts of bracken 

fern for 2 to 4 weeks.

Cattle are affected by a nor-sesquiterpene glycoside called ptaquiloside, which causes bleeding and 

damage to the bone marrow. The 

disease has a delayed onset: Cattle 

may graze the plant for several 

weeks and then get sick and die. 

Poisoned animals seldom recover. 

If consumed over time, ptaquiloside can also cause cancer in 

the urinary bladder and GI tract. 

These tumors often bleed, causing 

red urine (enzootic hematuria or 

redwater disease).

Bracken fern poisoning in horses 

can occur when they are fed hay 

containing about 20 percent bracken fern over a period of 30 days. 

Signs of poisoning include weight 

loss, incoordination, and lethargy. 

Horses may stand with their legs 

apart as though bracing themselves 

and may assume a crouching position with an arched back. Muscle 

tremors develop and the animal 

is unable to stand despite violent 

attempts to do so. Death will occur 

in several days to a week.

How to Reduce Losses

Animals seldom eat bracken fern 

if sufficient forage is available, so 

grazing should be delayed until adequate forage is available. Young 
15

shoots are the most toxic and are 

relatively palatable in early growth 

stages.

To eliminate livestock losses, do 

not overgraze pastures and ranges. 

Make sure sufficient forage is 

available at all times to animals in 

infested areas. If necessary, supplement forage near the end of the 

grazing period. Do not feed hay 

contaminated with bracken fern.

Poisoning can be treated with 

thiamine hydrochloride, saline 

cathartics, and possibly activated 

charcoal. Few cattle have recovered after signs of acute poisoning 

appear; however, horses in early 

stages of poisoning may be saved 

by intravenous injections of thiamine hydrochloride. The thiamine 

hydrochloride treatment should be 

given under the direction of your 

local veterinarian.

Bracken fern can be controlled. In 

areas where cultivation is practical, the plants can be destroyed by 

cultivating the soil for 2 to 3 years.
16

Chokecherry 

Distribution of Chokecherry

Signs and Lesions of 

Chokecherry Poisoning

•	 Death (animals consuming 

large amounts of this plant 

may die in 1 to 60 minutes 

and show only convulsions 

and death as signs of poisoning)

•	 Distress, rapid breathing, and 

gasping

•	 Cyanosis (blue coloring of 

lining of the mouth and mucosal membranes)

•	 Salivation

•	 Excitement may occur

•	 Muscular twitching, staggering, and convulsions

•	 Bloat may occur; rumen 

contents may have odor of 

almonds

•	 Coma

•	 Blood and tissue are bright 

cherry red

•	 Tracheal and pulmonary 

congestion

Western chokecherry (Prunus 

virginiana var. demissa) and black 

chokecherry (P. virginiana var. 

melanocarpa) cause livestock 

poisoning when drought and 

overgrazing strip the pastures and 

ranges of grass and other forage. 

Animals become poisoned if they 

eat considerable quantities of the 

leaves in a short time. Wilting, 

frost, or other damage to the plant 

enhances toxicity.

Both sheep and cattle may be poisoned by chokecherry. Although 

most losses occur when feed is 

scarce, losses are not uncommon 

when sheep graze chokecherry 

in the spring. Cattle sometimes 

are poisoned by eating leaves on 

branches trimmed from cultivated 

chokecherry trees.

The toxic substance in chokecherry, hydrogen cyanide (hydrocyanic acid), is found principally 

in the leaves. Leaves become less 

toxic as the growing season advances.

Chokecherry and arrowgrass cause 

the same type of poisoning because 

they both contain hydrocyanic 

acid. Other plants with cyanogenic 

potential include serviceberry, 

Sudan grass, Johnson grass, white 

clover, birdsfoot trefoil, mountain 

mahogany, and reed canary grass.
17

Where and When Chokecherry 

Grows

Chokecherry grows in damp and 

fertile soil. It is found in thickets 

on hillsides and canyon slopes. It 

appears as a shrub or small tree 

among willows, poplars, and alders 

that grow along mountain streams.

Chokecherry begins growing early 

in spring. Its growth is slow at high 

elevations.

Chokecherry trees (center) may reach a height of 20 feet. They are often found 

growing with other trees and bushes. The berries are not considered to be toxic. 

Chokecherry may grow as a shrub to about 6-8 feet in height. It is found in thickets, along hillsides, and on canyon slopes.

How Chokecherry Affects 

Livestock

Although the hydrocyanic acid 

content of chokecherry leaves 

varies, ingestion of about 0.25 

percent of an animal’s weight in 

leaves can be fatal. Wilted leaves, 

as well as fresh leaves, are poisonous. Poisoning occurs when an 

animal consumes a relatively large 

amount over a short period of time. 

For chokecherry to be fatal, an 

animal must eat a toxic dose in a 

relatively short period—30 minutes to an hour. Hydrocyanic acid 

inhibits cellular respiration in all 

body organs and causes respiratory 

failure. Signs of poisoning come 

on rapidly, and death may follow 

within a few minutes.

How to Reduce Losses

Keep hungry or thirsty animals off 

areas where chokecherry is abundant.

The action of hydrocyanic acid is 

so rapid that it is usually too late 

to treat an affected animal after the 

signs are recognized.
18

Chokecherry is a perennial that bears 

masses of white flowers in long clusters 

in the spring. Small ripe cherries range in 

color from purple to black. Leaves are dark 

green and glossy.

Some poisoned animals may be 

saved by immediate treatment. For 

both cattle and sheep, use 20 cc of 

a 10-percent solution of sodium 

thiosulfate mixed with 10 cc of 

a 10-percent solution of sodium 

nitrite given intraperitoneally or 

intravenously. Do not let animals 

become overexcited while they 

are being treated. For advice about 

treatment, consult your local veterinarian.

Control of chokecherry is not practical on a large scale.
19

Colorado Rubberweed 

(Pingue)

Distribution of Colorado 

Rubberweed

Signs and Lesions of Colorado 

Rubberweed Poisoning

•	 Salivation

•	 Nausea and vomiting (area 

about mouth may be stained 

green from vomitus)

•	 Loss of appetite, rumen stasis, 

abdominal pain

•	 Weakness and depression

•	 Irregular gait and trembling; 

gait will become stiff

•	 Emaciation and death may 

occur if animals are allowed 

to graze this plant too long; 

death may not occur for some 

time after poisoning

•	 Congested liver, lungs, and 

GI tract

•	 Liver pale and fatty

•	 Enlarged spleen

•	 Hyperemia and hemorrhage 

of upper GI tract

Colorado rubberweed (pingue; 

Hymenoxys richardsoni var.

floribunda) may cause serious 

losses principally in sheep herds in 

Colorado, Utah, and northern and 

western New Mexico. Poisoning 

is common in sheep, but occurs 

occasionally in cattle. The plant is 

poisonous to livestock throughout 

the growing season. Losses are 

heaviest when hungry animals are 

trailed through Colorado rubberweed or are placed on overgrazed 

ranges with heavy infestations of 

Colorado rubberweed.

All aboveground parts of the plant 

contain the poisonous substance, 

a sesquiterpene lactone. Animals 

grazing the plant may have a gradual buildup of the toxin to a level 

that is harmful or lethal, or they 

may eat large amounts of Colorado 

rubberweed and be poisoned immediately.

Where and When Colorado 

Rubberweed Grows

Colorado rubberweed is a perennial that grows in arid sites at 

elevations of 6,000 to 8,000 feet. 

It is found mostly on mountains 

and foothills and grows from 

early spring until the first frost. It 

readily increases and may replace 

more palatable forage plants when 

ranges have been overgrazed.

Pingue

Bitter rubberweed
20

How Colorado Rubberweed 

Affects Livestock

Most poisoning occurs in spring or 

fall. The plant seems to act primarily as a depressant of the digestive 

tract. In most cases, the first sign of 

poisoning to be observed is a green 

froth around the mouth and nose. 

A 100-lb sheep may die if it eats 

1⁄4 to 1⁄2 lb of Colorado rubberweed 

daily for 1 to 2 weeks, or it may 

die from one large feeding.

How to Reduce Losses

Animals seldom eat toxic amounts 

of Colorado rubberweed if desirable forage is available.

Heavy losses during trailing may 

be prevented by avoiding heavily 

infested areas. Keep hungry animals away from Colorado rubberweed ranges at all times. If sheep 

losses become excessive, it may be 

advisable to change from sheep to 

cattle on certain ranges.

When grazing sheep on rubberweed-infested ranges, they should 

be watched closely for signs of 

poisoning. The rubberweed should 

be observed for signs of being 

grazed. At the first sign of poisoning (stiffness or a green stain 

around the mouth) or grazing, 

the sheep should be moved to a 

rubberweed-free part of the range. 

Lambs poisoned on rubberweed 

perform poorly and it may not be 

economical to keep them.

Colorado rubberweed may reach a height 

of about 1 foot. The stalk is thick and 

woody. Stem bases are covered with 

a woolly growth. Colorado rubberweed 

belongs to the sunflower family.

There is no known treatment for 

Colorado rubberweed poisoning.

Colorado rubberweed causes a 

wasting disease similar to that seen 

from bitterweed and sneezeweed 

poisoning. Sheep are more likely 

to eat it than cattle, and are probably more sensitive to it.
21

If Colorado rubberweed invades a 

range, examine your range management program carefully. On a 

range that is overgrazed, the desirable forage plants are gradually 

crowded out and Colorado rubberweed begins to spread.

To control Colorado rubberweed, 

spray plants in the budding stages 

or during active growth with 2,4-D 

ester at 2 lb ae/acre.
22

Copperweed 

Distribution of Copperweed

Signs and Lesions of 

Copperweed Poisoning

•	 Loss of appetite

•	 Dullness

•	 Weakness

•	 Coma and death in 1 to 

several days after ingestion of 

a lethal dose

•	 Small hemorrhages on serosal 

surfaces

•	 Mild gastroenteritis

Cattle and sheep may be poisoned 

from grazing copperweed (Oxytenia acerosa). They usually graze 

this plant only when other feed is 

scarce. Cattle are more likely to eat 

the plant in the fall when they are 

being trailed from summer range. 

Sheep are occasionally poisoned in 

fall and winter by eating dry leaves 

that have fallen to the ground. 

Most losses occur in cattle.

Copperweed contains a toxin that 

is dangerous at all times. The toxin 

is not known but is probably a 

sesquiterpene lactone. Toxicity 

reaches a peak when the plant matures. Leaves and stems are equally 

toxic.

Where and When Copperweed 

Grows

Copperweed grows along streambeds or gullies where moisture is 

plentiful and the soils are usually 

alkaline.

Copperweed starts growing early 

in spring. Flowers appear during 

July and August.

Copperweed is a perennial that may reach 

a height of 4 feet. A large number of stems 

grow from the crown; each has many narrow 

leaves. Small, flowering heads turn orange 

to yellow when mature.

How Copperweed Affects 

Livestock

Cattle are more susceptible to 

copperweed poisoning than sheep. 

Three lb of copperweed or an 

amount equal to 0.5 percent of the 

animal’s weight may cause death. 
23

Poisoned cattle die in 24 to 28 

hours. Poisoned sheep may linger 

1 to 3 weeks before dying.

How to Reduce Losses

Animals seldom eat a toxic amount 

of copperweed if other forage is 

available. To reduce losses, provide adequate forage at all times. 

Supplemental feeding is beneficial 

before animals are driven through 

heavily infested copperweed 

ranges.

There is no known treatment for 

copperweed poisoning.
24

•	 Death within a few hours to a 

few days

•	 Congestion of lungs and 

kidneys

•	 Minimal necrosis of skeletal 

and cardiac muscle

Death camas (Zigadenus spp.) is 

the common name of several species of plants that are poisonous to 

livestock. The more toxic of these 

species are grassy death camas 

(Z. gramineus), meadow death 

camas (Z. venenosus), foothill 

death camas (Z. paniculatus), and 

Nuttall’s death camas (Z. nuttallii).

They are found principally in the 

western range States.

Death camas is one of the first 

plants to begin growth in early 

spring. Without sufficient other 

forage, death camas may be heavily grazed and will cause severe 

losses. Spring snow storms may 

cover all forage except death 

Death Camas 

Distribution of Death Camas

Signs and Lesions of Death 

Camas Poisoning

•	 Salivation and bloody 

frothing

•	 Nausea and vomiting

•	 Muscular weakness and 

staggering

•	 Pulse fast and weak

•	 Prostration, labored breathing, gasping

•	 Coma

•	 Death due to heart failure

Foothill death camas growing on a grassy hillside, a typical 

habitat where its density often reaches levels that are hazardous to grazing animals.
25

camas, which may protrude 

through the snow and is available 

to the livestock. Sheep are most 

likely to be affected by feeding on 

death camas. Occasionally, cattle 

and horses are poisoned.

Death camas contains toxic steroidal alkaloids that occur throughout 

the plant; plants are dangerous at 

all times.

The bulb may be mistaken for 

those of the edible camas or quamash (Cammassia spp.) and can 

cause severe illness in humans. If 

bulbs are eaten, take the affected 

person to the emergency room of 

the nearest hospital immediately.

Death camas is a perennial that produces grasslike leaves in groups of three from a deeply 

buried bulb. The plant may be 4 to 16 inches tall. Yellowish-white flowers grow in clusters 

atop the stalk. Left, meadow death camas; right, foothill death camas.

Where and When Death Camas 

Grows

Some species of death camas 

thrive on sandy soils; others grow 

on drier, rocky foothills. The more 

toxic species are seldom found 

above elevations of 8,000 feet. 

Death camas grows early in spring, 

matures, and enters dormancy 

during early summer when soil 

moisture declines.

The leaves appear very early in 

the spring. In the foothills, death 

camas generally flowers in April 

and May. At higher elevations, the 

plant may flower in late June and 

July.
26

How Death Camas Affects 

Livestock

Death camas causes marked disturbance in respiration and heart 

action. A 100-lb sheep may die if it 

eats 1⁄2 to 2 lb of green foliage. The 

amount of foliage that will cause 

an animal’s death depends on the 

species of plant eaten and the rate 

of consumption. Severely poisoned 

animals usually die; those less seriously affected may recover.

How to Reduce Losses

To avoid poisoning, delay turnout until adequate good forage is 

available. Do not introduce hungry 

sheep into heavy stands of death 

camas. Avoid feeding, bedding, or 

trailing sheep through heavy stands 

of death camas.

There is no known treatment for 

death camas poisoning.

Research results show that early in 

the season, when plants have three 

to six leaves, death camas can be 

controlled by spraying with 2,4-D 

at the rate of 11⁄2 to 3 lb ae/acre. 

After the flowering stalks appear, 

spraying is not effective.
27

False Hellebore 

(Veratrum)

Distribution of False Hellebore

Signs of False Hellebore 

Poisoning

•	 Excessive salivation with 

frothing

•	 General body weakness; 

animal may be unable to 

stand

•	 Irregular gait

•	 Vomiting

•	 Fast, irregular heartbeat

•	 Slow, shallow breathing

•	 Coma

•	 Convulsions

•	 Birth defects

False hellebore (Veratrum californicum), or veratrum (sometimes 

called wild corn and cow cabbage), 

is a range plant that causes severe 

poisoning in sheep. It also affects 

cattle and goats. If ewes, nanny 

goats, and cows eat it during early 

pregnancy, false hellebore causes a 

cyclopian-type (single eye) facial 

deformity in the offspring.

Sheep and goats readily eat the 

whole plant. Cattle may eat it if 

other forage is scarce.

False hellebore is poisonous from 

the time it starts to grow until after 

it is killed by freezing, but toxicity 

decreases as plants mature. Roots 

are 5 to 10 times as poisonous as 

leaves or stems. The toxins in false 

hellebore are cyclopamine and 

other steroidal alkaloids.

Where and When False 

Hellebore Grows

False hellebore grows on moist, 

open meadows and hillsides at 

elevations of 6,000 to 11,000 feet. 

It emerges as soon as snow melts 

in the spring. Flowers appear in 

July and August, and the plant 

produces seeds in late August and 

September.

How False Hellebore Affects 

Livestock

False hellebore poisoning may 

occur 2 to 3 hours after an animal 

eats the plant. Sheep may show 

slight or marked signs of poisoning 

after eating 6 to 12 ounces of green 

stems or leaves.

If pregnant ewes eat false hellebore 

on the 14th day after breeding, the 

young may have congenital deformities of the head. These offspring, 

commonly called monkey-faced 

lambs, may have a protruding 
28

Leaves of false hellebore may measure 9 to 12 inches long and 3 to 6 inches broad. 

Cream-colored flowers grow in clusters at the top of a single unbranched stalk in a 

way that resembles corn. Seed pods turn black as they ripen.

lower jaw, underdeveloped upper 

jaw, proboscis-like nose, cyclopia, 

hydrocephaly, and a variety of 

deformities of the eyes as well as 

related deformities. There is a high 

incidence of embryonic loss if the 

plant is ingested between the 15th 

and 19th day of gestation. When 

ewes eat the plant later in gestation 

(28th to 33th days), they give birth 

to lambs having tracheal stenosis 

or shortened limbs.

Ewes carrying deformed fetuses 

fail to lamb at the end of the normal gestation period. As the ewe 

approaches term, the udder will 

start to fill with milk and the external genitalia will swell. At term, 

all indications of parturition will 

disappear and the fetus continues 

to grow to an abnormal size and 

will eventually kill the ewe unless 

the lamb is removed by caesarian. 

Gestation has extended as long as 

240 days with the lamb weighing 

over 30 lb when removed from the 

ewe (normal birth weight is 8 to 

9 lb).

How to Reduce Losses

Losses of newborn animals from 

deformities can be avoided by 

keeping sheep, goats, and cattle 

away from false hellebore during 

early gestation. Ideally, a flock 

of sheep should not be grazed on 

veratrum for 60 days after the rams 

are turned in with the ewes.

Research results show that false 

hellebore may be controlled by 

applying amine salts of 2,4-D at 
29

Typical cyclopic lamb, caused when the 

pregnant ewe grazed false hellebore on the 

14th day of gestation.

the rate of 2 lb ae/acre after the last 

leaves have expanded and before 

bud stage. A second treatment may 

be required the following year. Picloram pellets at 1 lb ae/acre may 

also provide long-term control.
30

Greasewood

Distribution of Greasewood

Signs and Lesions of Greasewood 

Poisoning

•	 Depression

•	 Dullness, weakness, reluctance to move

•	 Breathing rapid and shallow

•	 Drooling

•	 Recumbency

•	 Coma

•	 Death between 2 hours and 

several days

•	 Uremia, hypocalcemia, death 

due to interference with 

energy metabolism

•	 Renal tubular necrosis with 

crystals

•	 Crystalluria

Greasewood (Sarcobatus vermiculatus) is a range shrub that 

livestock can safely eat in moderate amounts with other forage. It is 

quite palatable to livestock. Death 

occurs when livestock eat large 

amounts in a short period of time. 

Poisoning occurs in sheep and 

cattle.

Losses may occur when sheep or 

cattle eat large quantities of leaves 

that have fallen to the ground in 

fall and winter or new growth in 

spring.

The toxic substances, soluble 

sodium and potassium oxalates 

(also found in halogeton), accumulate in the leaves of the plant. 

The amount of toxin varies considerably among the different 

areas where it grows. Greasewood 

increases in toxicity as the growing 

season advances.

Where and When Greasewood 

Grows

This shrub is adapted to the heavy 

saline soils of arid and semiarid 

regions. It is confined to alkaline 

soils and may form the dominant 

vegetation on alkaline flats.

Greasewood starts growing in 

early spring. The leaves remain 

succulent until fall, when they 

dry and drop off. Buds remain on 

plants most of the year. 

How Greasewood Affects 

Livestock

Signs of poisoning may develop 

4 to 6 hours after an animal eats 

a toxic amount of greasewood. 

Greasewood poisoning in livestock 

is similar to that caused by 

halogeton.
31

A sheep may die if it eats as little 

as 2 lb of green leaves and fine 

stems in a short period. Cattle 

may die after eating 3 to 3 1⁄2 lb of 

greasewood in a short period. Most 

poisonings occur when hungry 

animals are turned into a patch of 

greasewood.

How to Reduce Losses

Rumen bacteria can metabolize the 

toxin to a nontoxic form. Therefore, introduce livestock into heavy 

stands of greasewood slowly so 

as to allow time for them to adapt 

to the toxic substance in the plant 

(2 to 3 days). Livestock can also 

be conditioned to this toxin by 

grazing them on shadscale, which 

contains nontoxic levels of oxalate. 

Make sure animals are not hungry 

when first allowed to graze greasewood. Supply adequate water and 

a good variety of forage.

There is no known treatment for 

greasewood poisoning.

Research shows that greasewood 

can be effectively controlled with 

2,4-D (2 lb ae/acre). Two or more 

successive years of treatment may 

be necessary for effective control 

because of its resprouting ability.

Greasewood is an erect, spiny, woody perennial shrub that grows 2 to 5 feet tall. 

Flowers are small and light green to whitish.
32

Groundsel (Threadleaf 

and Riddell) and 

Houndstongue

Distribution of Groundsels

Signs and Lesions of Groundsel 

and Houndstongue Poisoning

•	 Signs may not appear until 

6 months or more after the 

plant is eaten

•	 Lethargy; loss of interest in 

food and abdominal pain

•	 Crustiness around eyes and 

nose; eyes may also be red 

and watery, especially in 

bright sunlight

•	 There may be diarrhea or 

constipation

•	 Weakness as manifested by 

wobbling and dragging rear 

feet

•	 Animals may wander aimlessly and appear blind, and 

may become belligerent

•	 Cattle may develop an unpleasant odor with a sweetish 

quality

•	 Ascites

•	 Death may occur within a few 

days after symptoms appear

•	 Icterus and hyperbilirubinemia

•	 Liver cirrhosis, fibrosis, and 

bile duct proliferation

•	 Photosensitization

Threadleaf groundsel (Senecio 

longilobus), often called woolly 

groundsel, and Riddell groundsel 

(S. riddellii) contain pyrrolizidine 

alkaloids similar to those in 

tansy ragwort and thus may poison 

cattle, horses, and sheep. These 

groundsels occur in greatest abundance in the Southwest, notably in 

Texas, New Mexico, and Arizona. 

Riddell groundsel may also poison 

livestock in the Midwest. Both 

plants have similar leaves that are 

thickish, elongated, and narrow. 

Threadleaf groundsel leaves are 

gray, hence the name “woolly 

groundsel,” whereas Riddell 

groundsel leaves are bright green. 

Riddell groundsel has stems that 

are somewhat less woody than 

those of threadleaf groundsel, 

which also tends to be more 

bush-like.

Houndstongue (Cynoglossum 

officinale) is a biannual forb 

that infests pastures, ranges, and 

hayfields throughout the Western 

United States. It is sometimes 

harvested in hay where it can cause 

poisoning. Houndstongue also contains pyrrolizidine alkaloids (see 
33

tansy ragwort). There are a number 

of other plants that contain toxic 

amounts of pyrrolizidine alkaloids 

such as Amsinckia and Crotalaria.

In some areas of the world, these 

plants grow mixed in with small 

grains and subsequently end up 

in the food of people, with toxic 

consequences including carcinogenicity. There is some evidence that 

pyrrolizidine alkaloids can pass 

through the placental membranes 

and have an effect on the fetus. 

Threadleaf groundsel, often called woolly 

groundsel because of its gray color, has 

many stems. Each stem may have several 

branches.

Toxicity increases up until time of 

flowering; then it begins to decrease. Younger plants tend to be 

more palatable to livestock. Sheep 

and goats are more resistant to 

poisoning than cattle and horses. 

Younger animals are more susceptible than older animals.

Where and When Groundsels 

and Houndstongue Grow

Threadleaf groundsel typically 

grows in dry, gravelly, or hardpan 

soils and may be found on plains 

and foothill areas; Riddell groundsel is generally found in slightly 

moister sites, such as drainages 

and in sandy places. Houndstongue 

can be found growing in croplands 

and in the better soils.

Both groundsels flower in late 

summer, although in the Southwest 

threadleaf groundsel may grow and 

flower any time temperature and 

moisture conditions are right. Riddell groundsel usually dies back to 

the crown after flowering and follows a more definite growth cycle.

How Groundsels and 

Houndstongue Affect Livestock

These groundsels and houndstongue contain pyrrolizidine 

alkaloids, which primarily affect 

the liver. Cells of the liver are 

slowly killed or prevented from 

reproducing and are gradually 

replaced by scar tissue. Whether 

an animal survives depends on the 

number of liver cells it loses, and 

the duration of survival depends 

upon the rate at which it loses liver 

cells. 
34

central nervous system effects such 

as impaired vision, belligerency, 

and an incessant stumbling walk. 

The onset of symptoms may be dependent on other stresses imposed 

on the liver, such as cold weather, 

poor feed, shipping, or parturition, 

which it cannot handle in its weakened condition; thus, the true cause 

of death is often not ascertained. 

Cattle eating 5 percent or more 

of their total daily diet of mature 

plant for periods exceeding 15 consecutive days can be expected to 

die within 1 to 6 months. A lesser 

amount of young plant may cause 

the same symptoms. Intoxications 

are often subchronic or chronic 

with clinical signs developing only 

after long periods of time. Such 

animals perform poorly throughout 

their lives and are culled because 

they are inefficient producers. 

Young animals are more easily 

poisoned than mature animals.

How to Reduce Losses

When symptoms of poisoning 

appear, it is too late to save the 

animal; thus, the best prevention is 

avoidance of the plant.

Animals may graze pastures 

containing these plants without ill 

effects if an ample amount of good 

forage is present; thus, pastures or 

ranges should be maintained for 

good production of grasses and 

high quality forage.

Houndstongue is a biennial. The first year it 

produces a rosette with large rough leaves 

resembling a dog’s tongue. The second 

year it produces a flowering stalk with 

reddish-purple flowers that produce four 

prickly nutlets.

Animals may survive for 6 months 

or longer after they have ingested 

a lethal amount of plant and may 

show no outward symptoms during 

this period. They may suddenly become lethargic, fill with fluid in the 

abdominal cavity, and die within 

2 to 4 days. They may also show 
35

Groundsels may be controlled with 

2,4-D (1 lb ae/acre), picloram (1 lb 

ae/acre), or a combination of 2,4-D 

and picloram (0.75 + 0.25 lb ae/

acre) when the plants are growing 

rapidly, but plants are generally 

spread over large areas and herbicide treatment may not be economically feasible.

Riddell groundsel is a bright green plant which has several stems that originate 

from a woody base. Stems, if they branch, only branch terminally.

Houndstongue can be controlled 

with 2,4-D (2 lb ae/acre) or picloram and 2,4-D (0.25 to 0.5 lb ae/

acre). Herbicide should be applied 

in spring prior to bloom.
36

The toxic substance in halogeton is sodium oxalate. Halogeton 

becomes more toxic as the growing season advances, reaching a 

peak of toxicity at maturity. Cattle 

and sheep readily graze dried 

halogeton; thus, losses occur during fall, winter, and early spring. 

Losses generally occur when these 

livestock become hungry—during 

trailing, after trucking, or overgrazing.

Where and When Halogeton 

Grows

Halogeton often grows along 

railroad beds, roads, sheep trails, 

and in places where the soil has 

been disturbed. Dense stands are 

found on burned-over areas, overgrazed ranges, dry lakebeds, and 

abandoned dry farms. It thrives in 

the saline soils of colder arid and 

semiarid regions of the Great Basin, especially where native plant 

cover is thin. However, halogeton 

lacks the capacity to compete with 

vigorous perennial plants and the 

more aggressive annuals.

Halogeton is a prolific seed 

producer. New plants germinate 

from February to mid-August and 

produce a seed crop before the 

growing season ends. Seeds are 

spread by wind, water, animals, 

and vehicles and equipment such 

as road graders. Seed may remain 

alive in soil 20 years or longer.

Halogeton

Distribution of Halogeton

Signs and Lesions of Halogeton 

Poisoning

•	 Depression, weakness, and 

reluctance to move

•	 Respiration rapid and shallow

•	 Drooling

•	 Recumbency

•	 Coma

•	 Death between 2 hours and 

several days; death due to 

interference with energy 

metabolism

•	 Hypocalcemia, uremia

•	 Renal tubular necrosis and 

crystals, hemorrhage, and 

hyperemia

•	 Rumen wall may be hemorrhagic and edematous 

Halogeton (Halogeton glomeratus), an alien invasive annual plant 

of the Western States, frequently 

causes poisoning in sheep and cattle. Most losses occur when hungry 

animals are allowed to graze in 

heavy stands of halogeton.

1935-1957

1958-1969
37

Halogeton has a characteristic small hair—about one-twelfth inch long—on the 

end of each leaf.

Halogeton grows 3 to 18 inches tall; its height depends on the moisture available during 

the growing season. Each plant generally has five main stems that come directly from the 

base of the plant.
38

How Halogeton Affects Livestock

Toxicity is due primarily to sodium 

oxalate, which can accumulate to 

high levels in the plant. Oxalates 

precipitate calcium from the blood 

causing hypocalcemia; oxalate 

crystals damage the kidneys and 

rumen walls, and enzymes are 

inhibited in the citric acid cycle of 

energy metabolism, causing rapid 

death.

Sheep can tolerate large amounts 

of halogeton if they eat it slowly or 

with other forage. The tolerance of 

sheep doubles if they are preconditioned by grazing light stands or 

other plants containing low levels 

of oxalates.

About 12 ounces of halogeton will 

kill a sheep that has been without 

feed for a day or longer; 18 ounces 

are required to kill a sheep that has 

been feeding on other forage. First 

signs of halogeton poisoning occur 

2 to 6 hours after an animal eats a 

fatal amount; death usually occurs 

in 9 to 11 hours.

How to Reduce Losses

Livestock losses may be reduced 

by maintaining range in good condition and by proper management 

of animals. Supplemental feeding 

helps prevent halogeton poisoning when animals trail through or 

graze infested areas.

Do not introduce livestock into 

areas heavily infested with halogeton unless it can be done slowly 

to allow time for adaptation to the 

toxin. This can be accomplished 

by grazing plants such as shadscale or light stands of halogeton. 

Halogeton forms a solid line along the roadside and extends into the sagebrush.
39

Livestock should not be allowed 

to become hungry or thirsty while 

grazing in areas infested with halogeton as they graze indiscriminately. Death in livestock occurs when 

an animal eats a large amount of 

halogeton in a short period of time. 

Animals being trucked in should 

not be unloaded in halogetoninfested areas. These animals may 

benefit from supplemental feeding 

before grazing in the halogetoninfested areas. There is no known 

treatment for halogeton poisoning.

Halogeton does not compete well 

with other vegetation; therefore 

the best way to control halogeton is proper range management. 

Because each plant produces vast 

numbers of seeds, some of which 

may survive for 20 years or more 

in soil, it is not practical to eradicate any population that has been 

in existence for 2 years or more. 

Plants can be held in control by 

proper use of herbicides, and very 

small infestations can be eradicated if treated early. Research results 

indicate that few herbicides are effective for halogeton control. The 

low volatile ester of 2,4-D (2 lb ae/

acre) is effective when applied in 

late May or early June. Applications of 2 lb ai/acre of tebuthiuron 

as late as August will kill the halogeton and prevent reinvasion for 3 

to 5 years. However, tebuthiuron is 

a sterilant and also kills the broadleaf forbs and shrubs, resulting in 

further (and potentially stronger) 

invasion by halogeton (from seed 

in the soil) or other pioneer invaders, such as Russian thistle and 

rabbitbrush. 

Caution: Use the herbicide only to 

treat small infestations of halogeton. Repeated treatments are necessary for control.

Some of the 1,200 sheep that died from 

halogeton poisoning in a case from west 

central Utah.
40

Hemp Dogbane

Distribution of Hemp Dogbane

Signs and Lesions of Hemp 

Dogbane Poisoning

•	 Rapid pulse

•	 Dilation of pupils

•	 Vomiting

•	 Blue coloration of mucous 

membranes

•	 Progressive body weakness

•	 Convulsions may occur

•	 Coma

•	 Death

•	 Mild myocardial degeneration

Hemp dogbane (Apocynum cannabinum), a poisonous plant found 

throughout the United States, may 

cause occasional livestock losses 

in the western range States. The 

plant gets its name from the fact 

that American Indians used fiber 

from the bark for making rope. 

It also is called dogbane, Indian 

physic, American hemp, and rheumatism weed.

Normally, animals avoid hemp 

dogbane because of its bitter, 

sticky, milk-white juice. Sheep are 

more frequently affected than other 

animals; they will eat large quantities of hemp dogbane leaves and 

tops if other forb-type plants are 

not available. Hungry animals may 

eat hemp dogbane when they are 

turned onto harvested fields or onto 

new range in the fall or when other 

forage is scarce. Poisoning may 

also occur when sheep, cattle, and 

horses are trailed from summer to 

winter ranges.

Leaves are poisonous at all times, 

even when they are dry. The chief 

toxic substance in hemp dogbane is 

thought to be cymarin, a glycoside 

once used as a heart stimulant for 

humans.

Where and When Hemp 

Dogbane Grows

Hemp dogbane grows on plains 

and foothills at elevations up to 

7,000 feet. It commonly is found 

in gravelly or sandy fields, in 

meadows, and along creekbeds, 

irrigation ditches, and fence lines 

in cultivated pastures. The plant 

begins growing in late spring or 

early summer.

How Hemp Dogbane Affects 

Livestock

Death from hemp dogbane poisoning may occur 6 to 12 hours after 
41

Hemp dogbane is a perennial that 

grows 2 to 5 feet tall. Leaves turn 

yellow in the fall.

Leaves of hemp dogbane grow on opposite 

sides along reddish stems that contain 

a milky sap. The smooth-edged leaves 

are hairy on the lower surface. Flowers 

are greenish white. Two long pods, which 

develop from each flower, contain numerous seeds with tufts of silky white hairs at 

their ends.

animals eat the plant. A lethal dose 

for sheep is about 1⁄2 to 1 ounce 

per 100 lb of body weight. A lethal 

dose for cattle and horses is about 

1⁄2 to 3⁄4 ounce per 100 lb of body 

weight. A toxic dose depends 

largely on rate of consumption. 

Poisoned animals are usually 

found dead; post-mortem pathology shows heart lesions.

How to Reduce Losses

There is no known treatment for 

hemp dogbane poisoning.

Research results show that hemp 

dogbane may be controlled by 

repeated treatment of 2,4-D at 1 to 

4 lb ae/acre.
42

Horsebrush

Distribution of Horsebrush

Signs and Lesions of Horsebrush 

Poisoning

•	 Loss of appetite

•	 Depression

•	 Lagging behind the herd

•	 Weakness, recumbency; death 

may occur in severe cases, 

or photosensitization may 

develop

•	 Itching and uneasiness may 

develop with the head held in 

a “looking up” position

•	 Swelling of the ears, lips, and 

face

•	 Animal seeks shade

•	 Peeling of skin from face and 

ears

•	 Abortion may occur

•	 Liver is swollen, engorged, 

and often shows severe fatty 

changes

•	 Kidneys show low grade 

nephritis

•	 Petechial hemorrhages can be 

found in subcutis and 

serosal surfaces 

Two species of horsebrush that 

grow in the Great Basin region of 

the West are poisonous to sheep. 

Littleleaf horsebrush (Tetradymia 

glabrata) is commonly called 

coal-oil brush or spiny rabbitbrush. 

Spineless horsebrush (T. canescens

var. inermis) is also called gray 

horsebrush.

Sheep that feed on horsebrush just 

following or in conjunction with 

black sage (Artemesia nova) and 

then are exposed to bright sunlight 

may develop a characteristic swelling of the head (photosensitization) called bighead. Sheep grazing horsebrush may die without 

developing bighead; the liver is 

extremely friable. However, with 

care, many of these sheep survive.

Most losses from horsebrush occur 

during stormy periods when sheep 

change their grazing habits as they 

are trailed through heavily infested 

areas. Hungry sheep may also eat 

toxic amounts of horsebrush after 

they are watered. The plant is especially dangerous during the bud 

stage, perhaps because it is more 

palatable.

All plant parts of both species are 

poisonous, but sheep eat only buds, 

leaves, and fine stems.

Gray Horsebrush

Little-leaf Horsebrush
43

Where and When Horsebrush 

Grows

Littleleaf horsebrush is most 

abundant on benchlands, welldrained slopes, and low elevations 

on sheep winter ranges. It is one 

of the earliest desert range plants 

to start growing in spring; it may 

be green by late March and in full 

flower by the end of June. Leaves 

dry and drop off in early July, and 

the plant is dormant until the next 

spring.

Spineless horsebrush is most abundant in sagebrush areas and foothill 

regions. It starts growing later than 

littleleaf horsebrush and flowers 

in June or July. The plant usually 

remains green until fall.

How Horsebrush Affects 

Livestock

Horsebrush causes severe liver 

damage when large amounts are 

eaten, and sheep may die within a 

Severe photosensitization (bighead) on 

sheep that grazed horsebrush. As little as 

one-half pound of littleleaf horsebrush can 

cause bighead.

day or two. Survivors, if pregnant, 

often abort and may require weeks 

to recover. Sheep eating lesser 

amounts of the plant may become 

sensitive to sunlight and develop 

various degrees of photosensitivity. 

Severe photosensitization results in 

bighead wherein the sheep’s head 

is swollen. Sheep vary considerably in their susceptibility to horsebrush, but often 1⁄2 to 3⁄4 lb of littleleaf horsebrush will cause bighead, 

and larger amounts may result in 

death. Nearly twice that amount of 

spineless horsebrush must be eaten 

to cause similar symptoms.

Bighead develops only if the sheep 

has recently eaten black sagebrush. 

This plant enhances the action of 

horsebrush on sheep.

How to Reduce Losses

Bighead is principally a trail disease. To prevent losses, select trail 

routes devoid of horsebrush and 

do not let animals graze in infested 

areas. Sheep are more apt to graze 

horsebrush during stormy periods. 

Spineless horsebrush is also called gray 

horsebrush. Photo courtesy U.S. National 

Park Service.
44

Move affected sheep to shade as 

soon as signs of bighead appear. 

Give them water and supplemental 

hay. If possible, these sheep should 

be left undisturbed for a few days.

An effective economical method 

for the control of horsebrush has 

not been developed. Chemical 

and mechanical control in the area 

where littleleaf horsebrush grows 

is economically and physically 

impractical and ecologically unsound. Littleleaf horsebrush grows 

in areas where it would be difficult 

and impractical to replace it with 

better forage. It is most practical 

to avoid horsebrush populations 

where possible.
45

Kochia

Signs and Lesions of Kochia 

Poisoning

•	 Depression

•	 Dehydration

•	 Weight loss

•	 Muscular weakness

•	 Photosensitization

•	 Ocular discharge

•	 Crusty muzzle

•	 Blindness

•	 Chronic nephrosis

•	 Degenerative hepatopathy

•	 Elevated GOT (glutamic-oxaloacetic transaminase), GGT 

(gamma-glutamyl transpeptidase), and serum bilirubin

•	 Brain edema

•	 Fatty, cirrhotic, enlarged 

livers

•	 Gastrointestinal inflammation

•	 Icterus

•	 Ataxia

•	 Incoordination

•	 Polioencephalomalacia 

may occur

Kochia (Kochia scoparia), or summer cypress, is an annual weed 

introduced into the United States 

from Eurasia. This plant can now 

be found growing throughout the 

United States as one of our serious weed pests. Kochia has been 

promoted in some areas of the 

country as a forage plant. During 

drought years, it has been used 

both as forage and often as pasturage. However, kochia can cause a 

variety of problems in cattle and 

sheep. Although not common, it 

has been associated with oxalate 

and nitrate poisoning. On occasion, 

it has been associated with photosensitization, polioencephalomalacia, toxic nephrosis, and hepatitis. 

Diets having much kochia will 

result in decreased growth rates 

and death can occur. The principal 

manifestation of kochia poisoning 

is photosensitization. Poisoning 

due to kochia apparently depends 

on the environmental conditions 

under which the plant is growing.

Where and When Kochia Grows

Kochia weeds can be found 

growing on abandoned farm land, 

cultivated land, ditch banks, road 

sides, waste lands, and other 

disturbed areas. It thrives in a 

great variety of environments and 

soil types. Kochia is very drought 

tolerant. Kochia weed should not 

be confused with prostrate kochia 

(Kochia prostrata), which is considered excellent winter forage.

How Kochia Affects Animals

Cattle and sheep may become 

intoxicated after grazing kochia. 

Cattle are more susceptible to 

intoxication from kochia than are 

sheep. Cattle grazing pastures with 

a high percentage of kochia lose 

weight or gain it slowly. Cattle 

grazing near pure stands of kochia 

may show depression, dehydration, weight loss, photosensitiza-
46

tion, and discharge from the eyes 

and nose. They may show signs 

of polioencephalomalacia. Death 

frequently occurs. The toxin may 

be any or all of the following compounds: oxalate, nitrate, sulfate, 

saponin, and alkaloid.

How to Reduce Losses

Ensure that alternative feed is 

available. During periods of 

drought, livestock producers frequently ask if it is safe to feed kochia to their cattle. In general, the 

advice given is to dilute the kochia 

with other hay if at all possible and 

watch the cattle closely for signs 

of poisoning. Grazing cattle on this 

plant leads to unpredictable results.

Kochia is a bushy plant with stems either green or reddish. It is often confused with tumbleweed (Salsola kali) since it also breaks off and blows in the wind when dry.
47

Larkspur

Distribution of Larkspur

Signs and Lesions of Larkspur 

Poisoning

•	 Nervousness

•	 Weakness and staggering gait; 

animal may fall suddenly

•	 Salivation

•	 Muscular twitching

•	 Nausea and vomiting may 

occur

•	 Bloating may occur

•	 Rapid, irregular pulse

•	 Animal may die suddenly; 

excitement intensifies all 

signs of poisoning

•	 Lack of gross lesions

•	 Pulmonary congestion

Larkspur (Delphinium spp.) causes 

heavy cattle losses in western 

range States. Larkspur is highly 

palatable to cattle, and losses can 

be expected when cattle are allowed to graze larkspur-infested 

ranges, especially where the plant 

is abundant or grows in large, 

dense patches. Cattle consume tall 

larkspur most often after plants 

begin flowering; consumption 

increases into the pod stage. Summer storms may lead to increased 

consumption of tall larkspur.

Losses rarely occur in sheep or 

horses, but if subjected to sudden 

physical activity after ingesting 

large amounts of larkspur, these 

animals may show clinical effects.

Plants are most toxic during early 

growth, but toxicity gradually 

declines over the growing season. 

The toxic substances are alkaloids, 

and over 40 of these compounds 

have been evaluated. The relative toxicity and concentration of 

individual alkaloids varies among 

species. The toxic alkaloids cause 

death by muscular paralysis, leading to respiratory failure or bloat.

All parts of the plant are poisonous, but new growth and the seed 

contain the highest concentrations 

of toxic substances. Normally, 

seeds do not pose any special prob-
48

Tall larkspur is a perennial found on hillsides and in meadows above 7,000 feet. It 

ranges in height from 2 to 6 feet. A hollow 

stem distinguishes larkspur from poisonous 

monkshood, which has a similar blue or 

purple flower without a spur.

lem if cattle have grazed the area 

prior to seed maturity; however, 

under a rest-rotation system, where 

cattle enter an ungrazed unit after 

seeds have started to mature, losses 

can be significant.

Where and When Larkspur 

Grows

Based on height at maturity and 

geographic location, larkspurs 

have arbitrarily been divided into 

three groups: the tall larkspurs (D. 

barbeyi, D. occidentale, and D. 

glaucum), the low larkspurs (D. 

nelsonii, D. andersonii, and D. 

nutallianum), and the plains larkspur (D. geyeri).

Tall larkspurs tend to grow at higher elevations on deep soils where 

a plentiful supply of moisture is 

available. They grow in mountain 

meadows on sites where deep 

snowdrifts persist well into the 

growing season, under aspens on 

north-facing slopes, along streams, 

or around seeps and springs. Tall 

larkspur begins growing as soon as 

snow melts, but at the upper limits 

of their distribution this may not 

occur until July. 

Low larkspurs tend to grow at 

lower elevations where they mature and become dormant before 

the soil moisture is depleted. They 

begin growing in early spring, 

often before other forage begins 

growth. Low larkspurs grow best 

when springs are cold and wet. 

Cattle will graze low larkspur at all 

stages of growth, but most often 

graze it after flowering.

Plains larkspur is found primarily on the high plains of Colorado 

and Wyoming. It begins growth in 

spring before other plants.

How Larkspur Affects Animals

Plains larkspur may be eaten by 

cattle at any time during summer, 

but early green growth and pods 

may be most appealing to cattle. 

Both low and plains larkspurs may 
49

Low larkspur has spurred blue flowers 

that grow on the top third of a single, 

unbranched stem. It is found on grassy hillsides and in sagebrush areas, where it may 

reach a height of 2 feet. Leaves alternate 

and are divided into deep, narrow lobes. 

The stem is hollow.

be the only green herbage available 

to cattle in early spring.

The larkspurs contain a number 

of alkaloids of varying toxicity. 

The most toxic of these are the 

MSAL (methyl succidimino acetyl 

lycoctonine) types, which include 

methyllycaconitine.

How to Reduce Losses

Placing an affected animal on its 

brisket or chest with its head uphill 

may reduce bloating. Treatment for 

bloat (intubation or rumen puncture with a trocar) may save some 

animals. Avoid unduly exciting 

affected animals.

Toxicity of tall larkspurs declines 

as it matures through the growing 

season. Research has identified a 

toxic window of high risk during 

the flower and early pod stages 

when it becomes palatable and 

toxin levels are moderate.

Since cattle do not generally consume tall larkspurs before flowering, grazing early before plants 

flower may be an option. Cattle 

should be moved off of the larkspur areas during the flower stage 

but can graze larkspur in the late 

pod stage when toxicity declines. 

Using sheep to graze or trample 

tall larkspur patches ahead of cattle 

grazing may reduce cattle losses.

Low larkspur losses may be 

prevented by deferring grazing 

until plants lose their flowers and 

pods, as they rapidly senesce after 

producing pods.

The cholinergic drug neostigmine 

(0.02 mg/kg i.m.) has been successfully used under pen conditions to reverse clinical larkspur 

intoxication. This reversal lasts 

about 2 hours, and repeated injec-
50

tions of neostigmine are sometimes 

required. Under field conditions, 

neostigmine temporarily abates 

clinical signs and animals quickly 

(about 15 minutes) become ambulatory. Depending on the larkspur 

dose, the intoxication can resurface. Nonetheless, there are risks 

associated with the use of neostigmine. The use of neostigminebased treatments may actually 

aggravate losses in the absence of 

further treatment because suddenly 

mobile animals may later develop 

increased muscular fatigue and 

dyspnea and may die.

Research results show that low 

larkspurs can usually be controlled 

by applying 2,4-D at the rate of 

4 lb ae/acre when the vegetative 

development approaches its maximum but before the first flowers 

open.

Tall larkspur can be controlled 

with picloram (1 to 2 lb ae/acre) up 

through the flowering stage. Metsulfuron (1 to 2 oz of product/acre) 

is effective when applied in the 

early vegetative stage of growth. 

Plains larkspur can be controlled 

with picloram (0.25 to 0.5 lb ae/

acre) in the bud stage.

Do not graze cattle on larkspur 

ranges treated with herbicide until 

larkspur is senescent in the fall. 

Herbicide treatment may increase 

palatability to cattle, but toxicity 

remains high.

Toxic window theory of high risk for larkspur poisoning. When toxins are 

high, palatability is low; thus there is low risk of poisoning. Risk is highest 

when palatability is high and toxins are at moderate concentrations.
51

Locoweed

Distribution of Locoweed

Signs and Lesions of Locoweed 

Poisoning

•	 Depression

•	 Dull, dry hair coat

•	 Eyes dull and staring

•	 Irregular gait or some loss of 

muscular control

•	 Weakness

•	 Some animals show extreme 

nervousness

•	 Loss of sense of direction

•	 Withdrawal from other animals

•	 Some animals develop 

inability to eat or drink

•	 Abortions are common; 

hydrops may occur in some 

cattle

•	 Skeletal malformations may 

occur

•	 Animal may become violent 

if stressed

•	 Reduced libido

•	 Cessation of spermatogenesis 

and oogenesis

•	 Congestive heart failure when 

grazed at high elevations

•	 Vacuolation of neurons, renal 

tubular epithelium, hepatocytes, etc.

•	 Recumbency and death may 

follow prolonged consumption of locoweed

Horses, cattle, sheep, and goats 

are poisoned by eating locoweed. 

Wildlife such as elk and antelope 

also have been poisoned; locoweed is suspected in poisoning of 

deer and bighorn sheep as well. 

The locoweeds belong to certain 

species of the Astragalus and 

Oxytropis genera. Other species of 

Astragalus accumulate selenium or 

3-nitro-propanol, which cause different types of intoxication.

The plant gets its name from the 

Spanish word “loco” (crazy), 

which describes the abnormal 

behavior of poisoned animals. 

“Locoed” animals do not recover 

completely. Horses affected by 

locoweed have no value as saddle 

or draft animals. However, the females may be used as brood mares. 

Woolly loco is found from southwestern 

South Dakota south to Texas and New 

Mexico.

Oxytropis sericea belt

Astragalus lentiginosus belt

Astragalus pubentissimus belt

Astragalus mollissimus belt
52

Generally, beef cattle poisoned on 

locoweed do not make economic 

gains, although they may appear to 

recover. Calf, lamb, and foal losses 

from abortion may be high. 

Skeletal birth defects are common; 

many lambs are lightweight at 

birth.

The more common species include white locoweed (Oxytropis 

sericea), woolly loco (Astragalus 

mollissimus var. mollissimus),

spotted loco (A. lentiginosus),

bigbend loco (A. mollissimus var. 

earlei), and garboncillo (A. wootonii). Loco is poisonous at all stages 

of growth. Plants are dangerous 

throughout the year—even when 

they have matured, dried, and 

turned black. All plant parts are 

toxic. The toxin is the indolizidine 

alkaloid swainsonine, which is 

produced by an endophyte (fungus 

growing within the plant). Absence 

of the endophyte may result in 

toxicity being greatly reduced or 

absent in some plant populations. 

Locoweed is found on foothills and semiarid 

regions. It grows in tufts or clumps 4 to 24 

inches tall.

Locoweed flowers resemble sweetpeas. 

Blossoms may be blue, purple, yellow, 

or white. Each stem contains numerous 

leaves with a leaflet on its tip. Top, white 

locoweed; bottom, spotted locoweed.

Where and When Locoweed 

Grows 

Locoweed is commonly found on 

mountains, foothills, and plains 

and in semiarid desert regions. It 

starts growth in late fall, winter, or 

early spring—depending on locality, species, and moisture.

White locoweed grows from 

Montana, Idaho, and North Dakota 

south to Arizona, New Mexico, 

and Texas. Spotted loco grows 

from British Columbia, Canada, 

to Mexico and east to Kansas and 

Oklahoma. Bigbend loco is native 

to the region of Texas for which 
53

How to Reduce Losses

Locoweeds are relatively more palatable than other forage at certain 

seasons. Cattle prefer green-growing locoweed to dormant forage on 

short-grass prairies in early spring, 

but will cease grazing locoweed 

when it matures and warm-season 

grasses begin rapid growth. On 

mountain summer range, cattle 

prefer the young succulent pods of 

white locoweed. On desert winter 

range, cattle and sheep graze dry 

senescent spotted locoweed (which 

retains the toxin) in proportion to 

its availability. Livestock should 

not be allowed to graze locoweedinfested sites when they are likely 

to eat it. Once consumption of 

locoweed stops, swainsonine is 

rapidly cleared from the body.

Livestock owners can reduce 

losses by keeping animals off 

locoweed-infested ranges until 

good forage is available.

There is no effective treatment for 

locoweed poisoning.

Locoweeds are particularly susceptible to clopyralid (0.12 to 0.5 

lb ae/acre), picloram (0.25 to 0.5 

lb ae/acre), metsulfuron (0.25 oz 

product/acre), and 2,4-D (2 to 3 

lb ae/acre). All locoweeds have 

a large seed bank in the soil and 

will germinate and re-establish the 

population when environmental 

conditions are favorable.

it was named; it also occurs in 

southern New Mexico. Wooton 

loco (garboncillo) grows in eastern 

Arizona, southern New Mexico, 

and southwestern Texas. Seeds 

may remain viable in the soil 50 

years or more.

Populations of all locoweed 

species are cyclic. White loco is 

relatively long-lived but its populations die out during major regional 

droughts and gradually increase 

during wet cycles. Woolly and 

spotted loco are short-lived perennials, germinating during autumn 

or spring rains. They grow for 2 to 

3 years and then die from drought 

or insect damage. Wooton loco is a 

winter annual growing during wet 

winters. 

How Locoweed Affects Livestock

Signs of poisoning appear after 

2 to 3 weeks of continuous grazing on the plant. Locoweed has 

four principal effects on livestock: 

neurological damage; emaciation; 

reproductive alterations, such as 

abortion and birth defects; and 

congestive right heart failure 

when grazed at high elevations. 

The toxin is excreted in the milk; 

calves nursed by cows poisoned 

on locoweed have become intoxicated. The neurological signs of 

poisoning will disappear in time 

but may recur when an animal 

poisoned on locoweed is moved 

and stressed.
54

Lupines

Distribution of Lupine

Signs and Lesions of Lupine 

Poisoning

•	 Nervousness

•	 Excessive salivation, frothing 

at the mouth

•	 Depression

•	 Reluctance to move about

•	 Lethargy, inappetence

•	 Difficulty in breathing

•	 Twitching leg muscles

•	 Loss of all muscular control

•	 Convulsions

•	 Coma

•	 Death

•	 Cleft palate and skeletal 

defects in fetus when grazed 

during 40th to the 100th day 

of gestation

Sheep in the Western States are 

frequently poisoned by feeding on 

lupine. Poisoning usually occurs 

when hungry animals are allowed 

to graze lupine. Losses may be especially heavy when hungry sheep 

are trailed through lupine ranges in 

late summer. Sheep and cattle have 

been poisoned by eating lupine 

plants that have been cut and dried 

for hay.

Cows may give birth to calves with 

cleft palate and skeletal defects if 

the cows ingest certain lupines during early gestation (crooked calf 

syndrome). 

Five poisonous species are silky 

lupine (Lupinus sericeus), tailcup 

lupine (L. caudatus), velvet lupine 

(L. leucophyllus), silvery lupine (L. 

argenteus), and lunara lupine (L. 

formosus). Some lupine species are 

not poisonous to livestock, and not 

all species cause birth defects.

Piperidine and quinolizidine alkaloids (ammodendrine and anagyrine) are the compounds causing 

toxicosis and cleft palate as well as 

skeletal defects.

Poisonous species of lupine are 

toxic from the time they start 

growth in spring until they dry up 

in fall. Younger plants are more 
55

toxic than older plants; however, 

plants in the seed stage in late summer are especially toxic because 

of the high alkaloid content of the 

seeds. Under proper conditions, 

some lupines make good forage.

Where and When Lupines Grow

Lupines grow on foothills and 

mountain ranges in sagebrush and 

aspen areas.

Silky lupine grows in northern 

areas from Washington and Oregon 

east to South Dakota. Tailcup 

lupine is found in Oregon, California, Idaho, Utah, Montana, and 

Wyoming. Velvet lupine is found 

in an intermountain region from 

Oregon to Wyoming. Silvery 

lupine occurs from North Dakota 

and Idaho south to Arizona and 

New Mexico. Lunara lupine grows 

in California.

How Lupines Affect Livestock

The amount of lupine that will kill 

an animal varies with species and 

stage of plant growth. It is not safe 

to let sheep graze species such as 

L. argenteus under any condition.

Cattle may be poisoned by eating 

1 to 12 lb of lupine without other 

forage. Smaller amounts are poisonous if cattle eat lupine daily for 

3 to 7 days. Hay containing lupines 

has caused poisoning and death 

of cattle. Crooked legs and other 

congenital deformities occur in 

newborn calves if cows graze certain species of lupine (L. sericeus, 

L. caudatus, and L. laxiflorus)

between the 40th and 100th days 

of gestation.

Closeup shows typical circular pattern of lupine leaves.
56

Lupine is found on open and wooded 

hillsides. Poisonous species grow 1 to 3 

feet tall. Leaves are composed of several 

leaflets, which radiate from a central point. 

Although blue is the most common color, 

flowers may also be white, pink, yellow, or 

blue and white.

Cleft palate of calf whose dam grazed 

teratogenic lupine during the early part of 

the susceptible gestational period.

How to Reduce Losses

Poisoning can be reduced by keeping hungry animals away from 

lupines in the early growth stage, 

in late summer when the plant 

is in the highly toxic seed stage, 

and from dense plant stands at all 

times. Supplemental feeding is 

beneficial, especially when animals 

are trailed through lupine ranges. 

If animals are poisoned on lupines, 

do not try to move them until they 

show signs of recovery.

If cows in the susceptible gestational period (40th to 100th days 

of gestation) are kept from lupine 

when it is most teratogenic (very 
57

early growth or mature seed stage), 

most deformities can be prevented. 

The congenital deformity hazard is 

minimal at other gestation periods 

and after seeds have shattered from 

pods. The malformations can be 

avoided by adjusting the breeding 

season and the grazing of lupineinfested range to avoid the critical 

periods of gestation.

There is no known treatment for 

lupine poisoning. 

Lupine can be controlled with 2,4-

D (2 lb ae/acre), 2,4-D + dicamba 

(1 + 0.5 lb ae/acre), or triclopyr 

(0.5 to 1.5 lb ae/acre). Spray 

actively growing plants after they 

are 5 inches high but before they 

bloom. Reinvasion is rapid and retreatment may be necessary every 

4 to 5 years.
58

Milkvetches

Distribution of Milkvetches

Signs and Lesions of Milkvetch 

Poisoning

Acute Poisoning:

•	 Respiratory distress

•	 Muscular weakness primarily 

in pelvic limbs; prostration

•	 Death usually occurs in 3 to 

4 hours

•	 Lobular alveolar emphysema; 

collapsed lungs and constricted bronchioles with interlobular edema

•	 Forced movement may cause 

these animals to collapse 

and die

Chronic Poisoning:

•	 Nervousness

•	 Labored, rapid respiration

•	 As intoxication progresses, 

respiration develops a wheezing or roaring sound

•	 Knuckling of fetlocks

•	 Goose stepping, knocking 

of hocks and/or feet when 

walking

•	 Drooping of pelvic limbs and 

loss of control of hind limbs, 

which may be dragged when 

animal moves

•	 Indications of temporary 

blindness

•	 Drooling; rough hair coat; 

constipation or diarrhea may 

occur

•	 When forced to move rapidly, 

animal may collapse and die

•	 All signs of poisoning increase with forced movement

•	 Lactating cows are more 

commonly affected than nonlactating

•	 Animals with advanced 

poisoning seldom recover but 

waste and die after several 

months

•	 Sheep show more respiratory and less neuromuscular 

involvement

•	 Horses can be intoxicated; 

cannot get them to back up

•	 Focal hemorrhages in brain

•	 Wallerian degeneration in 

spinal cord in pelvic region

•	 Alveolar emphysema, interlobular edema

•	 Death

Some milkvetches contain nitro 

compounds that are poisonous to 

cattle, sheep, and horses. These 

include plants such as Wasatch 

milkvetch (Astragalus miser 

var. oblongifolius), Columbia 

milkvetch (var. serotinus), Yellowstone milkvetch (var. hylophilus), 

red stemmed pea vine (A. emorya-
59

nus), and other species and varieties of Astragalus. Cattle and sheep 

of all ages are highly susceptible 

to the poisoning. Even when other 

forage is available, cattle readily 

eat some species of milkvetch.

Plants are poisonous from the time 

they emerge but decrease in toxicity as they mature and dry up.

The poisonous substance in 

Wasatch, Yellowstone, and Columbia milkvetches is the ß-D-glucoside of 3-nitro-l-propanol, or miserotoxin. Other milkvetches contain 

glucosides of 3-nitropropionic 

acid. Poisonous nitro compounds 

are found in varying quantities in 

263 species and varieties of North 

American Astragalus.

Where and When Milkvetches 

Grow

Milkvetches grow throughout 

much of North America. Poisonous species grow on the meadows, 

deserts, and forests in the Rocky 

Mountain States. Milkvetches 

emerge from late April to June, 

depending on elevation and snowmelt. Leaves and stems become 

dry and are less dangerous after 

seed dispersal in July or August. 

Red-stemmed pea vine (Astragalus emoryanus) occurs in western 

Texas and New Mexico.

How Milkvetches Affect 

Livestock

The poison in milkvetches acts 

quickly. Two lb of green milkvetch 

may cause acute poisoning or 

death in a 1,000-lb cow. Some 

deaths occur within 1 hour, so fast 

that cattle show no signs; more 

often, animals die within 3 or 4 

hours after eating the plant. Lactating cows are more readily affected 

than dry cows. Do not stress cows 

that are grazing or have recently 

grazed milkvetch.

Acute poisoning is characterized 

by a general muscular weakness 

so that affected animals fall after 

the slightest excitement. The heart 

beats very rapidly before the animal dies from heart failure.

Chronic intoxication may occur 

in cattle and sheep from grazing any of the toxic varieties of 

Astragalus miser, A. emoryanus,

and A. Canadensis—or other 

nitro-containing Astragalus species over a period of several days 

or weeks. Intoxication in cattle is 

characterized by goose stepping 

(cracker heels), varying degrees of 

posterior paralysis, and respiratory 

problems characterized by loud 

breathing sounds (roaring disease). 

This condition occurs in most of 

the Western States and Western 

Canada.
60

Flowers of Wasatch milkvetch resemble sweetpeas. They vary in color from creamy white 

to shades of violet.

Cow poisoned on milkvetch.

How to Reduce Losses

To reduce losses, prevent animals 

from grazing these plants for 

extended periods. Feeding protein 

supplements has been shown to 

reduce intoxication. Avoid stressing cattle that have grazed these 

milkvetches. Cattle 3 years or 

older are less susceptible than 

younger ones.

There is no known treatment for 

milkvetch poisoning.

Milkvetches can be controlled with 

2,4-D (2 lb ae/acre), picloram, 

or clopyralid (0.25 lb ae/acre). 

Treat plants before they reach full 

bloom.
61

Milkweed

Distribution of Milkweed

Signs and Lesions of Milkweed 

Poisoning

•	 Depression, weakness, and 

staggered gait

•	 Difficulty in breathing with 

expiratory “grunting” sounds

•	 Dilation of pupils

•	 Rapid, weak pulse

•	 Loss of muscular control

•	 Elevated temperature

•	 Violent spasms

•	 Bloating

•	 Respiratory paralysis

•	 Congestion of visceral organs

•	 Renal tubular degradation and 

necrosis

•	 Gastroenteritis

Several species of milkweed are 

poisonous to livestock. Labriform 

milkweed (Asclepias labriformis)

is the most toxic. Other species, in 

order of toxicity, include western 

whorled milkweed (A. subverticillata), woollypod milkweed (A. 

eriocarpa), and Mexican whorled 

Milkweed is a perennial that often bears 

blossoms and fruit at the same time. The 

plant may be 1 to 3 feet tall. Greenish-white 

flowers are borne in umbrella-like clusters. 

Leaves may be narrow or broad.

milkweed (A. fascicularis). The 

whorled, narrow-leaf milkweeds 

are most toxic while the common 

broad-leaf milkweed is relatively 

nontoxic.

Milkweed poisoning occurs in 

chickens, turkeys, rabbits, horses, 

cattle, sheep, and goats, with avian 

species being less susceptible than 

mammals. Most livestock losses 

are a result of hungry animals 

being concentrated around heavily infested milkweed areas (such 

as corrals, roadways, and bedding 

grounds). However, poisoning 

may also occur when animals are 

fed hay contaminated with milkWestern whorled milkweed

Mexican whorled milkweed

Labriform milkweed

Woolly pod milkweed
62

weed. The narrow-leaf, whorled 

milkweed species appear to be 

more palatable than the broadleaf 

species. Thus, poisoning incidents 

from contaminated hay are more 

commonly associated with the 

whorled milkweeds. Similarly, 

field poisoning cases are more 

common from the whorled milkweeds. Milkweed may cause losses 

at any time, but it is most dangerous during the active growing 

season. Livestock may be more apt 

to graze these plants after a frost 

or when other available forage is 

limited.

Illustration of broadleaf (left) and narrow-leaf milkweed (right). Drawing courtesy of Holly 

Broome-Hyer, graphic artist, Logan, Utah.

Leaves and other aboveground 

parts of the plant are the typical 

cause of poisonings, but roots may 

also contain toxic constituents. The 

nonwhorled milkweeds contain a 

variety of glycosidic substances 

called cardenolides that are highly 

toxic. In contrast, the whorled 

milkweeds generally contain very 

low cardenolide concentrations. 

The whorled milkweed species are 

thought to contain as yet uncharacterized neurotoxin(s).
63

sheep and cattle and should not be 

fed to them. When possible, rid the 

areas of milkweed and then manage to prevent reinvasion.

Milkweeds can be controlled with 

2,4-D plus picloram (1 + 0.5 lb ae/

acre) or glyphosate as a spot spray. 

Where and When Milkweed 

Grows

Milkweed is often found in sandy 

soils of plains and foothills. It 

grows on ranges and abandoned 

farms, along roadsides, in pastures, 

in ditches, and in waste places or 

overgrazed areas. This plant gets 

its name from the milky, sticky 

juice that oozes out quickly when 

any plant part is broken.

How Milkweed Affects Livestock

The toxicity of milkweed species 

is quite variable, ranging from 

relatively nontoxic to highly toxic. 

An average-size sheep that eats 1 

to 3 oz of green leaves of one of 

the more toxic species is likely 

to die of poisoning within a few 

hours to 2 to 4 days. On a body 

weight basis, for the milkweeds 

that have been identified as being 

toxic, ingestion of as little as 0.05 

percent to greater than 2 percent of 

an animal’s body weight can result 

in poisoning.

How to Reduce Losses

Animals usually do not eat milkweed unless good forage is scarce 

or when plants have been frosted.

Livestock owners can reduce 

losses by keeping animals out of 

milkweed-infested areas. Supplemental feeding usually is beneficial 

during trailing. Hay contaminated 

with milkweed can be poisonous to 
64

Nightshades 

(Solanum spp.)

Distribution of Nightshades

Signs and Lesions of Nightshade 

Poisoning

•	 Labored breathing and expiratory grunt

•	 Salivation and nasal discharge

•	 Body temperature may be 

slightly elevated

•	 Yellow discoloration of the 

skin may occur in chronic 

poisoning

•	 Apathy, drowsiness, progressive weakness, paralysis, and 

trembling

•	 Increased heart rate

•	 Fat may be yellowed and 

gelatinous

•	 Gall bladder may be distended

•	 Gastrointestinal irritation 

including inflammation, hemorrhage, and ulceration

There are several species of nightshades that are toxic to horses, 

cattle, swine, sheep, and poultry. 

The genus includes annual and 

perennial herbs and shrubs that can 

be found throughout the United 

States.

The principal species that serve as 

examples of the genus are black 

nightshade (Solanum nigrum),

silverleaf nightshade (S. eleagnifolium), and buffalo burr (S. rostratum). Black nightshade is an introduced herbaceous annual weed that 

can be found growing mostly on 

disturbed soils and waste areas in 

the Eastern United States and into 

the Midwest. Silverleaf nightshade 

is a perennial with long creeping 

rootstocks. Buffalo burr is an annual native to the Great Plains and 

introduced to the West Coast.

The toxins include a combination 

of a number of sugars and at least 

six different steroidal amines combined to form a variety of glycoalkaloids. One example is the toxin 

solanine. Potatoes are included 

with this group because the vines 

and tubers that have been exposed 

to light can be toxic to livestock. 

Drying does not destroy the toxin. 

Nightshade species are not very 

palatable to livestock. However, 

these plants often grow as weeds 

in hay and silage crops and small 

grains where they can be harvested 

with the crop and then fed to livestock.
65

Where and When Nightshades 

Grow

Black nightshade (both the native 

and introduced varieties) is an annual 6 inches to 3 feet tall. Leaves 

are simple, ovate to lanceolate, entire to sinuate-dentate. Flowers are 

white; berries are black when ripe. 

It grows peripherally in moist areas 

of fields and pastures of disturbed 

loamy or gravelly soils throughout 

the United States.

Silverleaf nightshade is a perennial that grows 1 to 3 feet tall with 

white, hairy leaves and stems. 

Leaves are simple, thick, lanceolate to linear, entire to sinuate. 

Stems and ribs usually have short 

stiff spines. Flowers are violet or 

blue; berries are yellow or orange. 

Silverleaf nightshade grows in 

fields, pastures, and roadsides from 

Missouri to Texas and California.

Buffalo burr is an annual spiny 

weed 1 to 2 feet tall. Leaves are 

irregularly round-lobed or once or 

twice pinnately deeply lobed; veins 

are spiny. Flowers are yellow, and 

the berries are enclosed. Native to 

the Great Plains and introduced to 

the West Coast, buffalo burr grows 

in old fields, overgrazed pastures, 

and roadsides.

How Nightshades Affect 

Livestock

Nightshades are generally unpalatable and are not grazed by 

livestock except under the stress 

of overgrazing or in contaminated 

hay and grain. Poisoning by this 

group of plants does not always 

end in death. In acute poisoning, 

the nervous symptoms develop 

rapidly. Death or recovery occurs 

within a few hours to 1 or 2 days. 

Death apparently is related to the 

paralysis. Chronic poisoning is 

accompanied by emaciation, rough 

hair coat, anorexia, constipation, 

and ascites.

How to Reduce Losses

Losses can be kept at a minimum 

by good pasture management and 

weed control. Harvested forage such as hay, grain, or silage 

can be contaminated with nightshades. Contaminated forage can 

be fed if it is diluted (mixed) with 

nightshade-free forage: an on/off 

feeding strategy should be used. 

Animals being fed this diluted 

forage should be kept under close 

surveillance and immediately removed from the contaminated feed 

if signs of poisoning appear.
66

Nitrate-accumulating 

Plants

Signs and Lesions of Poisoning 

by Nitrate-accumulating Plants

Acute poisoning:

•	 Blue coloration of membranes of mouth, eyes, and 

other mucous membranes 

(cyanosis)

•	 Shortness of breath

•	 Staggering gait

•	 Death

•	 Chocolate-brown blood

•	 Muddy, cyanotic mucus 

membranes

•	 Congestion of rumen and 

abomasum

Subacute poisoning:

•	 Watering eyes

•	 Unthrifty appearance

•	 Reduced milk flow

•	 Reduced weight gain

•	 Abortion and infertility

Many plants, both crops (oat hay, 

sorghum, corn, sudangrass, Johnsongrass, and beets) and weeds 

(carelessweed, kochia, pigweed, 

Russian thistle, and nightshade), 

can accumulate nitrate. Plants 

containing more than 1.5 percent 

nitrates (as KNO3

) dry weight may 

be lethal to livestock. Sublethal 

effects may occur in livestock from 

eating feed containing between 

0.5 percent and 1.5 percent nitrate. 

Nitrate poisoning can also occur 

in animals that consume nitrate 

fertilizers, machine oil, and some 

natural well and pond waters.

Plants differ in their ability to accumulate nitrate. Often the type of 

soil present and the form of nitrogen therein influences the amount 

of nitrate that accumulator plants 

may contain. Drought conditions 

or cloudy weather may enhance 

nitrate accumulation. Treatment of 

nitrate-accumulating plants with 

2,4-D may also cause plants to accumulate excessive amounts of nitrate. Nitrate accumulates primarily in the vegetative tissue of plants 

while the seed remains safe.

Where and When Nitrate 

Poisoning Occurs

Nitrate poisoning occurs throughout the United States. Livestock 

may be poisoned after eating either 

harvested or nonharvested plants, 

feed materials high in nitrate, 

nitrogen fertilizer, etc.

How Nitrate Poisoning Affects 

Livestock

Nitrates are converted to nitrite in 

ruminants. Nitrite causes the production of methemoglobin, a form 

of hemoglobin that cannot carry 

oxygen. Thus, the effects of nitrate 

poisoning result largely from oxygen starvation or suffocation.

The amount of plant material required to poison an animal depends 

on the amount of nitrate in the 
67

plant and on the rate at which the 

plant is eaten. Many factors affect 

toxicity, but in general about 0.05 

percent of an animal’s weight of 

nitrate is near a minimum lethal 

dose. Abortions in cattle have been 

associated with the consumption of 

high-nitrate forage or with maternal poisoning resulting in fetal 

hypoxia.

How to Reduce Losses

Crops that accumulate nitrate and 

grow under conditions favoring 

nitrate accumulation should be 

checked for nitrate content. Highnitrate forage should be diluted 

with low-nitrate forage to decrease 

nitrate intake; or if there are indications of nitrate toxicity, the feeding of nitrate-accumulating forage 

should be discontinued. Adequate 

levels of readily fermentable 

carbohydrates (such as corn) can 

provide some protection against 

nitrate intoxication. Ruminants can 

adapt to relatively high dietary nitrate levels if the high-nitrate feed 

is increased gradually in the diet. 

Otherwise, mix a low-nitrate feed 

with the high-nitrate feed.

If the condition is identified 

soon after onset of clinical signs, 

animals poisoned on nitrate can 

be successfully treated by giving 

methylene blue intravenously at 2 

to 4 mg/kg body weight.
68

Oak

Distribution of Oak

Signs and Lesions of Oak 

Poisoning

•	 Lack of appetite

•	 Gaunt, tucked-up appearance

•	 Constipation, frequently followed by profuse diarrhea

•	 Weakness

•	 Rough, dry hair coat; dry 

muzzle

•	 Tendency to remain near 

water, excessive thirst

•	 Reluctance to follow the herd

•	 Emaciation

•	 Mucus in feces

•	 Frequent urination; 

dark-colored urine

•	 Swelling under the jaw

•	 Subnormal temperature

•	 Collapse

•	 Death

•	 Gastritis: abomasum and 

small intestine inflamed

•	 Swollen kidneys

•	 Nephritis with necrosis and 

renal tubular casts 

•	 Ascites and subcutaneous 

edema

•	 Uremia; elevated BUN (blood 

urea nitrogen)

Cattle may be poisoned by browsing on oak in fairly large amounts 

over a period of 2 to 3 weeks. 

Shinnery oak (Quercus havardii)

and Gambel oak (Q. gambelii) are 

the species responsible for most 

losses. However, many other species can cause poisoning when a 

large amount of the oak plant material is ingested. Shinnery oak, or 

shinnery, is common in the Southwest. Gambel oak, also called 

scrub oak, is found throughout the 

central part of the Western States.

Poisoning occurs primarily when 

animals graze buds and early 

growth leaves, sprouts in cut-over 

areas, mature foliage, and acorns. 

Oak is most dangerous in the budding and leafing stages and when 

acorns are available. As leaves 

mature, oak decreases in toxicity.

Cattle may get as much as 50 

percent of their diet from oak 

browse without showing signs of 

poisoning. More than 50 percent of 

oak browse in the diet will cause 

sickness, and more than 75 percent 

will cause death. Poisoning is most 

likely during times of drought.

The toxic substance in oak is probably a complex of tannins called 

gallotannins.

Gambel Oak

Shinnery Oak
69

Scrub oak may be a shrub 3 to 4 feet high or a tree up to 20 feet high.

recover once oak consumption 

ceases. Milk production will decrease in lactating cows, and they 

will become emaciated. Goats are 

less susceptible than cattle.

How to Reduce Losses

Livestock losses from oak poisoning can be reduced by conservative 

grazing and proper seasonal use of 

shinnery and Gambel oak ranges. 

Oak leaves decrease in toxicity as 

they mature.

In shinnery areas of the Southwest, 

livestock owners should reserve 

pastures with the least amount of 

oak for early spring grazing. The 

use of supplemental feed containing 10 percent calcium hydroxide 

will reduce losses.

Where and When Oak Grows

Shinnery oak is a low spreading 

shrub that grows in sandy areas. It 

is found primarily in western Oklahoma, western Texas, and eastern 

New Mexico.

Gambel oak is a shrub or small 

tree. It grows in dense thickets on 

foothills and mountain slopes, up 

to an elevation of 9,000 feet.

Oak usually starts growing in early 

spring before other range plants.

How Oak Affects Livestock

Death from oak poisoning may 

occur from a few days to 2 weeks 

after the cattle first show signs. 

Chronic poisoning results in poordoing animals that never fully 
70

In Gambel oak areas, animals 

should be kept off oak ranges until 

other forage becomes available and 

the oak leaves mature.

At first signs of poisoning, cattle 

should be moved to an oak-free 

area. In some cases, the use of a 

mild laxative, such as mineral oil, 

may be beneficial.

Oak can be controlled with tebuthiuron at 0.5 to 1 lb ai/acre applied 

to the soil in winter. 

Caution: tebuthiuron is a sterilant 

and will kill all vegetation.
71

Poison Hemlock

Distribution of Poison Hemlock

Signs and Lesions of Poison 

Hemlock Poisoning

•	 Nervous trembling

•	 Neuromuscular stimulation 

followed by depression and 

paralysis

•	 Ataxia, especially lower and 

hind limbs

•	 Salivation

•	 Lack of coordination

•	 Dilation of the pupils

•	 Rapid, weak pulse

•	 Respiratory paralysis

•	 Coma

•	 Death

•	 Convulsions have been 

reported

•	 Occasionally bloody feces 

and gastrointestinal irritation

•	 Skeletal birth defects and 

cleft palate in calves and 

piglets if cows or sows eat 

poison hemlock during susceptible stage of gestation: 

40th to 100th days for cows, 

30th to 60th days for sows

Poison hemlock (Conium maculatum) can be found growing 

throughout the United States. 

Sheep, cattle, swine, horses, and 

other domestic animals are poisoned by eating a small amount. 

It is also extremely poisonous to 

humans.

Poison hemlock has white flowers that grow in small erect 

clusters. Each flower develops into a green, deeply ridged 

fruit that contains several seeds. After maturity, the fruit 

turns grayish brown.
72

Poison hemlock grows 4 to 10 feet tall. 

Leaves are delicate, like parsley, and it 

has a white taproot.

Poison hemlock is sometimes 

confused with western waterhemlock—a more deadly plant— 

because the names are similar. 

(See Waterhemlock chapter in 

this volume.) Poison hemlock 

has a number of common names, 

including deadly hemlock, poison 

parsley, spotted hemlock, European hemlock, and California or 

Nebraska fern.

Roots of poison hemlock may be 

mistaken for wild parsnips and 

eaten by people. The stem of 

poison hemlock has purple spots 

on it.

All parts of poison hemlock—

leaves, stem, fruit, and root—are 

poisonous. Leaves are especially 

poisonous in spring up to the time 

the plant flowers. Fresh leaves are 

unpalatable, so livestock seldom 

eat hemlock when other feed is 

available. The toxic compounds 

are coniine, γ-coniceine, and related piperidine alkaloids.

Where and When Poison 

Hemlock Grows

Because of its attractive flowers, 

poison hemlock was brought to 

the United States from Europe as 

a garden plant but has escaped 

cultivation and can be found growing in many pastures and in some 

areas on rangeland. Poison hemlock is found at roadsides, along 

fences and ditch banks, on edges 

of cultivated fields, along creekbeds and irrigation ditches, and in 

waste areas and may invade fields 

or pastures.

Poison hemlock is a biennial and 

belongs to the carrot family. It 

starts growing in early spring but 

does not flower until its second 

year. In favorable locations it may 

be a perennial. Poison hemlock 

harvested with hay can be toxic 

to livestock and produce birth 

defects.

How Poison Hemlock Affects 

Livestock

Poison hemlock ingestion is often 

fatal. Sheep may be poisoned by 

eating as little as 4 to 8 ounces of 

green leaves. Cattle that eat 10 to 

16 ounces may be affected. Signs 
73

usually appear within an hour after 

an animal eats the plant. Animals 

die from respiratory paralysis in 2 

to 3 hours. Convulsions, which are 

common in waterhemlock poisoning, seldom occur with poison 

hemlock.

Skeletal deformities or cleft palate may be induced in offspring 

of cows, sheep, goats, and pigs if 

poison hemlock is ingested by the 

mother during susceptible stage 

of gestation: 40th to 100th days 

in cows and 30th to 60th days in 

sheep, goats, and pigs. Palate and 

skeletal deformities in calves are 

indistinguishable from the lupineinduced crooked calf disease.

How to Reduce Losses

Avoid stressing poisoned animals 

that are not recumbent. For recumbent animals, support respiration 

and treat with activated charcoal 

and a saline cathartic. Gastric 

lavage may be beneficial, with 

atropine therapy to control parasympathetic signs.

Animals that recover seldom show 

lingering effects. 

Research results show that poison 

hemlock may be controlled by 

treating plants before they begin to 

bud with 2,4-D plus dicamba (2.5 

lb + 1 lb ae/acre). Repeat applications may be needed.

Hemlock Poisoning in Humans

People may be poisoned by eating 

any part of a hemlock plant. Often 

poisoning occurs when the victim 

has confused hemlock root with 

wild parsnips, hemlock leaves 

with parsley, or hemlock seed with 

anise. 

The hollow stem is marked with purple spots, a distinguishing 

feature.
74

Ponderosa Pine Needles

Distribution of Ponderosa Pine

Signs and Lesions of Ponderosa 

Pine Needle Poisoning

•	 Abortion characterized by 

weak parturition contractions, 

excessive uterine hemorrhage, and incomplete dilation of the cervix

•	 Calves are weak but may survive if abortion is near term 

and extra care is provided

•	 Persistently retained placenta

•	 There may be indications of 

the impending abortion

•	 Following the abortion, cows 

may develop endometritis 

and septicemia accompanied 

by a marked increase in body 

temperature; cow may die if 

treatment is not immediately 

provided

The needles of ponderosa pine 

(Pinus ponderosa) cause abortion when grazed by cattle. The 

abortions occur primarily from 

late fall to early spring, during the 

last trimester of pregnancy. Pine 

needles are generally grazed by 

cattle during cold winter weather 

when forage is lacking because of 

previous grazing or snow cover. 

However, cows may incidentally 

ingest dry fallen pine needles when 

grazing under tree cover. They may 

also eat needles from slash piles 

or windfall branches. The abortifacient compounds are diterpene 

acids including isocupressic acid 

and its metabolites.

Where and When Ponderosa 

Pine Grows

Ponderosa pine grows in all of the 

States west of the Great Plains and 

in Western Canada. Lodgepole 

pine, some cedars, junipers, and 

Monterey cypress can also cause 

abortions when consumed by 

cows. 

How Ponderosa Pine Needles 

Affect Livestock

Abortions may begin within 48 

hours after pine needles are ingested. Some cows abort as much 

as 2 weeks after having ingested 

the needles. Only a small amount 
75

of needles is required to cause 

an abortion. Incidence can vary 

from only a few to 100 percent 

of the cows involved. There are 

no indications of overt toxicity to 

cattle eating the needles. If calves 

are far enough developed when the 

cow eats pine needles, they will be 

small and weak but may survive 

with proper care. Surviving calves 

may not nurse or may not be allowed to suckle by the dam; the 

dam may not have sufficient milk 

to feed the calf.

A persistently retained placenta is 

a constant finding regardless of the 

gestational stage of the abortion. 

Cows should be observed closely 

the first few days following an 

abortion. In case of complications 

from the retained placenta, consult 

a veterinarian. Some of these cows 

will die. The mortality of cows 

aborting from eating pine needles 

can be significantly higher than 

normal.

How to Prevent Poisoning

Prevent access to pine trees during 

the last trimester of pregnancy.

The ponderosa pine is a hardy tree extensively harvested for lumber. Both the dry 

and green needles and bark from the tree 

can cause abortion in cows.
76

Rayless Goldenrod

Distribution of Rayless 

Goldenrod

Signs and Lesions of Rayless 

Goldenrod Poisoning

•	 Lassitude and depression

•	 Standing in a humped-up 

position; stiff gait when walking

•	 Trembling of muscles of nose 

and legs, especially after 

exercise; as the condition 

worsens, the whole body may 

shake

•	 Weakness

•	 Constipation and dribbling of 

urine

•	 Recumbency

•	 Acetone odor on the breath

•	 Coma

•	 Terminal respiration consists 

of prolonged inspiration, a 

short pause, and forced expiration

•	 Death

•	 Myocardial necrosis and fibrosis of cardiac and skeletal 

muscles in horses and goats

•	 Degenerative changes of the 

liver

Rayless goldenrod (Isocoma 

wrightii or pluriflora), rosea, or 

jimmy weed, is an erect, bushy, 

unbranched perennial shrub, growing 2 to 4 feet tall. The leaves are 

alternate, linear, and sometimes 

sticky, and the flowers are yellow. 

It is toxic to horses, cattle, sheep, 

and goats. The toxin, referred to as 

tremetol (a mixture of compounds 

including tremetone, dehydrotremetone, 3-hydroxytremetone 

and 3-oxyangeloyl-tremetone), is 

excreted in the milk of lactating 

animals, so the offspring of the 

animal or humans drinking the 

milk may become poisoned by 

the consumption of contaminated 

milk. The toxin is cumulative and 

is present in both green and dry 

plant material.

Where and When Rayless 

Goldenrod Grows

This shrub grows on the dry rangelands from southern Colorado into 

Texas, New Mexico, and Arizona. 

It grows especially well in river 

valleys and along drainage areas. 

Poisoning is most common in late 

fall and winter.
77

How Rayless Goldenrod Affects 

Livestock

Daily consumption of 1 to 1.5 

percent of an animal’s weight of 

the green plant for 1 to 3 weeks 

will produce signs of poisoning 

in horses, cattle, and sheep. Death 

will result if the affected animals 

are not removed from access to the 

plant. The condition it produces in 

cattle is known as trembles.

How to Reduce Losses

Poisoning of livestock by rayless 

goldenrod can best be prevented by 

not overgrazing livestock on ranges infested with this plant and by 

feeding hay following snowstorms 

that cover other forage. There is 

no treatment for poisoning by this 

plant but livestock may recover if 

they are not stressed and are given 

fresh feed and water; long-term 

effects are unknown.

Closeup of rayless goldenrod showing the leaves and flowers.

Rayless goldenrod in its natural environment. Photo 

courtesy of Dr. Samantha R. Uhrig, Desert Willow Veterinary 

Services, LLC, Carlsbad, NM.
78

Rayless goldenrod can be controlled by picloram or dicamba 

(1 to 2 lb ae/acre) in late summer 

following adequate rainfall.

White Snakeroot

White snakeroot (Eupatorium 

rugosum) contains the same toxin 

as rayless goldenrod (tremetol 

compounds), and it is toxic to 

cattle, horses, sheep, and goats. 

It affects all animals, including 

humans who consume milk from 

affected animals (“milk sickness”). 

It damages nearly all muscle types 

including the heart muscle, disrupting cardiac function. Death may 

result, especially when an animal 

is stressed. White snakeroot grows 

in the Midwest and south into eastern Texas and is most commonly 

found in moist, shady, wooded 

areas.

White snakeroot.
79

Selenium-accumulating 

Plants

Distribution of Seleniumaccumulating Plants

Signs and Lesions of Selenium 

Poisoning

Acute Poisoning:

•	 Abnormal posture

•	 Unsteady gait

•	 Diarrhea

•	 Abdominal pain

•	 Increased pulse and respiration rate

•	 Prostration

•	 Death

•	 Petechial hemorrhage, endocardia, acute congestion 

and hemorrhage of the lungs; 

enteritis and passive congestion of the liver

Sheep do not show the typical 

signs of poisoning observed in 

cattle, horses, and pigs. Depression, increased respiration, and 

sudden death are seen in sheep.

Chronic Poisoning:

•	 Dullness

•	 Rough hair coat

•	 Emaciation

•	 Lack of vitality

•	 Lameness

•	 Hooves may become 

overgrown

•	 Loss of long hair

Selenium is accumulated by a 

number of plants in sufficient 

amounts to be chronically toxic, 

and in some cases acutely toxic, 

if consumed by livestock. Plants 

have been divided into three 

groups, based on their seleniumaccumulating ability.

Plants containing more than 5 ppm 

(parts per million) selenium are 

potentially toxic.

Two-grooved milkvetch (Astragalus bisulcatus) is a selenium-accumulating plant.

Primary selenium accumulator or 

indicator plants may accumulate 

up to several thousand parts per 

million selenium. This group 

includes species of milkvetch 

(Astragalus), woody aster (Machaeranthera section Xylorrhiza),

goldenweed (Haplopappus section 
80

Oonopsis), and princes plume 

(Stanleya pinnata). Selenium 

accumulated by these plants is 

largely water soluble and in the 

form of low-molecular-weight 

organic compounds and selenate. 

The selenium is not incorporated 

into protein.

Secondary selenium accumulator plants may contain up to 

several hundred parts per million 

selenium, but lesser amounts are 

much more common. This group 

includes species of aster (Aster),

milkvetch (Astragalus), saltbush 

(Atriplex), Indian paintbrush 

(Castilleja), toadflax (Comandra),

gumweed (Grindelia), snakeweed 

(Gutierrezia), woody aster (Machaeranthera), and stickleaf (Mentzelia). In rare instances, these plants 

will accumulate up to several 

thousand parts per million. As in 

the first group, selenium appears 

primarily as water-soluble selenate 

with smaller amounts of lowmolecular organic forms.

Aster sp., a secondary selenium 

accumulator 

The nonaccumulator group includes grasses such as western 

wheat grass, small grains, and 

alfalfa. Selenium absorbed by 

these plants is metabolized into 

plant proteins. These plants rarely 

accumulate more than 50 ppm 

selenium and usually only 5 to 12 

ppm. On rare occasions, however, 

several hundred parts per million 

may be taken up. 

Where Selenium-Accumulating 

Plants Grow

The major seleniferous areas of the 

West can be found in North and 

South Dakota, Montana, Wyoming, 

Colorado, and Utah. Selenium 

poisoning occurs in the areas that 

have soils high in selenium.

How Selenium Affects Livestock

Selenium intoxication can occur 

as acute (rapid death) or as chronic 

(hair loss, hoof lesions, etc.) poisoning. Selenium is an essential 

nutrient. The problem in dealing 

with selenium is that the difference 

between the amount required for 

good nutrition and the amount that 

is toxic is very small.

The nonaccumulator plants are the 

most problematic of the selenium 

accumulators because they are 

commonly grazed by livestock. 

Cattle and sheep grazing on these 

plants may have problems with 

overgrown hooves and reproduction. Animals (both males and 
81

females) may show few obvious 

signs of selenium poisoning but 

may suffer reproductive effects.

How to Reduce Losses

The only practical method of reducing losses in livestock to selenium poisoning is to prevent animals 

from eating excessive amounts of 

selenium-containing plants. Soil 

and forage surveys or maps of the 

selenium content over a ranch or 

a range can be of great assistance 

in developing a grazing or forageproduction program. The amount 

of selenium in soil and forage can 

vary markedly over an area. 

Hooves of pigs fed selenium-accumulating 

plants. Note the cracks on the tops of the 

hooves.

The chemical form of selenium 

in the soil can dramatically affect plant uptake. Identifying 

high-selenium and low-selenium 

areas, and when possible the form 

of selenium present, can help in 

deciding where to graze animals 

or if selenium supplementation is 

needed. Breeding horses or cows 

should not be pastured in a highselenium area. Affected animals

Princes plume (Stanleya pinnata), a primary 

selenium accumulator.

that are removed from seleniferous 

forage may recover without apparent permanent effects; however, 

recovery depends on the severity 

of intoxication.
82

Snakeweed (Broom and 

Threadleaf)

Distribution of Snakeweed

Signs and Lesions of Snakeweed 

Poisoning

•	 Listlessness

•	 Periodic mucopurulent nasal 

discharge with crusting and 

sloughing of nasal mucosa

•	 Anorexia and weight loss

•	 Rough hair coat

•	 Diarrhea followed by 

constipation

•	 Hematuria may occur

•	 Gastroenteritis

•	 Hydropic degeneration and 

necrosis of the liver; mild 

icterus

•	 Toxic nephrosis

•	 Uterine edema and possible 

hydrops of fetal membranes

•	 Pregnant cows may have 

periodic vulvar swelling and 

earlier-than-normal udder 

development; they may abort 

and retained placenta is 

present.

Broom snakeweed (Gutierrezia sarothrae) and threadleaf snakeweed 

(G. microcephala) are perennial 

weeds common on rangelands 

from Canada to Mexico. Cattle, 

sheep, and goats have been poisoned in large numbers from eating 

snakeweed; however, most losses 

occur in cattle. Snakeweed should 

be considered for its toxic proper-
83

ties and for its abortifacient effects. 

Death may occur, but the principal 

effect of poisoning is abortion. 

Toxin levels increase through the 

growing season. Cattle will not 

eat snakeweed unless other feed 

is scarce. Abortions often follow 

a snowstorm because snow covers 

the grasses leaving only the snakeweed for the animals to graze.

Snakeweed is a densely branched perennial 

shrub that grows to 2 feet tall on dry range 

areas from Texas to California north to 

Colorado and Idaho and south into Mexico.

Where and When Snakeweed 

Grows

Broom snakeweed and threadleaf 

snakeweed are very similar in appearance. They are distinguished 

by the number of ray flowers per 

head: three or more ray flowers for 

broom snakeweed and only one 

or two for threadleaf snakeweed. 

Snakeweed grows on the drier 

range areas. Snakeweed is said 

to be more toxic when growing 

on sandy soils than on limestone 

soils (referred to as hard soils). In 

the Southwest, it resumes growth 

following flowering in the fall and 

remains green over the winter. Farther north it begins growth in the 

spring and flowers in the late summer and early fall. Its populations 

are cyclic, increasing in wet years 

and dying back during drought.

How Snakeweed Affects 

Livestock

The amount of snakeweed needed 

to cause death or abortion in cattle 

varies greatly. Cows near term 

may abort or give birth to small, 

weak calves that may survive 

if properly cared for. Cows that 

abort have a persistently retained 

placenta. Cows aborting may 

develop endometritis and septicemia accompanied by an increase 

in body temperature. These cows 

are at risk unless properly treated 

by a veterinarian. Factors affecting dosage include site and stage 

of growth and rate of consumption. The toxins are thought to be 

diterpene acids.

How to Reduce Losses

Snakeweed increases with disturbance (overgrazing, fire, drought). 

Maintaining ranges in good condi-
84

tion can prevent dense concentrations of snakeweed. Snakeweed is 

not palatable. Adequate forage will 

prevent consumption of snakeweed. Cows in poor body condition probably eat more snakeweed 

than cows in better condition 

because the former graze less 

selectively. 

Poisoned cows should be removed 

from snakeweed areas and given 

proper care until they recover. 

In the Southwest, snakeweeds can 

be reliably controlled by spraying 

in the fall using picloram (0.25 

to 0.5 lb ae/acre) or metsulfuron 

(0.5 g ai/acre). Further north in the 

Plains and Intermountain regions, 

these same herbicides and rates 

must be applied in early summer 

while snakeweeds are in the vegetative stage and growing rapidly.
85

Sneezeweed

Distribution of Sneezeweed

Signs and Lesions of Sneezeweed 

Poisoning

•	 Decreased appetite

•	 Lips and muzzle become 

stained green from vomiting 

(spewing sickness)

•	 Lambs become stiff and 

wasted

•	 Depression

•	 Weakness with irregular pulse

•	 Frothing at the mouth

•	 Coughing

•	 Emaciation and wasting

•	 Ascites

•	 Gastrointestinal hyperemia

•	 Renal tubular necrosis

•	 Liver degeneration

Animals that feed on sneezeweed 

may become affected with “spewing sickness.” The disease gets its 

name from its most characteristic 

sign—chronic vomiting or spewing.

In the Western States, western 

sneezeweed (Hymenoxys hoopesii;

formerly Helenium) is common 

to many mountain ranges. Sheep 

are frequently poisoned by eating sneezeweed; cattle are rarely 

poisoned. Animals eat sneezeweed 

during summer and fall, when other forage is scarce or has become 

less palatable. Lambs poisoned on 

sneezeweed become unthrifty and 

are difficult to market. Poisoned 

ewes are often emaciated (wasting) 

and may not die until some time 

after removal from sneezeweed.

All plant parts are poisonous. The 

toxin is a sesquiterpene lactone. 

Sneezeweed, bitterweed, and rubberweed have the same type of 

toxin.

Where and When Sneezeweed 

Grows

Sneezeweed grows at elevations 

of 5,000 to 12,000 feet on moist 

slopes and well-drained meadows 

from western Montana and eastern 

Oregon southward to California 

and New Mexico. It starts growing 

in early spring and matures in late 

summer and early fall. Sneezeweed increases with overuse of the 

range. Heavy stands of sneezeweed 

will inhibit growth of other plants.

How Sneezeweed Affects 

Livestock

An animal may die if it eats small 

quantities of sneezeweed over a 

long period. Sheep may be poisoned by eating about 2 lb of green 
86

sneezeweed leaves daily for 10 

days.

Some animals die within a few 

days after the first signs appear. 

Others that develop a chronic form 

of poisoning may live for 2 to 3 

weeks or more. Complete recovery 

from the poisoning is possible if 

animals are taken off the plants as 

soon as the first signs are observed. 

Lambs usually show signs of 

stiffness before other symptoms appear. Lambs left to graze 

sneezeweed after signs first appear 

become unthrifty (waste) and are 

unprofitable to keep. Ewes left on 

sneezeweed after signs appear will 

waste and die.

How to Reduce Losses

Proper range management and 

improved range conditions will 

reduce the risk of sneezeweed 

poisoning. Alternate grazing (on 

and off) of sneezeweed areas at the 

proper times allows time for recovery. As soon as signs of poisoning 

appear, remove all animals from 

sneezeweed-infested range for at 

least 14 days.

Practice open herding. Allow 

animals free movement. Avoid 

grazing sheep continuously on 

sneezeweed-infested rangeland.

Sneezeweed can be controlled with 

2,4-D at 4 lb ae/acre.

Sneezeweed has one or several stems. Leaves are alternate, lance shaped, and smooth 

edged. Orange flowers with darker orange centers grow in clusters. Sneezeweed is a perennial of the sunflower family and is closely related to bitterweed and Colorado rubberweed.
87

Spring Parsley

Distribution of Spring Parsley

Signs of Spring Parsley 

Poisoning

•	 Sunburn of exposed areas

•	 Reddening and blistering of 

exposed areas of the body 

(nose, udder, external 

genitals)

•	 Scabs form after blistering

•	 Ewes and cows may refuse to 

allow young to nurse

Spring parsley (Cymopterus 

watsonii) causes a severe sunburn—or photosensitivity—in 

sheep and cattle. The plant also 

is known as cymopterus or wild 

carrot.

Animals do not die from eating 

spring parsley, but losses occur 

when affected ewes or cows with 

blistered, sore udders refuse to let 

their offspring nurse. Lamb losses 

are often high; calf losses usually 

are low.

Spring parsley poisoning differs 

from bighead poisoning, a type of 

Spring parsley is a perennial that grows 4 to 6 inches tall. It gets its name from the finely 

divided leaves that resemble parsley. Small white or cream-colored flowers are borne in 

umbrellalike clusters about one inch across. The plant has a long taproot. Spring parsley is 

a member of the carrot family.
88

photosensitivity caused by horsebrush, but is similar to St. Johnswort poisoning. The poisonous 

substances in spring parsley are 

two furocoumarins—xanthotoxin 

and bergapten.

Plants are poisonous from early 

spring until they mature and dry in 

early summer.

Where and When Spring Parsley 

Grows

Spring parsley grows on welldrained soils, on rolling foothills, 

and with sagebrush, piñon pines, 

and junipers. It occurs at elevations 

of 4,000 to 8,000 feet. This is one 

of the first plants to begin growing 

in early spring. It flowers from late 

April to June and disappears by 

early summer.

How Spring Parsley Affects 

Livestock

Sheep and cattle are especially susceptible to spring parsley poisoning during March, April, and May.

Sheep are affected if they are 

exposed to direct sunlight after 

eating as little as 1⁄4 lb of the green 

plant. The photosensitization varies from slight to severe; blisters 

form on areas of the sheep’s body 

not covered by wool. In advanced 

poisoning, all of the white areas of 

the body may be affected. 

Losses are primarily confined to 

lambs. On ranges where spring 

parsley is one of the first spring 

plants to emerge, a ewe may eat 

it soon after lambing. The udder 

and teats become so painful that 

the ewe will not allow the lamb 

to nurse. Newborn lambs may die 

of starvation or dehydration. The 

growth of surviving lambs is usually stunted from lack of milk.

Cattle are affected if they are 

exposed to direct sunlight after eating about 1 lb of the green plant. 

White areas on the body become 

“sunburned.” Cows refuse to let 

calves nurse. In severe poisoning, 

all of the white areas of the body 

may blister, and animals may lose 

weight rapidly.

Sheep and cattle gradually 

recover after they stop eating 

spring parsley.

How to Reduce Losses

To reduce losses, keep sheep and 

cattle off ranges infested with 

spring parsley in early spring until 

adequate forage is available.

There is no known treatment for 

animals that are poisoned by spring 

parsley, but they will recover if 

kept in the shade and if skin lesions are treated.

Research results show that spring 

parsley can be controlled by 
89

spraying plants in the bud to early 

bloom stages of growth with an 

amine salt of 2,4-D applied at the 

rate of 2 lb ae/acre.
90

St. Johnswort

Distribution of St. Johnswort

Signs and Lesions of 

St. Johnswort Poisoning

•	 Restlessness

•	 Scratching head with hind 

legs and rubbing head against 

solid objects

•	 Crouching

•	 Rapid pulse, increased 

temperature

•	 Redness and swelling of 

white-skinned areas (sunburn)

•	 Swollen eyelids, clouded 

eyes; possibly blindness

•	 Peeling or sloughing of 

affected skin

•	 Convulsions

•	 Necrotic dermatitis

St. Johnswort (Hypericum perforatum), or Klamath weed, is a range 

plant that, when grazed by livestock, results in photosensitization. 

Animals that eat St. Johnswort and 

then are exposed to direct sunlight 

develop severe photosensitization 

in white areas of the body.

Young cattle and sheep are most 

often affected, but almost all 

white-skinned cattle, sheep, and 

horses react to eating the plant. 

Recently sheared sheep are especially susceptible. Although 

St. Johnswort seldom kills, it can 

cause severe economic losses.

St. Johnswort is toxic at all stages 

of growth. Young tender shoots 

may attract animals in spring. Normally, cattle and sheep will not eat 

mature St. Johnswort if they have 

other forage. Hay containing dry 

St. Johnswort can cause poisoning.

St. Johnswort is a perennial that grows 

along roadsides and in meadows, pastures, rangelands, and waste places. In 

the Pacific Coast States, it may reach a 

height of 5 feet; in other areas, it grows 1 

to 3 feet tall.
91

Where and When St. Johnswort 

Grows

St. Johnswort is an aggressive 

weed. It grows in old meadows, 

on pastures, along roadsides, on 

rangeland, and in waste areas. It 

usually is found growing on dry, 

gravelly or sandy soils. It may 

grow in dense patches or mixed 

among other plants. It is considered a noxious weed in many 

States.

How St. Johnswort Affects 

Livestock

When an animal eats St. Johnswort, the poisonous compound in 

the plant, hypericin, sensitizes the 

skin to sunlight. Pigments in the 

skin shield colored skin from the 

sun’s rays so that only white or 

unpigmented areas are affected. 

These areas itch and become red, 

swollen, and sore, and the skin 

may peel or come off in large 

sheets (photosensitization).

White-skinned cattle are more 

susceptible to St. Johnswort poisoning than white-skinned sheep. 

Cattle are poisoned by St. Johnswort if they eat an amount equal 

to approximately 1 percent of their 

body weight and are then exposed 

to direct sunshine for 2 to 5 days. 

In experimental feedings, sheep 

fed 5 percent of their body weight 

showed symptoms.

Signs of poisoning usually appear 

2 to 21 days after animals begin to 

graze St. Johnswort.

St. Johnswort is a smooth-branched, erect 

plant. Leaves are covered with clear, small 

dots that contain the toxic substances. Fivepetaled flowers grow in clusters; they are 

orange-yellow with occasional black dots 

along the edges.

Photosensitization due to eating 

St. Johnswort.
92

How to Reduce Losses

At the first signs of poisoning, 

move affected animals out of direct 

sunlight to shady or dark quarters. 

Treat affected skin areas as directed by your veterinarian. Give 

animals free access to fresh water 

and feed.

Research results show that St. 

Johnswort may be controlled by 

applying 2,4-D at 2 to 3 lb ae/acre. 

Biological control with the Klamath beetle is recommended for 

extensive infestations. For information about using the Klamath 

beetle, see your county agricultural 

agent.
93

Sweet Clover

Distribution of Sweet Clover

Sweet clover grows throughout the 

Western United States.

Signs and Lesions of Sweet 

Clover Poisoning

•	 Signs occur 3 to 6 weeks after 

first exposure to spoiled plant

•	 Bleeding into muscles, joints, 

or other tissues

•	 Hematomas appear on neck, 

flanks, and hips

•	 Excessive bleeding during 

minor surgery

•	 Sudden death due to massive 

hemorrhage

Where and When Sweet Clover 

Grows

White sweet clover (Melilotus 

alba) and yellow sweet clover (M. 

officinalis) are biennials that can 

be found growing along roadsides, 

ditch banks, and often invading 

fields throughout the United States. 

These plants have been used 

extensively as a forage crop and 

soil builder. They are the cause of 

sweet clover poisoning, a severe 

hemorrhagic disease of cattle. 

Only minor losses have occurred 

in sheep. This bleeding condition 

is the result of the consumption of 

moldy or spoiled sweet clover hay 

or silage by cattle.

Yellow sweet clover.
94

How Sweet Clover Affects 

Livestock

Sweet clover contains coumarin, 

which is nontoxic but can be converted to the dicoumarol by molds 

that grow on spoiled sweet clovers. 

The anticoagulant dicoumarol is an 

antagonist to Vitamin K. Dicoumarol interferes with the synthesis in 

the liver of the vitamin-K-dependent clotting protein prothrombin. 

The likelihood of poisoning depends on the level of dicoumarol in 

the clover and the time over which 

the moldy clover is consumed by 

an animal.

The signs of poisoning usually 

occur 3 to 6 weeks after the start of 

feeding spoiled sweet clover. Sudden death due to massive hemorrhaging may occur. Bleeding may 

occur in muscles, joints, or other 

tissues. Hematomas usually occur 

in the neck, flanks, hips, and other 

body areas where the animal may 

be bumped, such as when eating 

in a stanchion or similar device. 

Excessive bleeding is associated 

with minor surgery.

How to Reduce Losses

Treatment consists of removing 

the moldy clover from the diet. A 

blood transfusion can be given to 

badly poisoned animals or 

vitamin K can be administered.

Prevent poisoning by not feeding 

moldy clover to cattle, especially 

just prior to castration, dehorning, 

or any surgical procedure. Cattle 

grazing sweet clover also bloat and 

die.
95

Tansy Ragwort

Distribution of Tansy Ragwort

Signs and Lesions of Tansy 

Ragwort Poisoning

•	 Signs may not appear until 

6 or more months after the 

plant is ingested

•	 Lethargy and loss of interest 

in food

•	 Crustiness around eyes and 

nose; eyes may also be red 

and watery, especially in 

bright sunlight

•	 There may be diarrhea or 

constipation

•	 Weakness as manifest by 

wobbling and dragging rear 

feet

•	 Animals may wander 

aimlessly and appear to be 

blind and may become 

belligerent

•	 Cattle may develop an 

unpleasant odor that has a 

somewhat sweetish quality

•	 The abdominal cavity may 

fill with fluid up to several 

gallons, and death may occur 

within a few days after symptoms appear

•	 Liver cirrhosis (necrosis and 

fibrosis) and bile duct 

proliferation

•	 Ascites

•	 Gastroenteritis

Mature tansy ragwort may grow 4 or 5 

feet tall. It has sturdy stems, has a strong 

“weedy” odor, and produces great numbers of seed. Photo courtesy of Michael 

Shephard, USDA Forest Service.

Tansy ragwort (Senecio jacobaea) is a weedy biennial plant 

that infests woodlands, pastures, 

and hayfields of the coastal northwest United States. It is generally unpalatable to livestock and, 

therefore, is eaten only when other 

food is scarce or when it cannot be 

avoided as a contaminant in hay, 

ensilage, and lush pastures. The 

toxins are pyrrolizidine alkaloids 

that are toxic to all classes of 

livestock but most toxic to cattle 

and horses. They cause a chronic, 
96

cirrhosis-like condition of the liver, 

which may lead to death of the 

animal several months after the 

tansy ragwort has been eaten. The 

poisoning is thus difficult to diagnose and death is often attributed 

to other causes. Death losses have 

been reported from short-term 

grazing of these plants.

The rapid spread of the plant has 

been slowed due to the development of biological control procedures.

Where and When Tansy 

Ragwort Grows

Tansy ragwort grows in areas with 

over 20 inches of rainfall annually; 

however, it could possibly grow 

in heavily irrigated locations with 

less rainfall. In the United States, 

tansy ragwort occurs principally 

in coastal Washington, Oregon, 

northern California, and in the 

New England States.

How Tansy Ragwort Affects 

Livestock

Tansy ragwort contains pyrrolizidine alkaloids, which primarily 

affect the liver. Cells of the liver 

are slowly killed or prevented 

from reproducing and are gradually replaced by connective tissue. 

Whether an animal survives 

depends on the number of liver 

cells it loses, and the length of 

survival depends on the rate at 

which it loses liver cells. Animals 

may survive for 6 months or longer 

after they have ingested a lethal 

amount of plant and may show 

no outward symptoms during this 

period. They may suddenly become lethargic, fill with fluid in the 

abdominal cavity, and die within 

2 to 4 days. They may also show 

central nervous system effects such 

as impaired vision and continuous 

walking with a stumbling gait. The 

onset of symptoms may be dependent on other stresses imposed on 

the animal, which it cannot handle 

in its weakened condition. Animals 

eating 5 percent or more of their 

total daily diet of prebloom tansy 

ragwort for periods exceeding 20 

consecutive days can be expected 

to die within 6 months.

How to Reduce Losses

The poisoning is irreversible and 

the animal will die. The best way 

to prevent tansy ragwort poisoning 

is to avoid the plant. Young animals are more easily poisoned than 

mature animals. Pastures for horses 

and cattle with over 5 percent 

tansy ragwort should be avoided 

until the tansy ragwort has been 

controlled. Avoid hay and ensilage 

contaminated with tansy ragwort 

because animals cannot sort out the 

tansy ragwort. 

Tansy ragwort can be controlled by 

cultivation. In other areas, research 

results show that tansy ragwort 

can be controlled with 2,4-D (low 
97

volatile ester or emulsifiable acid) 

at 1 to 3 lb ae/acre, dicamba at 0.5 

to 1 lb ae/acre, picloram at 0.25 to 

0.5 lb ae/acre, or metsulfuron at 1 

to 1.5 oz product/acre. Spray tansy 

ragwort in the rosette stage. These 

herbicides will injure or kill legumes. Biological control methods 

have been developed; contact your 

extension agent. 
98

Waterhemlock

Distribution of Waterhemlock

Signs and Lesions of 

Waterhemlock Poisoning

•	 Nervousness

•	 Excessive salivation and 

frothing

•	 Muscle twitching

•	 Dilation of the pupils

•	 Rapid pulse

•	 Rapid breathing

•	 Tremors

•	 Violent convulsions, grand 

mal seizures

•	 Coma

•	 Death may occur as early as 

15 minutes after a lethal dose 

is consumed

•	 No significant gross lesions

Waterhemlock (Cicuta douglasii)

is the most violently toxic plant 

that grows in North America. 

Only a small amount of the toxic 

substance in the plant is needed to 

produce poisoning in livestock or 

in humans. The toxin, cicutoxin, 

acts on the central nervous system 

and is a violent convulsant.

Waterhemlock may be confused 

with poison hemlock because of 

their similar flowers. However, 

these two are different plants and 

cause different types of poisoning. 

(See Poison Hemlock chapter in 

this volume.)

The underground portions of the 

plant, especially the tuberous 

roots, are very toxic. People are 

sometimes poisoned by eating the 

roots, which they mistake for wild 

parsnip.

Waterhemlock grows in wet seepage areas 

such as meadows, pastures, and along the 

banks of streams. It reaches a height of 

2 to 4 feet. The plant is a perennial in the 

carrot family.

In cases of waterhemlock poisoning in humans, take the affected 

person to the emergency room of 

the nearest hospital immediately. 
99

Call poison control and seek emergency treatment immediately.

Cattle have been known to eat 

lethal amounts of waterhemlock 

in pastures having adequate forage; therefore, animals should 

be prevented from grazing over 

waterhemlock-infested areas. Animals have been poisoned by eating 

roots that have been brought to 

the surface by plowing or cleaning 

ditches.

The toxic substance in waterhemlock is cicutoxin, a highly poisonous unsaturated alcohol that has a 

strong carrot-like odor. It is found 

principally in the tubers but is also 

present in the leaves, stems, and 

immature seeds. Leaves and stems 

lose most of their toxicity as they 

mature.

Where and When Waterhemlock 

Grows

Waterhemlock is most commonly 

found growing in wet meadows 

and pastures and along stream 

banks. It starts growing in spring. 

Waterhemlock usually flowers in 

June or July.

How Waterhemlock Affects 

Livestock

Livestock usually show signs of 

poisoning 15 minutes to 6 hours 

after eating the plant. They develop 

violent convulsions and may die 

within 15 minutes to 2 hours after 

signs appear.

Waterhemlock has small, white flowers that 

grow in umbrella-like clusters. Side veins of 

the leaves lead to notches, not to tips at the 

outer margin.

How to Reduce Losses 

The toxic substances act so rapidly 

that an affected animal can seldom 

be saved. Treatment consists of 

preventing seizures with barbiturates or tranquilizers and supporting respiration. Gastric lavage, 

activated charcoal, or saline cathartic may be helpful. Seek immediate 

medical or veterinary treatment.

To reduce losses, keep animals 

away from places where waterhemlock grows. Prevent waterhemlock poisoning in livestock by 

carefully surveying pastures and 

ranges at a time when the plant can 

be identified, and eradicate it.

The plants, which usually grow in 

small patches, are easy to locate. 
100

They can be eradicated by spraying or grubbing. Actively growing plants can be controlled with 

2,4-D at 2 lb ae/acre. Repeat spray 

treatments until eradication is 

complete. The stems and leaves of 

waterhemlock increase in palatability immediately after being 

sprayed with herbicide. Therefore, 

keep animals away from treated 

plants for 3 weeks after spraying. Most losses occur early in the 

spring or after the plants have been 

sprayed with 2,4-D.

Note: If grubbing the waterhemlock, use gloves and be careful to 

get all of the plant, including roots. 

Gather and burn every part.

The thick rootstalk of waterhemlock contains a number of small chambers. These hold a highly poisonous brown or straw-colored liquid that is 

released when the stem is broken or split. Thick, fleshy tubers and slender 

individual roots grow from the bottom of the rootstalk.
101

Yellow Star Thistle and 

Russian Knapweed

Distribution of Yellow Star 

Thistle and Russian Knapweed

Both plants grow throughout the 

Western United States.

Signs and Lesions of Poisoning

•	 Clinical signs occur after the 

horse has eaten large quantities of either plant for 30-60 

days

•	 Chewing disease (dysfunction 

of facial, mouth, and throat 

muscles)

•	 Facial paralysis

•	 Depression

•	 Dehydration and malnutrition

•	 Incoordination

•	 Muscle tremors

•	 Irreversible necrosis of the 

brain

How and When Yellow Star 

Thistle and Russian Knapweed 

Grow

Yellow star thistle (Centaurea 

solstitialis) is an annual weed 

growing throughout much of the 

Eastern, Southern, and Western 

United States. Russian knapweed 

(C. repens) is an invasive perennial weed that spreads via seed and 

rhizomes. It is abundant throughout the intermountain west and 

the northern plains. They are both 

characterized as noxious plants.

How Yellow Star Thistle and 

Russian Knapweed Affect 

Livestock

Yellow star thistle and Russian 

knapweed are toxic primarily to 

horses. They are grazed only after 

other forage is gone.

It takes weeks to months of exposure to large amounts of yellow 

star thistle or Russian knapweed 

before clinical signs develop. 

Horses must consume 86 to 200 

percent of their weight in green 

plant.

Yellow star thistle is an annual weed that 

grows up to 12 inches tall. Leaves are 

covered with cottony hair, and the yellow 

flowers are surrounded by the characteristic 

stiff yellow spines up to an inch long. 
102

Horses develop chewing disease; 

signs of poisoning include twitching of lips, tongue flicking, involuntary chewing motion, drowsiness, weight loss, and emaciation. 

Eating and drinking are severely 

impaired. Prehension and mastication are affected, but swallowing 

is unaffected. The mouth is often 

held partly open with the tongue 

partially protruding. 

Most poisoning cases are in 

younger horses. 

How to Reduce Losses

There is no effective treatment 

for poisoning. The necrosis in the 

brain is irreversible.

The best prevention is to control 

the plant and keep pastures where 

horses graze in good condition, 

provide adequate good quality 

feed, and avoid overgrazing.

Russian knapweed is a perennial that grows 1 to 3 feet tall. The flowers are similar to some 

thistles and are lavender to white. There are no spines around the flowers.
103

Yew (Taxus)

Signs and Lesions of Yew 

Poisoning

•	 Gastric distress

•	 Diarrhea

•	 Vomiting

•	 Tremors

•	 Dyspnea

•	 Dilated pupils

•	 Respiratory difficulties

•	 Weakness

•	 Fatigue

•	 Collapse

•	 Coma

•	 Convulsions

•	 Bradycardia

•	 Circulatory failure

•	 Death (may be so rapid that 

signs of poisoning may not 

have time to develop)

•	 Survival is rare

•	 Moderate irritation of the 

upper digestive tract

Yews (Taxus spp.) are shrubs that 

are used extensively in landscaping 

around homes and other buildings. 

Yews have long, slender, alternate 

dark-glossy-green flat needles and 

bright-scarlet fleshy cup-shaped 

fruits. In some areas, the yew is 

considered the most toxic tree or 

shrub and is probably one of the 

most toxic of all poisonous plants.

Yew is toxic to all classes of 

livestock, large game animals, and 

humans. Poisonings usually occur 

when these plants are trimmed and 

the trimmings are fed to animals. 

Children are poisoned when they 

eat or chew on the scarlet fruit. 

Closeup of leaves of Japanese yew (Taxus cuspidata). Japanese yew is commonly used in 

horticulture.
104

Foliage, bark, and seeds are all 

toxic. The foliage is readily eaten 

by livestock.

Where and When Yew Grows

There are about 40 species of 

Taxus that can be found growing 

throughout the United States. Four 

of these are commonly used in 

horticulture.

How Yew Affects Animals

Green foliage is toxic to horses 

and other monogastric animals at 

about 0.1 percent of body weight. 

In ruminants, about 0.5 percent of 

body weight of foliage is toxic. 

The toxin is an alkaloid, taxine. 

The compound is a cardiac depressant causing the heart to stop.

How to Reduce Losses

Do not allow animals access to 

this group of plants. Control is 

mostly a matter of horticulture and 

landscaping decisions to prevent 

grazing animals from access. The 

general public should be educated 

not to put clippings of those plants 

where animals have access.
105

Other Poisonous Plants

Cocklebur.

Cocklebur (Xanthium strumarium)

is an annual plant that grows in 

dry lakebeds, river bottoms, and 

disturbed and flooded areas of 

fields, pastures, and roadways after 

water disappears. Poisoning occurs 

primarily in cattle, sheep, horses, 

and swine when the plant is eaten 

in the cotyledon stage (seedling). 

Signs of poisoning include rapid, 

weak pulse, labored breathing, 

nausea, vomiting, and spasmodic 

contractions of the legs and neck 

muscles.

Desert baileya (Baileya multiradiata) is a small annual that grows 

in dry, sandy and gravelly areas 

from Texas to southern California. 

Sheep are sometimes poisoned 

on this plant. Signs of poisoning 

include depression, anorexia, and 

slobbering of a green material from 

the mouth.

Drymary or inkweed (Drymaria 

pachyphylla) is a short-lived annual that grows close to the ground 

on alkaline clay soil in western 

Texas, southern New Mexico, and 

Arizona. Poisoning occurs primarily in cattle. Signs of poisoning 

include loss of appetite, diarrhea, 

restlessness, arched back, depression, coma, and death. Drymary is 

exceedingly distasteful to livestock.

Horsetail (Equisetum spp.) is an 

herbaceous perennial. It is rushlike in appearance with hollow, 

jointed stems. This group of plants 

is common throughout the United 

States. It is toxic primarily to 

horses and cattle.

Horsetail.

Jimsonweed or thornapple (Datura

spp.) is a large annual herb with 

worldwide distribution. It is toxic 

to all classes of livestock as well 

as humans. Signs of poisoning 

include dilated pupils, subnormal 
106

temperature, restlessness, gastric 

stasis, bloat, muscular twitching, 

incoordination, paralysis, rapid 

heart rate, and respiratory 

paralysis. 

Tansy mustard (Descurainia pinnata) is an annual weed that grows 

on dry, sandy soils in arid areas. 

Intoxication occurs primarily in 

cattle only after large amounts of 

this plant have been eaten over extended periods. Signs of poisoning 

include partial or complete blindness, inability to use the tongue, 

and aimless wandering.

Hundreds of plants are poisonous 

to livestock. Many are toxic at all 

times, whereas many others are 

toxic only under certain conditions. 

Livestock producers are urged to 

become acquainted with the plants 

on their ranges and pastures that 

are potentially dangerous to their 

livestock. Help in identifying these 

plants can usually be obtained 

from the local county agricultural 

agent. Help with poisonous plant 

problems can also be obtained 

from local veterinarians.

Jimsonweed. Tansy mustard.
107

Noxious Weeds

A noxious weed is any plant that 

is designated by a Federal, State, 

or county government as injurious to public health, agriculture, 

recreation, wildlife, or property 

and must be controlled by the legal 

owner of the land on which it appears. There are several poisonous 

plants that have also been classified as noxious weeds. The following is a partial list:

•	 Mustards: white top, hoary 

crest, perennial pepperweed. 

Tansy mustard has not been 

declared noxious as yet.

•	 Knapweeds: diffuse, Russian, 

spotted, squarrose, yellow 

star thistle

•	 Leafy spurge

•	 Goatsrue

•	 Houndstongue

•	 St. Johnswort

•	 Nightshades: sliver leaf, buffalo bur, black nightshade

•	 Kochia weed

•	 Milkweeds

•	 Johnson grass

•	 Poison hemlock

Under ordinary conditions, these 

plants are seldom grazed. However, poisoning can and does occur 

under stress conditions such as on 

overgrazed pastures or after a frost. 

Noxious weeds compete with useful forages such as grasses, some 

legumes, etc. for space, nutrients, 

and moisture. 

Some noxious weeds can be found 

growing in crops and may be 

harvested with hay or small grains. 

Care must be taken when these 

crops are fed to livestock.

Most of these plants are aggressive 

and spread rapidly. It is important 

to monitor all range and pasture 

land for poisonous and noxious 

plants to prevent infestations and 

manage these plants. Early treatment to control these plants is 

the most effective. The spread 

of noxious weeds may signal the 

decline of entire ecosystems. They 

severely affect the biodiversity of 

natural areas and cause economic 

losses to those relying on range 

resources.