Some Major Plant Toxicities of the Western

United States

LYNN F. JAMES AND A. EARL JOHNSON

Highlight: Poisonous pluntr rank high among the causes of

economic loss fo the livestock industry. Losses come nor only through
death and disabiliry of livestock but through co.m nssociared wirh
interference with management progmms such a addirional fencing
and a/wed &7-‘IZiQ’ pro,$‘UJm.
One of the best meant of avoiding poisonous plant problems is by
complrre familiariry with poisonousplmm likely fo be encountered by
livestock. Impoportantplants causing congeniral birth dcfecrs; plants
containing cyanide, oxalate, nirrates, selenium, and pyrrolizidine
alkuloids; as well as ~1few specific plants a.~ lrrrkspurs and hemlock
and those producing phorosensitizarion are reviewed briefy nnd
resu,rs of more recenf research ore considered.

Poisonous plants rank high among the causes of economic

loss to the livestock industry (Schmitzet al., 1968; Sperry etal.,
1968). They take their toll through death of livestock, abortions,
birth defects, photosensitization, chronic illnesses, debilitation,
etc. Additionally, land managers and livestockmen have
stgniftcant costs ana problems generated by the presence of
poisonous plants on ranges and pastures. These include con-
struction of additional fences, altered grazing programs, de-
creased forage production and utilization, and in some in-
stances, supplemental feeding programs.
The National Academy of Science, 1968, estimated that
8.7% of the nutritionally sick animals in western United States
were sick as a result of eating poisonous plants and it has been Several important causes are: deficiencies or excesses of
estimated (Sampson, 1952) that the mortality rate, due to nutrients (Palludon, 1961), chemicals (James and Keeler,
“oisonous
1~
“lants. of livestock erazine the western ranees
Y _
1968), and plants containing natural teratogens (Keeler, 1972).
approaches’5%. Veratrum californicum, or western false hellebore, a plant
Annroximatelv 75% rf the land area of the western United growing in the mountain meadow areas ofthe West, was show”
Stat& is rangela~d. The forage on this land can be utilized only to be the cause of cyclopian and related cephalic malformations
by ruminants, i.e., cattle, sheep, and wildlife, which convert
in lambs born t” ewes that had ingested the plant on the 14th day
forage into red meat and fiber for human “se. However, this is of gestation (Binns et al., 1963). This condition occurs in
economically feasible only if the ranges can be developed and
southwestern Idaho, where the incidence varies from less than
maintained in productive condition by proper grazing programs. 1% to 25% of the lambs born in a band of sheep. The anomaly is
Many of these ranges cannot be properly and fully utilized characterized by the following which occur in varying degrees:
because of poisonous plants that grow on them. They may also cyclopia, anophthalmia, kydrocephalus, harelip, cleft palate,
interfere with the development of grazing programs by land and a proboscis protruding above the eye. These deformed
management agencies. lambs may live and continue to grow in ufero, and prolonged
One of the first steps in preventing livestock losses due t” gestation may occur. Lambs weighing up to 14 kg have been
poisonous plants is to recognize the plants and understand their taken from ewes in prolonged gestation, while the normal birth
effects on animals.
weight of lambs is about 3.6 kg.
Ii veratrum 1s eaten on the 28th or 30th day of gestation,
Plants Producing Teratogenic Effects in Animals
lambs may be born with shortened metatarsal and metacarpal
For many years the main problem of plant poisoning of live- bones (Binns et al., 1972).
stock was considered to be that of acute intoxication. In recent Signs of intoxication are rare in ewes producing malformed
years, however, another inlportant dimension has been recog- young.
“ized-that of teratology, wherein the congenital malfornx- Approximately 50 to 60 alkaloids occur in the plant, “early all
tions are related to dietary factors. of which are toxic t” animals, but only three are teratogenic.
These are the steroidal alkaloids I I-deoxojervine, jervine, and
3.glucosyl-1 I-deoxojervine (Keeler, 1972).
Research has provided the livestock industry with a practical
solution t” the problem. Malformations can be avoided by
 Astragalus Plants
The teratogenic problems associated with the Astragalus
plants just discussed are only one of several toxic phenomena
ascribed to this group of plants. Over 300 species ofAsrragalus
grow in North America (Kingsbury, 1964). These can be
divided into groups according to their effect on animals: (I)
those that are acutely toxic (Anonymous, 1968), (2) those
chronically toxic (MacDonald, 1952, (3) those that cause the
locoweed syndrome (Marsh, 1909), (4) those that are toxic due
to their selenium content (Rosenfeld and Beath, 1964), and (5) a
group that is nontoxic.
A. miser represents the species that are acutely toxic to
animals. Animals grazing this plant die quickly after consuming
a lethal dose. The toxic agent is an organic nitro compound,
miserotoxin (Stermitz et al., 1969). The signs of poisoning
include nervousness, weakness, rapid weak pulse, coma, con-
vulsion, and death (Anonymous, 1968).
Those species causing chronic toxicity characterized by
huskiness in the voice and posterior paralysis include A.
enolyanus (Mathews, 1940) and A. tempterus (Marsh and
Clawson, 1920). There is an overlap in symptoms between
Astragalus plants causing acute intoxication and those causing
chronic poisoning. The toxic agent is the same, and the
preventing sheep from grazing the V. californicum plant during difference in effect appears to be related to rate of consumption.
the critical stages of gestation. The locoweeds are so called because of their effect on
Lupinus sericeus and L. caudatus, when ingested by cattle animals. Approximately 13 species of Astragalus are included
between the 40th and 70th days of gestation canse congenital in this grouping, which also includes some species of the genus
skeletal malformation in the offspring known as “crooked calf Oxyrropis. The consequences of animals grazing the locoweeds
disease” (Shupe et al., 1967). This disease occurs in nearly all include: (1) habituation, (2) emaciation, (3) neurological dis-
the western states and Alaska and herd incidence mav- varv. from turbances, and (4) reproductive disturbances (James et al.,
0 to 35%. 1969).
The deformity is characterized by malformation of the legs,
back. and neck and occasionallv bv cleft oalate (Shuoe et al..
1967). Affected calves appear’to’be not&al o&e&e. Thd
joints are generally immobile because of a malalignment and
malpositioning of the articular surfaces and the limbs are usually
rotated laterally. These animals do not recover and the condition
should not be confused with contracted tendons, wherein the
joints are all in proper alignment without lateral or medial
rotation. Joints of calves with contracted tendons can be
extended with pressure, whereas the joints of lupine-deformed
calves cannot.
Lupine toxicosis is related to the high alkaloid content of the
plant. Current research suggests that the teratogenic agent may
be the alkaloid anagyrine (Keeler, 1973).
Traditionally, lupine has been considered a poisonous plant
affecting orimarilv sheeo and we rarelv hear of luoine uoisonine
--~~-~c. , &

of cattle on the ranges. Cattle, however, are more susc’eptible o; l”<0wwl iA\ira&ll”s le”ugin”\“r, one <>I& piu,ii\ mos, &zmuginXI0 ,ii,e-
a weight basis to poisoning by this plant than are sheep. This srock in r,,e wesi.
suggests that more sheep than cattle are poisoned by lupine
because of differences in management procedures. Locoweeds are not especially palatable to livestock (Marsh,
Some of the Astragalus species that are classified as loco- 1909); however, when the loco is green and other forage dry,
weeds may cause malformations and abortions in livestock livestock may be enticed to eat it (James et al., 1968). When an
grazing them. Skeletal malformations induced by consumption animal starts to graze the plant, it develops a liking for it and
of the plant may be any or all of the following: curvature and may graze it to the exclusion of other forage (Marsh, 1909).
rigidity of the joints, aplasia of the mandible, hypermobility of Signs of poisoning do not develop until animals have grazed this
the stifle joint, flexture of the carpus, and a greatly increased plant for about 30 days. They include depression, dullness,
incidence of contracted tendons (James et al., 1967). Abortions excitement when disturbed, and loss of sense of direction
mav occur in as maw as 60% of the sheer, Doisoned bv (Marsh, 1909). Symptoms may disappear after an animal is
locbweed, and can oc& any time during the &&ion perioh prevented from grazing the plant; however, it may show signs of
(James et al., 1967, 1969; Mathews, 1932). poisoning the remainder of its life when placed under stress
Ewes fed locoweed between their 90th and 120th davs of (James et al., 1968). If grazing of the locoweed is allowed to
gestation produce fetuses with enlarged hearts, spleens, and continue, the animal becomes recumbent and eventually dies
thyroids. Bones of lambs from these ewes appear osteoporotic. (James et al., 1968).
Fetal edema may also be present (James, 1972) and many lambs In addition to the reproductive consequences already dis-
are small and weak at birth, and may not survive. There appears cussed, sexual desire and spermatogenesis of the male (James
to be a higher than normal death rate in normal appearing lambs and Van Kampen, 1971) and estms of the female is suppressed
that are born to locoed ewes (Balls et al., 1973). in locoweed poisoning. If the animal is removed from the plant,
The toxic agent(s) in the locoweed is not known. these functions are recovered.
 Pathologic changes in locoweed-poisoned animals have been toxic to sheep. Larkspur are of two types, low and tall. Low
described as cytoplasmic vacuolation of the neurons of the larkspurs are smaller plants that inhabit the drier plains and
central nervous system and the cells of certain internal organs foothill areas, while the tall larkspurs are larger, more robust
(Van Kampen and James, 1969). plants growing in the higher mountains or sites with abundant
Poisoning can best be diagnosed by observation of the gross soil moisture. Low larkspurs include species as D. nelsonii and
symptoms, by identifying the histopathologic lesions, and by D. andersonii, while the most important representatives of the
determining that the plant has been grazed. tall larkspurs are D. barbeyi, D. occident&, and D. glaucum.
Approximately 2 1 species of Asrragalus, including A. Both groups of larkspur arc toxic and animal responses to
bisulcatus (Rosenfeld and Bath, 1964) and A. pattersonii, poisoning are similar. However, there are variations in toxicity
accumulate the toxic element selenium from the soil (Rosenfeld associated with the species eaten and stage ofplant growth. Low
and Bath, 1964). Plants other than Astragalus can accumulate larkspurs grow early in the season and poisonings occur in the
selenium. These include Stanleya pinnata, Atriplex nuttallii, spring prior to hot weather. Tall larkspurs found at higher
and certain grasses (Rosenfeld and Bath, 1964). elevations grow later in the year, and poisonings occur primarily
Intoxication of livestock by seleniferous plants has been in the summer and fall.
classified as both acute and chronic (Moxon, 1937; Rosenfeld Young plants of both groups of larkspur are most toxic,
and Beath, 1964). In acute poisoning the animal dies rapidly Toxicity decreases as the plants mature, but it again increases in
after eating the seleniferous plant. the seed stage.
Chronic selenosis has been classified into two types: blind I’he larkspurs are readily grazed by cattle, which makes
staggers and alkali disease. Blind staggers is characterized by prevention of poisoning more difficult than with most poisonous
the animal wandering, moving in a circle, having little desire to plants. However, as with many other poisonous plants, cattle
eat or drink, and frequently having impared vision. Alkali may graze and utilize small amounts of the plant over prolonged
disease is characterized by lack of vitality, anemia, stiffness of periods without apparent effect. Rapid consumption of lzger
joints, lameness, roughened hair coat, and hoof deformities amounts in short periods of time may result in death in a very
(Rosenfeld and Beath, 1964). The selenium content of the hair short time. Compounds responsible for larkspur toxicity are
can be used as a diagnostic aid. Jensen et al. (1956) have alkaloids which appear to affect the nervous system principally.
suggested that blind staggers is not due to selenium intoxication Thus, signs are related to a general weakness of the animal. It
but to some other etiologic agent. may display a straddle-legged stance as it attempts to stand and
Plants such as A. bisulcarus, A. patrersonii, and Stan[eya may suddenly collapse if pushed or pressed (Anonymous,
pinnata have been termed as obligate species because they 1968). After collapse it may or may not regain sufficient
require selenium for growth and are therefore termed indicator strength to arise. Thus, the quieter a poisoned animal can be
or converter plants. Other plants may accumulate selenium if kept the better chance it has for survival. At present prevention
they grow on soil high in selenium. In these areas, the grasses or lies either with avoiding grazing or control of the plants with
other shallow-rooted plants that accumulate selenium may be herbicides. Tall larkspur can be successfully controlled by
dependent on the deeper rooting plants to bring selenium to the spraying it two successive years with 2,4,5-T (Cronin, 1974).
soil surface before they can accumulate it.
Hemlock
Larkspur
Two common poisonous plants which are often confused due
The larkspurs (Delphinium spp.) cause more cattle deaths to their names and similar appearance (Kingsbury, 1964) are
than any other plant species grazed on the ranges of the western water hemlock and poison hemlock. Water hemlock, Cicuta
United States and Canada (Kingsbury, 1964). They are less species, is found only in swampy or wet habitats as along
streams, in marshes, or other areas which are wet at least part of
the year. It is of the Limbelliferae family and has as its known to be in the area, little concern has been shown until the
distinguishing features fascicled tuberous roots, chambered past 10 years (Johnson, 1976). It has now gained such a strong
swollen rootstock, and a characteristic odor (Anonymous, foothold that eradication is virtually impossible and numerous
1968). It is toxic to all classes of livestock and humans, and losses occur annually in horses and cattle grazing the young
poisoning in humans is not uncommon. plant and eating contaminated ensilage and hay. Additionally,
Cicutoxin, the toxic principle of water hemlock. is one of the there are oublic health concerns as PAS are known to he
most powerful of the piant t&ins. Cicutoxin acts directly on the hazardous ?o humans.
nervous system, causing violent convulsions. Death follows
rapidly after consumption of a lethal dose. Control of the plant Some Related Members of the Compositae Family
or avoiding it is about the only means of the prevention of
A few plants in the compositae family are especially trouble-
poisoning.
Poison hemlock can be distinguished from the water hemlock some to the livestock industry. These include sneezeweed
(Helenium hoop&i), bitterweed (Hymenoqs odorata), rubber-
by observing that the stems are usually spotted with purple on
weed (Hymemnys richardsonii, xx. floribunda) and broom-
the lower portions and that the root is usually an unbranched
white tap root. Poison hemlock has a mousy odor (Anonymous, weed (Gutierrezia microcephala). Their effects on livestock are
similar. All four plants green early in the spring and remain
1968).
green into late fall. Livestock generally eat these plants (with the
The toxic principle is coniine, a volatile alkaloid which is also
exception of sneezeweed) only when hungry or searching for
toxic to all classes of livestock and humans. The signs of
green feed in early spring. Increased populations of these plants
poisoning include nervousness, trembling, ataxia, dilation of
have been considered indicative of overgrazing. All are more
the pupils, weakened and slowed heartbeat, coldness of extrem-
troublesome to sheep than to cattle except broomweed. All have
ities, coma, and death from respiratory failure.
caused considerable losses to the livestock industry. All except
This plant has recently been shown to be responsible for a
broomweed have recently been shown to have the same toxic
birth defect in calves similar to the “crooked calf disease”
principle, a sesquiterpene lactone (Ivie et al., 1975).
caused by lupine (Keeler, 1974). Prevention of poisoning lies in
control of the plant and avoidance of it. Animals eat this plant
only when forced to do so.

Plants Containing Pyrrolizidine Alkaloids

Some of the most insidious problems in livestock are caused
by plants which contain pyrrolizidine alkaloids (PAS) (Bull et
al., 1968). There are many PAS, all of which arc structurally
similar and found in several plant genera throughout the world.
Senecio, Crotalaria, and Heliotropium are representative gen-
era, with three Senecio species being of most importance in this
country: tansy ragwort (Senecio jacobaea), found in coastal
Washington, Oregon, and California; threadleaf groundsel
(Senecio km&bus);’ and Riddell’s groundsel (Senecio rid-
d&i), found in semidesert areas of the Southwest.
Powming caused by PA-containing plants is usually chronic
unless abnormally large quantities of plants are consumed in a
short time. The primary target in the animal is the liver, and
most animals are susceptible to PAS. Sheep are generally more
resistant than horses and cattle.
PAS produce a cirrhosis-like condition of the liver, which
may not manifest itself until weeks or months after a toxic dose
has been consumed (Bull et al., 1968). Signs of poisoning may
appear gradually and include: depression, anorexia, weakness, Sneezeweed is a herbaceous perennial growing in the Inter-
uneasiness, emaciation, and reduced sensibility; or the affected mountain West at elevations above 7,000 feet. Sneezeweed
animal may suddenly fill with fluid in the abdominal area, poisoning (spewing sickness) occurs primarily when over-
become either diarrheic or constipated, may become very dull grazing encourages the plants to increase in number. Both cattle
rapidly, and may walk or pace aimlessly and die suddenly in a 2. and sheep arc poisoned by this plant, hut it is principally a
to 4-day period. Due to the delay in appearance of symptoms, it problem in sheep. Poisoning occurs only when sheep graze the
is difficult to diagnose and many poisonings go unrecognized or plant continually over extended periods (about 2 weeks). Signs
are blamed on other causes. The most consistent postmortem of poisoning include dullness, depression, weakness, and in
findings are a tough? fibrotic liver with an enlarged gall bladder. more advanced intoxication, vomiting, which is a sign of
Definitive diagnosis may be made through histopathologic permanent injury. Lesions include gastrointestinal irritation and
examination of the liver. congestion of the liver and kidneys (Anonymous, 1968).
Since symptoms often do not appear until an animal has Prevention lies in alternating (at IO-day intervals) between
received a lethal dose of the plant, treatment in PA poisoning is grazing sneezeweed-free and infested ranges.
usually of little value. Rubberwed, or pingue, is a perennial herbaceous plant that
The grounds& flourish principally in time of overgrazing grows in dry soils at elevations of 4,COO to lO,ooO feet in the
and drought, and plants are eaten primarily when ranges are dry southern parts of Utah and Colorado, and the northern part of
and other food IS scarce (Sperry et al., n.d.). As I” tansyragwort Arizona and New Mexico. It is principally a problem in range
poisonings, many toxicities may go unrecognized and the sheep. Signs of poisoning include salivation, anorexia, turnen
relationship of groundsel poisoning to other stresses may be of stasis, abdominal pain, uneasiness, weakness, and prostration.
more importance than is realized. Lesions are those associated with gastrointestinal irritation and
Tansy ragwon was introduced into the northwest United degeneration of the liver.
States probably through a seaport early in this century. Though Bitterweed, an annual, grows primarily in southwestern
it was recognized as a plant poisonous to livestock and was United States. Signs of bitterweed intoxication include anor-
exia, salivation, vomiting, depression, and weakness (Sperry et Awareness of the cyanide-producing plants and avoiding
al., n.d.). Lesions are confined primarily to the lungs and them during periods of potential danger is the best means of
gastrointestinal tract. Prevention of intoxication at the present prevention.
time lies in avoiding areas where these plants can be grazed in
excessive amounts. Oxalate-Producing Plants
Broomweed is a perennial that grows on the drier ranges of
Oxalate-producing plants are worldwide in distribution. A
the West (Sperry et al., n.d.). In snme areas it covers many fairly com&te list of plants that may contain dangerous
thousands of acres of rangeland but toxicity to livestock is amounts of soluble oxalates may be found in Kingsbury (1964).
related to the soil types on which it grows; it is reported to be
Oxalates are found in plants in both soluble and insoluble
most toxic on sandy soil. Cattle and sheep are. poisoned if forced forms. Soluble oxalates are toxic to livestock; insoluble oxalates
to graze heavily on broomweed. Signs of broomweed poisoning are not. The soluble oxalates have a strong affinity for calcium.
in cattle and sheep arc listlessness, anorexia, rough hair coat,
Calcium oxalate is the principal insoluble form. The two most
diarrhea or constipation, mucus in the feces, and vaginal
important toxic oxalates are sodium oxalate found in sap that is
swelling in females. The principal result of such poisoning is.
mildly acidic (pH6), and acid potassium oxalate found in sap
abortion and the production of light-weight and weak offspring,
that is highly acidic (pH2) (James, 1968).
and retention of the placenta, which may also occur in dams
giving birth to normal young. Lesions in the dam include severe
digestive tract irritation, and degenerative changes of the liver
and kidneys.

Cyanide-Producing Plants
There are. a number of plants that under the proper conditions
produce an excess of the glycoside of the hydrocyanic acid. The
two important range plants that accumulate hydrocyanic acid
are chokecheny (Prunus virginiana) and arrowgrass (Tri-
glochin maritima). The hydrocyanic acid is produced in exces-
sive amounts during drought, frost, or other conditions that
might stress the plants (Kingsbwy, 1964).

There are two principal oxalate-producing plants in North

America. They are halogeton (Ha&won glomerarus), a natur-
alized annual introduced from Asia, and greasewood (Sarco-
batus vermiculatus), a native perennial. Both plants belong to
the Chenopodiaceae family and are readily grazed by sheep and
cattle. They have caused a multitude of sheep deaths but only
occasional deaths in cattle.
Halogeton usually contains 15% to 18% of its dry weight as
oxalate hut may reach as high as 36%; greasewood contains
slightly less. Oxalate content varies with factors such as
moisture, site of growth, stage of growth, and leaching
(Williams, 1960).
When oxalate is consumed by a ruminant it combines with
calcium to form insoluble oxalate and is excreted; or it may be
degraded by the turnen microorganisms; or it is absorbed from
Four factors are of importance in cyanide poisoning: (1) the mmen where it may exert its toxic effects.
cyanide content of the plant, (2) rate of intake, (3) speed of Oxalate produces its toxic reactions in three principal ways.
release of cyanide from the plant material, and (4) relative rate (1) It may be absorbed into the blood stream from the rumen,
of absorption and detoxification by the animal’s tissue where it may combine with calcium resulting in a hypocal-
(Kingsbury, 1964). The cyanide content of the plant as indi- cemia (James, 1968). (2) Accumulation of calcium oxalate
cated varies with environmental conditions. If the toxic plant crystals may mechanically damage renal tubules and rumen
material is eaten slowly, enzymatic processes in the body can mucosa and thus interfere with kidney and rumen function (Van
detoxify the cyanide. The release of the toxic plant material Kampen and James, 1969). (3) Oxalate may interrupt energy
requires a certain amount of moisture. Thus, drinking water metabolism by interfering with the enzymes succinic and lactic
may prompt a quick release of cyanide material and rapid death dehydrogenases (James, 1968). The immediate cause of death
of the animal may result. may be the disruption of energy metabolism (James, 1968).
Signs of intoxication include nervousness, abnormal respira- Halogeton poisoning in sheep is characterized by depression,
tion, trembling, blue coloration of the lining of mouth, spasm or weakness, and some salivation. There is increased heart rate,
convulsion ending in death (Anonymous, 1968). complete stasis of the digestive tract, and finally cnma and death
 Factors that influence the nitrate content of plants include
drought and fertilization. Treatment with the herbicide 2,4-D
may increase nitrate accumulation by the plant as well as cause
some unpalatable plants to become palatable.
In the rumen of an animal the nitrate is converted to nitrite.
The nitrite is about IO times more toxic than is nitrate.
The gross symptoms of acute nitrate poisoning include
cyanosis, severe dyspnea, trembling, and weakness. Nitrate
poisoning can be successfully treated.
Chronic poisoning can occur when animals eat feeds contain-
ing between 0.5% and 1.5% nitrate. The response is varied but
the principal result is unthriftiness.

Photosensitization
Photosensitization is an allergy-like disease caused by a
hypersensitivity of animals to sunlight (Johnson, 1974). It
occurs in livestock more frequently than realized. Photosensi-
tivity results when a phototoxic substance is allowed to reach the
skin from an internal route, i.e., it is eaten by the animal, is
absorbed from the digestive tract into the bloodstream, and thus
circulated to the skin (Johnson, 1974). Here it is acted on by
sunlight to cause its irritating effect. This type is called primary
photosensitization and may be caused by many chemical
compounds, usually pigments which may contaminate water or
(Cook and Stoddart, 1953), which usually occurs within about feed consumed by livestock. Plants which contain primary
12 hours. Some animals may linger for several days.
Oxalate poisoning appears to be an all or none situation: i.e., photosensitizers include buckwheat (Polygonurn fagopyrum),
a sheep either eats enough to kill it, or there are few sympto- St. Johnswort (Hypericum perforatum), and desert parsley
matic effects (James and Butcher, 1972). Sheep can eat large (Cymopterus watsonii) (Kingsbury, 1964).
amounts of halogeton with no ill effects if they consume the
plants slowly, but are poisoned when they eat large amounts in a
short period of time. This usually occurs when they arc
excessively hungry Thus, the problem is principally one of
management. There is no effective treatment for sheep or cattle
poisoned by halogeton.
Prevention of oxalate poisoning can best be attained by
following three rules:,(l) Move sheep slowly into areas where
oxalate-producing plants grow to allow mmen microflora time
to become accustomed to degrading oxalate. Oxalate is rapidly
degraded by rumen microflora (James et al., 1967) and theirde-
gradative effectiveness can be increased if oxalate is supplied
over a time at small nontoxic levels. The efficiency of these
organisms can be increased by as much as 75% (James et al.,
1970) by exposing livestock to gradually increasing amounts of
oxalate-producing plants or first allowing them to graze low
oxalate-producing plants such as shadscale. (2) Prevent hungry
sheep from grazing heavy stands of halogeton. Hunger can
result from either insufficient feed or water (James et al., 1970).
However, if water is withheld, feed intake declines. (3) Develop
grazing plans that allow critical halogeton areas to be ap-
proached only after proper preparations have been made for the
sheep to graze these areas (James and Butcher, 1972).
Various calcium-containing mineral supplements have been
recommended for the prevention of halogeton poisoning (James Of far more .importance to livestock, however, are those
and Binns, 1961). However, they are ineffectwe because the classes as secondary photosensitizers. In this type the photo.
high level of calcium necessary to prevent poisoning can be toxic agent is a pigment called phylloerythrin, a product of
maintained for only a short time after the calcium is consumed chlorophyll breakdown. Normally chlorophyll is broken down
(James and Johnson, 1970). in the stomach and the resultant phylloerythrin absorbed into the
blood which goes to the liver. The normal functioning liver
Nitrates - Nitrites removes the phylloerythrin and it is excreted in the bile. A liver
damaged in such a way that it cannot remove phylloerythrin
Several plants have the potential for containing nitrate at toxic allows this pigment to reach the skin and thus be activated by
levels. These include crop plants such as oat hay, corn, and sunlight.
soybeans, and weeds such as pigweed (Amaranthus rem- Photosensitization occurs only in skin that is unprotected by
jlexus and A. palmerii), and lambsquarter (Chenopodium thick wool or hair, or by skin coloration. Thus, in sheep the
album) (Kingsbury, 1964). Plants containing more than 1.5% problem occurs principally in the face, ears, udder, or unpro-
nitrate (KNO, dry weight) may prove lethal to livestock. Nitrate tected rear parts. In cattle it occurs in the white or light-colored
poisoning also results from animals eating fertilizers and drink- skin areas. Symptoms of photosensitization are: uneasiness,
ing water high in nitrate. itching and thus rubbing of sensitive areas, redness of the skin,
 fluid accumulation in the affected areas which may be so severe 4. Avoid grazing hungry animals in areas infested with
that the skin cracks and fluid leaks out. Affected skin may die poisonous plants. Animals can be made hungry by withholding
and slough off in large sheets, especially in cattle. Sheep may feed or water and overgrazing. Provide animals with adequate
also lose their herding instinct as they seek shade. forage, of good variety and quality, and water.
Though there are several plants in the western United States
5. Provide an adequate mineral and salt supplement.
which have been incriminated in secondary photosensitization,
only the horsebrushes (Tetradymia glabrata and T. canescens) 6. Where possible, control or eradicate poisonous plants,
are responsible for sizeable losses to livestock. Photosensiti- especially from problem areas.
zation caused by these plants in sheep is known as “bighead” 7. Where possible, develop a grazing plan.
because tissue swelling may cause the head to be almost twice 8. Keep your range in good condition. Avoid overgrazing.
its normal size. Though the extremely large losses of years ago 9. It is the consensus of most people who have written on
no longer occur, many sheep are still affected when they are poisonous plants that good management will prevent most cases
trailed through horsebrush infested areas. Livestockmen using of plant poisoning.
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