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Poisonous Plants Affecting Livestock on Colorado’s Eastern
Plains
1/18/2002
Ron F.
Meyer
Area Extension Agent (Agronomy)
Colorado State University
Extension
Golden Plains Area |
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Tony Knight
Colorado State University
January
2002
Photosensitization
Photosensitization
that resembles severe sunburn is most commonly due to animals that eat certain
plants that cause severe liver disease. Once the liver is damaged, it is unable
to detoxify plant toxins and by-products, and these compounds enter the
animal’s blood and are carried to the non-pigmented skin, they react with
UV light to cause damage to the blood vessels and skin in the area. Acute
inflammation results, and the skin eventually dies and peels
off.
Hounds tongue (Cynoglossum
officinale)
Distribution: Fields, roadsides and waste places.
Imported from Russia with grain, the plant has become widespread in Colorado
and many western States.
Description: A biennial, forming a
rosette the first year of basal leaves up to 18 inches long, densely hairy, and
tongue-shaped. The second year the plant produces a 2-4 feet tall, erect, stout
and hairy flowering stems. The flowers are reddish-purple in color. The fruit
is pyramidal, separating into 4 nutlets at maturity, that are covered with
hooked (velcro-like) barbs enabling adherence to clothing and animal
hair.
Toxic principle: Hounds tongue contains significant
quantities of pyrrolizidine alkaloids comparable to the levels found in the
most toxic Senecio species. The plant is rarely eaten when green, but
livestock find it quite palatable when it is dried in hay. As little as 6% of a
horse's daily intake of food of dried hounds tongue is
poisonous.
Control : Hounds tongue is a prolific seed producer
that is best controlled by preventing seed production. In limited areas the
plant can be eliminated by digging it out, or by regular mowing to prevent seed
production. Herbicides can also be used to help control the plant over larger
areas. The most effective herbicides against hounds tongue include 2-4,D if
applied in the spring before blooming occurs, and metsulfuron (Escort R
) if applied before blooming. Because of the dense covering of hairs on
the leaves and stems of hounds tongue, it is important to add a nonionic
surfactant to the spray solution.
Threadleaf Groundsel
(Senecio ridellii)
Description: Threadleaf groundsel is a
perennial growing up to 30 inches tall. Widely distributed throughout the
United States, it is commonly found in disturbed soils and waste
areas.
Leaves are alternate, linear. Flowers numerous, with yellow disk
flowers surrounded with a single layer of bracts. The seeds have white hairs
attached that aid in wind distribution.
Toxic Principle:
Pyrrolizidine alkaloids similar to those found in hounds
tongue.
Flix weed (Descurainia sophia)and Tansy Mustard
(D. pinnata)
Flix weed, and the very similar tansy mustard,
are common annual weeds that emerge in early spring often forming dense stands
in cultivated fields. When moisture is plentiful these mustards germinate
quickly and pose a threat to cattle and horses that graze them in the
preflowering stage. Poisoned animals exhibit difficulty in eating and drinking
sometimes referred to as "paralyzed tongue". Blindness, weight loss, and severe
photosensitization with sloughing of the white skinned areas also develops
after a few days. Once other forages become available and the flixweed forms
seed pods and becomes unpalatable, less severely affected animals recover if
they are provided shelter from the sun until the skin is healed. Alfalfa hay
with a high percentage of flix weed has low nutritional
value.
Russian Knapweed (Centaurea repens (Acroptilon
repens) )
Introduced from Russia in alfalfa seed, Russian knapweed
has established itself in cultivated soils, waste ground, roadsides, etc. It is
a poisonous noxious weed.
Description: A perennial, branched,
herbaceous weed, growing up to 3 feet tall. The stems and leaves are covered by
fine hairs or knap that give the plant a grayish appearance. Flowers, produced
terminally on the stems, are thistle-like, reddish purple to white in color.
The seeds are gray, flattened about 4mm in length. Unlike Canada thistle
(Cirsium arvense) and spotted knapweed (Centaurea maculosa) for
which it is often mistaken, Russian knapweed has no spines on its leaves, stems
or flowers. The roots are extensive, being brown to black in color, and woody.
The plant is highly invasive and spreads readily via its roots and to a lesser
extent by its seeds.
Toxic Principle: The toxin destroys the
specific area in the brain that coordinates prehension and chewing of food. The
plants are toxic in the green, and dry state to horses only. Horses will eat
yellow star thistle in all its stages of growth and will acquire a preferential
taste for the plant. Russian knapweed (1.8-2.6 kg/100 kg body weight) eaten
over a period of 28-35 days produces disease in horses. Cattle and sheep graze
the plants without problems but since the plants may accumulate nitrate there
is always a potential for nitrate toxicity.
Clinical Signs:
Russian knapweed causes increased tonicity and incoordination of the muscles of
prehension and chewing. Horses show a sudden onset of inability to prehend and
chew food. Affected horses tend to wander about with their head down, trying to
graze but, in time give up attempting to eat. Swallowing is not affected. The
tongue has increased tone and the horse will often curl the tongue from side to
side. Yawning is common. The continual chewing movements cause frothing of the
saliva which can resemble that seen in rabies. Some horses may show more
involvement of one side, so that the lips, tongue and head movements are to one
side. Circling to the same side may also occur. Weight loss and depression are
common. Pneumonia resulting from inhalation of feed is a serious sequel to the
disease. There is no effective treatment, and although horses can be kept alive
by supportive feeding, they do not recover. Marked weight loss and pneumonia
frequently require the horse to be euthanized to avoid unnecessary
suffering.
Control: Russian knapweed may be partially controlled
using competitive crops and perennial grasses, but combinations of regular
cultivation and herbicides are usually needed to eradicate the plant. The most
effective herbicides against Russian knapweed include Tordon
(picloram), and Banvel (Dicamba). Some control may
be achieved using higher application rates of 2,4-D (4 pounds of 2,4-D amine
per acre). For best effects the herbicides should be applied in the spring when
the knapweed is actively growing and again in the fall before the plants go
dormant. Use of a wetting agent with the herbicide will help ensure better
penetration of the protective knap on the leaves allowing plant-herbicide
contact.
Poison Hemlock (Conium maculatum)
Poison
or spotted hemlock contains several alkaloids, the most important of which is
coniine. These alkaloids are present in all parts of the plant but especially
in the root and the seeds. The alkaloids are toxic to all animals with cattle
being the most susceptible and sheep being relatively resistant to the
alkaloids. Since the concentration of alkaloids in poison hemlock varies with
the growth stage of the plant, it is difficult to predict with any accuracy the
quantity of green plant that must be ingested to cause death. Early studies
indicated that somewhere between 2 and 4% of the animal's body weight in green
plant have to be consumed before clinical signs develop. Conium alkaloids have
two major effects in animals. In large quantities they act predominantly on the
central nervous system, causing initial stimulation followed by paralysis. A
progression of signs starting with muscle tremors, incoordination, nervousness,
dilation of the pupils, rapid heart rate, coma and death due to respiratory
paralysis can be expected. If consumed in smaller, nonlethal quantities during
the first trimester of pregnancy, cows and sows have been shown to produce
offspring with skeletal deformities identical to those associated with lupine
poisoning. Calves born to cows that have grazed poison hemlock in their first
trimester develop crooked legs and cleft palates. Problems with calving often
occur in cows trying to deliver deformed
calves.
Nightshades
Nightshades, a large genus of at least
1500 species found worldwide and represented by the following important
species. Most are annual or perennial herbs and shrubs with alternate, simple
or compound leaves, and axillary flowers with 5 petals and 5 sepals. The
flowers are star shaped and range in color from white to deep blue or violet.
The fruits are berries containing many seeds.
Solanum nigrum --
Black nightshade
S. americanum -- Garden huckleberry, wonder
berry,
S. sarrachoides -- Hairy nightshade
S. triflorum --
Cutleaf nightshade
S. rostratum -- Buffalo burr
Toxic
principle: A variety of alkaloids (atropine-like), and glycoalkaloids are
found in the nightshades, especially in the green parts of the plant and the
unripe fruits.
Poisoning from different members of the nightshade family
has been recognized in cattle, pigs, horses and poultry. Animals rarely eat the
plants unless they are hungry and deprived of other food. Green potatoes (S.
tuberosum), and potato and tomato vines (S. lycopersicum) have been
the most common cause of poisoning in people and animals. Cattle grazing post
harvest corn, bean and other arable croplands may become poisoned by eating the
green hairy or black nightshade that may be abundant.
In the case
of Jimson weed (Datura stramonium), it is the seeds that are likely to
cause poisoning as they may contaminate cereal grains. Cattle develop signs of
atropine toxicity after eating feeds containing 881 seeds/kg of feed.Deaths are
unlikely as poisoning appears to be self-limiting because of loss of appetite
and decreased intestinal activity.
Clinical Signs: Decreased
salivation and gastrointestinal motility leading to constipation and colic.
Bloating is common in cattle. The alkaloids also have a direct irritant effect
on the digestive system causing colic and hemorrhagic diarrhea. Affected
animals will have dilated and unresponsive pupils. Increased heart rate, and
cardiac arrhythmias are common. Depression, dullness and indifference to the
environment are typical in livestock.
Treatment: No specific
treatment exists, and animals should be treated symptomatically. Oral
administration of activated charcoal as an adsorbent may be effective if given
soon after the plants have been eaten.
Field Bindweed, morning glory
(Convolvulus arvensis)
Bindweed is an extremely persistent,
invasive, perennial, twining or creeping weed with alternate leaves, and white
or pink funnel shaped flowers. The plant reproduces readily from seed and its
extensive root system.
Toxin: Tropane alkaloids with
atropine-like action are present in all parts of the plant.
Clinical
Signs: Colic as the result of intestinal stasis and flatulence, and dilated
pupils may result if toxic levels of the bindweed seeds are consumed. No
specific treatment is known, and affected horses should be given symptomatic
therapy for colic.
Kochia weed, Mexican fireweed, summer cypress
(Kochia scoparia)
Habitat: Kochia weed was introduced
from Europe and is now widespread in North America, especially in the Western
States. It is a common weed of disturbed soils along roadsides, edges of
cultivated fields and wastes areas.
Description: A rapidly
growing, drought tolerant annual weed growing to a height of 6 feet under ideal
growing conditions. It is a bushy plant with a many-branched stem, soft hairy
lanceolate, and alternate leaves. In the autumn the stems turn bright
red.
Toxic Principle: A variety of toxicity problems in cattle,
sheep, and horses have been associated with Kochia weed. The toxicity of Kochia
weed varies with the growing conditions of the plant which possibly accounts
for the variety of syndromes associated with the plant: Nitrate poisoning,
Oxalate poisoning and Photosensitization secondary to liver disease.
Sulfate
toxicity - Kochia weed may accumulate high levels of sulfate which can result
in sulfide production in the rumen and subsequent brain necrosis. If the water
is also high in sulfates, the problem can be exacerbated by hot weather that
increases water consumption and therefore total sulfate consumption.
In
some areas of the arid south western States Kochia weed is grown as a forage
crop for cattle because it has a higher yield per acre than alfalfa and various
grasses. The nutritive value of Kochia is also comparable to alfalfa although
it may be less palatable and digestible. The toxicity of Kochia weed is poorly
understood and appears to be influenced by the conditions in which it is
grown.
Locoweed Poisoning
Members of the genera
Astragalus and Oxytropis, referred to as locoweeds or
vetches, are probably the most important toxic plants in the Rocky Mountain
area. Several hundred species exist in North America many of them being
concentrated in the western States. Not all species of Astragalus and
Oxytropis are poisonous. Horses, cattle, sheep, goats, elk, cats and
possibly other animals that eat locoweeds are susceptible to their toxic
effects. Signs of poisoning do not become evident until animals have consumed
significant quantities of locoweeds over many weeks and the toxic threshold is
reached. Animals must consume locoweed for at least 2 weeks and in large
quantities before clinical signs develop. Locoweeds are palatable and once
animals have learned to eat them they frequently will continue to do so even
when normal forages are present. Although horses, cattle, and sheep were
thought to develop an addiction to locoweeds, it is more likely an habituation
as there is no dependence on the plants and they do not actively seek them out
as would be the case if they were addicted. It is entirely possible that the
sole reason animals eat locoweeds is that they find them
palatable.
Principle Toxin
The alkaloid swainsonine is the
principle toxin in locoweed. It is present in all parts of the plant and
persists in the dried plant. The amount of swainsonine in locoweeds varies
depending on the species, stage of growth and the growing conditions. The
succulent flowering plants appear to be the most palatable with animals
preferring to eat the immature seed pods.The palatability of locoweed does not
have any relationship to the quantity of swainsonine in the
plant.
Swainsonine inhibits the action of two cellular enzymes that aid
in the metabolism of complex sugars. As a result, these complex sugars
accumulate in the cells of the brain and many other organs interfering with
their normal function. Young animals are most severely affected, as maturing
cells are more vulnerable to the effects of the toxin. Compounding this is the
fact that swainsonine is also secreted in the milk, so that suckling animals
will acquire additional alkaloid to that acquired from locoweed they may
eat.
Clinical Signs: Locoism, is characterized by abnormal
neurological behavior, reproductive failure, congenital abnormalities, poor
growth and weight loss. All grazing animals are affected. Horses appear to
manifest the nervous signs of locoweed poisoning more commonly than do cattle
or sheep. Depression, incoordination, staggering gait, and unpredictable
behavior especially if the animal is stressed or excited are common signs of
locoism. Some animals become totally unpredictable in their response to being
handled. Poor vision, incoordination, sudden changes in behavior such as
rearing and falling over backwards, make horses dangerous and unsafe to ride.
If removed from the source of the locoweeds and fed a nutritious diet, animals
will show improvement and appear relatively normal after several months.
However, horses with neurologic signs from chronic locoism usually only
partially recover making them a liability to human safety.
Cattle and
sheep may also exhibit neurologic signs of locoweed poisoning, but from an
economic perspective the effects of the locoweed on reproduction are of far
greater significance. Cows may experience poor conception rates, abortions,
hydrops, and produce calves with fetal deformities. In bulls eating locoweed
semen quality is affected.
Cattle grazing locoweed at high altitude will
develop heart failure. Young cattle grazing locoweed often grow poorly and have
markedly decreased weaning weights. Response to vaccination is often reduced in
locoed cattle because their immune system is compromised by the toxic
alkaloid.
Diagnosis: Locoweed poisoning should be suspected in
animals that exhibit abnormal behavior, abortions, deformed offspring,
infertility, and there is evidence that they have been eating locoweeds. It is
possible to detect swainsonine levels and measure alpha-mannosidase activity in
the serum of affected animals that gives a direct means of diagnosing locoweed
poisoning. However the serum half-life of swainsonine is approximately 20
hours, andalpha-mannosidase activity returns to normal in 6 days after the
animals stop eating locoweed.Post mortem examination of animals suspected of
locoweed poisoning should be done to obtain a positive
diagnosis.
Treatment of Locoism: There is no proven effective
treatment for locoweed poisoning. Affected animals denied further access to
locoweed often regain reproductive function provided they are not chronically
affected. Horses with nervous signs of locoism may never fully
recover.
Control of Locoweeds and Pasture Management Since it is
inevitable that livestock will have access to locoweeds in much of the western
United States, grazing management systems need to be developed to enable
horses, cattle and sheep to utilize natural rangeland. Systems to reduce
livestock losses from locoweeds should utilize optimum stocking rates, multi
species grazing, and rotational grazing to provide areas of range or pasture
that are free of locoweed. Such "safe areas" can be naturally free
of locoweed, or can be created by the strategic use of appropriate herbicides.
Herbicides alone are seldom effective in the control of locoweeds as they are
costly to apply to large acreages, and locoweed seeds can remain dormant in the
soil for many years, ready to germinate under favorable
conditions.
Sage Poisoning (Artemisia spp.)
A
syndrome called "sage sickness" has been reported in horses that eat sand sage
(Artemisia filifolia) in winter time when heavy snow-falls cover the
lower growing range grasses. Horses can eat sage without problem provided they
are not forced to eat it exclusively when other forages are scarce. Under
adverse conditions horses will readily eat sagebrush and become intoxicated.
Horses wintered on a pasture overgrown with fringed sage (Artemisia
frigida) also develop a neurologic disease similar to that seen with
sand sage poisoning. Cattle are not susceptible to sage
poisoning.
Indigenous sages are generally perennials ranging from the
common big sage (A. tridentata) which can grow to a height of 10 ft, to
fringed sage (A. frigida) that grows to 1ft. in height. Considerable
variation exists in the 200 or more species of sagebrush. The leaves are
alternate, and are covered by fine white hairs that give the leaves a silvery
appearance. Most sages have a characteristic odor when crushed. The flowers are
inconspicuous and are produced in the leaf axils.
The toxic principle
has not been determined in sand or fringed sage, but extensive work on big sage
(A. tridentata) has shown that volatile oils are present in significant
quantity, being highest in the fall and winter.
Sage poisoned horses
exhibit abnormal behavior characterized by ataxia especially of the front legs,
and a tendency to fall down or act abnormally to stimuli that would not
normally elicit such a response. Tying the horse to a coral post, for example,
will cause the sage poisoned horse to pull back violently and throw itself to
the ground. Normally docile horses will become excitable and unpredictable. The
smell of sage is often very noticeable on the breath.
The clinical signs
closely resemble those of horses that have been poisoned by locoweeds
(Oxytropis and Astragalus spp.) However, unlike "locoed" horses
that do not recover once clinical signs are evident, sage poisoned horses
generally recover once they are removed from the sage and are fed a normal
balanced diet.
Control of invasive sages such as fringed sage (A.
frigida) can be accomplished by the use of common herbicides. It is
important to avoid overgrazing which allows fringed sage to increase rapidly on
range land.
Plants causing Sudden
Death
Poison Suckleya (Suckleya
suckleyana)
Suckleya is found in localized areas from Montana to New
Mexico. It is a small, prostrate plant that grows in moist conditions
preferring the edges of receding reservoirs and ponds. It may become a large
plant when growing around the edges of irrigated fields where run-off water
collects.
Description: Annual, succulent, prostrate herbaceous
plant with reddish fleshy stems 3-6 cm long. The leaves are alternate,
triangular or spade-shaped with dentate margins and long petioles. The
inconspicuous small flowers are formed in the leaf axils. The fruits are
reddish-brown, enclosed by two papery, dark-colored scales joined at the
tip.
Principle Toxin: Suckleya contains variable quantities of
cyanogenic glycosides. Poisoning from suckleya varies, being troublesome
in some years when cattle and sheep find it palatable.This may be due to the
fact that it often grows around ponds, and in years of drought livestock eat it
as something green when they come to drink and congregate in the area. The
glycoside content of the plants is also quite variable.
The first
indication of suckleya poisoning is sudden death of cattle that have grazed the
plant. Affected animals, if seen alive, show severe difficulty in breathing,
and their venous blood is "cherry-red" in color.
Johnson grass
(Sorghum halepense )
Habitat:A common weedy grass in alluvial
bottom land, growing along roadsides and ditches throughout most areas east and
south of the Rocky mountains. Sudan grass (broom corn), Sorghum
sudanense and its hybrids are grown as a forage crops.
Johnson grass
is a drought resistant perennial growing 3-8 feet tall, with scaly root stalks
and relatively broad leaves with a prominent mid vein. Seeds are yellow-purple
and occur in a large, many branched panicle. Sudan grass and its hybrids are
very similar in appearance but are annuals, and tend to be a more robust plant
than Johnson grass, having broader leaves and thicker
stems.
Principle Toxin: Johnson and Sudan grasses are the most
common cause of cyanide poisoning in cattle and sheep, and are especially toxic
when growing rapidly. Fertilization with nitrogen increases the potential for
cyanide and nitrate toxicity. Regrowth of sorghums after cutting has high
potential for poisoning. Cyanide-free hybrids of sudan grass are available as
forage crops for animal consumption. All species of sorghum may also accumulate
toxic levels of nitrate.
Nitrate Poisoning:
Nitrate poisoning
is a universal and economically important problem for ruminants caused by the
ingestion of plants that have accumulated toxic levels of nitrate. Normally
plants absorb nitrates from the soil converting them into plant proteins.
Excessive application of organic or inorganic nitrogenous fertilizers can
result in excessive accumulation of nitrates in crop plants and common weeds.
Consumption of these plants in quantity by livestock leads to nitrate
poisoning. The chance of nitrate poisoning is increased when livestock water
sources also contain high levels of nitrates. Nitrate fertilizers themselves
are highly toxic chemicals capable of causing fatal poisoning in ruminants and
horses that gain access to them accidentally.
Common weeds, forage crops
and cereal grain plants have the potential for accumulating nitrate. Nitrate
poisoning is most often seen in cattle eating sorghums. Nitrate levels in
plants vary depending upon the plant species, stage of growth, water and
organic content of the soil, and application of nitrogen fertilizers. Drought
conditions, acidic soils, and soils deficient in sulfur, phosphorous and
molybdenum result in nitrate accumulation in plants. Cool, cloudy days enhance
nitrate formation in plants because the light and warmth dependent enzyme,
nitrate reductase, is inhibited, thus allowing nitrate accumulate in the plant.
Nitrate levels are therefore highest in plants at night and early morning when
the nitrate reducing enzymes are least active. Highest levels of nitrate tend
to be found in the stems where nitrate reduction normally takes place, and not
the leaves. Nitrate does not accumulate in the flowers or fruits of the plant
and therefore is not a problem in grains fed to livestock. Properly prepared
silage from forage crops high in nitrates reduces the nitrate content by 60%,
while there is little reduction of nitrate in dried hay. The application of
herbicides such as 2,4 - D , not only increases the nitrate content of plants,
but also the palatability, of the plants thereby increasing the potential for
poisoning.
Nitrate Toxicology: There is considerable variation as
to what constitutes a safe level of nitrate in animal feeds because of
different factors that influence nitrate metabolism. In general, nitrate is
reduced in a series of steps in the rumen from nitrate to nitrite, to ammonia
and eventually microbial proteins. It is the rapid formation and absorption of
large quantities of nitrite and not nitrate, that causes poisoning. The rate at
which nitrate is converted to highly toxic nitrite is dependent on the rate of
adaptation of rumen microorganisms to nitrate, the rate and amount of nitrate
ingested, and the amount of carbohydrate available in the rumen. Diets high in
carbohydrates such as corn and molasses enable rumen bacteria to convert
nitrates are more rapidly to ammonia and microbial proteins without the
accumulation of nitrite. Low energy diets on the other hand increase an
animal's susceptibility to nitrite poisoning.
Plants or hay containing
more than 1% nitrate (10,000 ppm) dry matter are potentially toxic and should
be fed with caution. Forages containing more than 1% nitrate should only be fed
if the total nitrate intake can be reduced to less than 1% by diluting the
nitrate-forage with nitrate-free forages.
The addition of monensin to
rations high in nitrate may precipitate poisoning. This has been reported in
cattle fed turnips, and forage high in nitrate that produced no clinical signs
until monensin was given as a feed additive.
Water containing up to
100ppm of nitrate can be considered safe for all classes of livestock assuming
that the animals are on a normal diet that does not have high levels of
nitrate. Water levels above 200ppm of nitrate should be considered toxic to
pregnant animals. Both the water and the animal’s forage should be
analyzed to ensure that total nitrate does not exceed potentially toxic
levels.
Clinical Signs: The first sign of nitrate poisoning is
the unexpected finding of dead animals. If observed before death, ruminants
with nitrate poisoning may exhibit drowsiness, and weakness, followed by
muscular tremors, increased heart and respiratory rates, staggering gait and
recumbency. Signs of poisoning develop within 6-8 hours of the consumption of a
toxic dose of nitrate. Stress or forced exercise will increase the severity of
clinical signs and hasten death. Examination of the mucous membranes,
especially the vaginal mucous membranes, usually reveals a brownish
discoloration. Venous blood also has a chocolate brown discoloration. Death
usually occurs within 2-10 hours of consumption of a lethal dose of
nitrate.
Cattle that consume sublethal quantities of nitrate forages may
develop chronic nitrate poisoning symptoms that include abortion, reproductive
failure, hypothyroidism, poor growth rates, and vitamin A deficiency. Fetal
death and abortion may occur at any stage of gestation.
Treatment:
Animals showing signs of nitrate poisoning should be handled carefully to
avoid stress or excitement. The suspected nitrate food source should be
removed. The preferred treatment for nitrate poisoning is methylene blue
solution administered intravenously. The recommended dose range for methylene
blue is from 4-15 mg/kg body weight administered as a 2-4% solution. A dose of
8 mg/kg body weight intravenously has been reported to be effective in
cattle.
The administration of several gallons of cold water with added
broad spectrum antibiotics orally will help reduce further nitrate reduction to
nitrite by rumen microorganisms. Similarly, a gallon of vinegar mixed with 2
gallons of water and given orally via stomach tube will help prevent further
nitrite formation.
Diagnosis: Sudden deaths in ruminants grazing
post-harvest crops, sudan grass (Sorghum spp.) and weeds should raise
suspicion of nitrate poisoning. Confirmation should be based on demonstrating
toxic levels of nitrate in the forage and/or water source, and in the rumen
contents and tissues of the animal. Animal tissue and plant samples should be
frozen if they cannot be analyzed immediately.
If the animal has been
dead for several hours or more the best sample to submit for nitrate analysis
is the aqueous humor from the eyes. Nitrate levels in aqueous humor of 20-40
ppm should be considered suspect, and over 40 mg/L (40 ppm) could be considered
diagnostic of nitrate poisoning if there are corroborating clinical signs and
evidence of high nitrate levels in the forage and/or the water. Ocular fluid
from an aborted fetus is useful for determining the cause of abortion provided
the levels detected are interpreted in light of forage and water nitrate levels
to which the dam would have had access.
As a general rule, levels of
nitrate in forages over 0.5%, and water levels exceeding 200 ppm are
potentially hazardous to pregnant animals especially if fed continuously.
Forages containing in excess of 1% nitrate dry matter should be considered
toxic. Water levels of 1,500 ppm or greater are potentially toxic to ruminants
especially if consumed with forages high in nitrate.
Prevention of
nitrate Poisoning: Nitrate poisoning can be prevented if the nitrate levels
in forages are predetermined and managed accordingly. Forages such as sudan
grass and its hybrids, oat hay and corn stalks should be tested especially
where heavy nitrogen fertilization has been used or drought has affected the
plants. Forages containing 1% nitrate or more should be fed cautiously and only
when the nitrate content in the total ration has been reduced to less than 0.5%
by diluting the toxic forage with grass hay containing no nitrates. Hay
containing high nitrate levels that is exposed to rain can have the nitrate
leached out into the lower bales making them especially high in nitrates. It is
also prudent to check the water of the animals to ensure it is not a source of
nitrates that would be additive to any nitrate in the food. Increasing the
total energy content of the ration also enhances the metabolism of nitrate in
the rumen thereby helping ruminants tolerate higher nitrate levels in their
diet.
Cocklebur (Xathium strumarium)
Cockleburs are
annual, bushy weeds 2-5 feet tall, with stout stems, often with dark spots. The
leaves are large, rough, glandular, and triangular from 2-14 inches long and
1-8 inches wide. Flowers are produced in the leaf axils. Hooked spines cover
the characteristic oval burs. Each bur contains 2 seeds, which can remain
dormant in the soil for years. Cockleburs can reappear many years after the
parent plant disappeared.
Principle Toxin: Carboxyactractyloside,
a sulfated glycoside, is the primary liver toxin present in cockleburs. The
glycoside is present in high concentration in the seeds and the 2-leafed
cotyledonary stage. The toxin disappears by the 4-leaf stage, and is not
present in the mature plant. The liver appears to be the primary target organ
with pigs, ruminants and horses being susceptible to poisoning. Fatalities
occur when 0.75% to 3.0% body weight of cotyledons are consumed. Acute deaths,
convulsions, blindness and recumbency have been encountered in cattle eating
hay contaminated with cockleburs.
The spiny burs are a source of
mechanical injury to the mouth of animals when consumed. Significant economic
losses can also occur to wool producers when the burs become entangled in the
fleece.
Clinical signs: Poisoning usually occurs when animals eat
large numbers of the 2-leafed stage of the cocklebur or eat the seeds that may
contaminate cottonseed or other food sources. Pigs and cattle show similar
signs of poisoning including depression, reluctance to move, hunched back,
ataxia and recumbency. Paddling of the limbs, convulsions succeeded by coma and
death in 24 hours are common. There is no known effective treatment for
cocklebur poisoning.
Reference: A Guide to Plant Poisoning of
Animals in North America. A. P. Knight and R. G. Walter. Teton New Media,
Jackson Hole, Wyoming. Order from 877-306-9793 |
Page Created and Maintained by: Perry D. Brewer, Area
Extension Agent (Technology Education/Youth)
1/16/2003 |
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