Quick Facts...
- Prussic acid poisoning can be a lethal problem for cattle grazing sorghums.
- A characteristic sign of prussic acid toxicity is bright cherry-red blood, a symptom that persists several hours after death.
- Treatment of prussic acid poisoning, with a mixture of sodium nitrate and sodium thiosulfate or with methylene blue, can be successful if administered by a veterinarian soon after symptoms appear.
- There is a qualitative test for prussic acid potential in forages.
Prussic acid, also called hydrocyanic (HCN), normally is not present in plants.
However, several common plants can accumulate large quantities of cyanogenetic
glycoside. When plant cells are damaged by wilting, frosting or stunting, the glycoside
degrades to form free HCN. Conditions in the rumen also favor degradation of the
glycoside to free HCN. Thus plants that contain the glycoside have the potential to cause
HCN toxicity when consumed by ruminants.
In Colorado, plants most likely to cause HCN poisoning are sorghums. The
potential is greatest for johnsongrass and least for true sudans. Other materials with
HCN potential include white clover, vetch seed and chokecherry.
As with nitrate buildup, some stress usually triggers accumulation of
cyanogenetic glycoside in plant tissue. The potential for accumulation and HCN toxicity
increases during drought. Occasionally, poisoning occurs when hot, dry winds induce
temporary moisture stress in plants. The potential for poisoning is greater with excessive
soil nitrogen and young plants. Toxicity also is more likely when periods of rapid
growth are followed by cool, cloudy weather. Lush regrowth after cutting for hay,
grazing or frost is particularly dangerous.
Unfortunately for the livestock producer, often the only indication of prussic
acid poisoning is dead animals. HCN is one of the most potent, rapid-acting poisons
known. It interferes with oxygen use at the cellular level. When a lethal dose is
consumed, animals die from asphyxiation in a few minutes.
When seen, clinical signs occur in rapid succession. Initially there is
excitement and muscle tremors. Rapid and difficult breathing follows. The animal goes
down, gasps for breath and may convulse. The pupils are dilated and mucous
membranes are bright pink. A characteristic sign of HCN toxicity is a bright cherry-red
color to the blood, a symptom that persists for several hours after death. Although blood is
oxygenated, HCN interferes with the release of oxygen from oxyhemoglobin to other
tissues. This situation contrasts with nitrate toxicity, where oxygenation of blood is
restricted. The rumen may be distended with gas, and the odor of "bitter almonds" may
be detected when the body cavity is opened.
Treatment of HCN poisoning, with a mixture of sodium nitrate and sodium
thiosulfate or with methylene blue, can be successful if administered soon after
symptoms appear. Consult a veterinarian for diagnosis and drug treatment, because
HCN toxicity often is confused with nitrate poisoning and other toxins of plant origin. A
veterinarian also can assist in collecting plant and animal tissues for analysis and in
interpreting laboratory results.
Preventing Prussic Acid Poisoning
As with nitrate, most problems with prussic acid can be avoided with proper
management of forage and animals. Test any forage crop thought to contain HCN before
animals are grazed or fed. Sorghums fertilized heavily with nitrogen and stunted by
drought or cool, cloudy weather should be suspected. Reduce risk of poisoning from
sorghums by using a maximum of about 50 pounds of nitrogen per application.
Young plants have a higher HCN potential than more mature ones, so do not
graze sorghums until plants are 18 to 24 inches high. This practice also applies to
regrowth that occurs after cutting for hay or grazing. If regrowth occurs following frost,
delay grazing until a hard freeze kills the entire plant. Do not pasture sorghums
following a killing frost until plants thaw and wilt for a few days. Spraying of
cyanogenetic plants with a herbicide may increase the toxic hazard.
Graze pastures to a uniform height, then remove animals to prevent selective
consumption of lush regrowth. Rotation grazing and heavy stocking rates help in this
regard. To acclimate cattle to new pasture, fill animals on native grass or hay during the
day, then graze sorghums in late afternoon and evening.
Proper field curing or ensiling results in considerable loss of HCN. If the forage
is questionable as pasture, harvesting for hay or silage reduces the potential for HCN
toxicity. However, if hay is poorly cured before baling, extremely high in HCN potential
at cutting, or contains johnsongrass, it still may cause problems.
Plant varieties differ in their potential for prussic acid poisoning. As with
nitrate, chances for HCN toxicity are somewhat lower with true sudans and sudan-sudan
hybrids than with sorghum-sudan or sorgo-sudan hybrids.
There is a quick qualitative test for HCN potential in plant tissue.
It also can be used to confirm the presence of HCN in rumen contents of animals
that die from prussic acid poisoning. Leaves are higher in HCN potential than stems.
Glycoside levels increase during the morning, then level off and begin declining in the
afternoon and evening. Therefore, samples for prussic acid analysis must include leaf
tissue and should be collected in late morning or early afternoon.
Randomly sample fresh forage from several locations. For hay, take cores from
several bales. Seal two or three handfuls per sample in a plastic bag, store in the dark,
refrigerate unfrozen, and deliver to the laboratory without delay.
Test for Prussic Acid
This is a qualitative test to evaluate
forages (hay, pasture, silage) for prussic
acid poisoning potential in ruminants.
- Prepare picrate paper by wetting filter paper with a solution of 5.0 grams of
sodium bicarbonate and 0.5 gram picric acid in 100 ml water.
- Dry the paper and cut into strips about 1/4 inch by 1 1/2 inch. Store dried strips in
a stoppered bottle or sealed plastic bag.
- Finely chop or crush a small quantity of plant material and place it in a test tube or
bottle that can be sealed with a cork or rubber stopper. Slit one end of the stopper
to hold a picrate paper strip.
- If plant material is dry, moisten with a few drops of water and allow to hydrolyze
several minutes in stoppered tube.
- Moisten the picrate paper with water.
- If the temperature is below 80 degrees F, warm the solution by holding the container
in hand. If the paper changes from yellow to brick red within 30 minutes, prussic acid is
present.
Toxic Levels
The level of HCN required to cause toxicity varies, depending on rate
of intake and individual animal tolerance. Generally speaking, view as
dangerous any forage analyzing more than 200 ppm HCN on an as-fed basis.
Summary
Prussic acid (HCN) causes acute poisoning in ruminants grazing sorghums,
especially johnsongrass. Many of the same factors that tend to cause nitrate
accumulation -- drought, reduced sunlight, excessive soil nitrogen, young plants -- also
increase HCN potential. HCN potential is greater in leaves than stems. Proper curing for
hay or ensiling greatly reduces the potential for HCN poisoning. Lush regrowth in
sorghums after cutting for hay, grazing or frost is often dangerous.
Contrasted to nitrate toxicity, HCN poisoning is characterized by a bright
cherry-red color to the blood. As with nitrate, minimize HCN potential through proper
fertility programs and variety selection and by testing questionable forage. Treatment of
prussic acid poisoning, with a mixture of sodium thiosulfate or with methylene blue, can
be successful if administered by a veterinarian soon after symptoms appear.
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