Nitrate vs. Prussic Acid Toxicity
Sometimes confused, the effect may be similar, but the cause is from two different mechanisms. Knowing the cause can help
reduce potential problems.
Nitrate Toxicity
Soil nitrogen absorbed by the plant roots is in the nitrate form. The enzyme nitrate reductase in the plant rapidly converts the
nitrate to amino acids. However, when the plant is stressed, the nitrate-to-protein conversion is disrupted and nitrates begin to
accumulate.
Although a misnomer, nitrite, not nitrate, is what poisons the animal. In cattle, the rumen bacteria rapidly reduces nitrates to
nitrites. The nitrites are normally converted to ammonia to be used by rumen microorganisms as a nitrogen source. If nitrate
intake is faster than its breakdown to ammonia, the nitrites will begin to accumulate in the rumen. Nitrite is rapidly absorbed
into the blood system where it oxidizes the hemoglobin to methemoglobin. Red blood cells containing methemoglobin cannot
transport oxygen, and the animal dies from asphyxiation.
Although all livestock are susceptible to nitrate toxicity, cattle and horses are affected the most often. Toxicity is related to the
total amount of forage consumed and how quickly it is eaten, in general, forages containing 3,000 - 6,000 ppm of nitrates is considered moderately safe in most situations. However, limit use for stressed animals to 50% of the total ration. If forage contain
more than 6,000 ppm of nitrate, it should be considered potentially toxic. Signs of chronic nitrate toxicity are nonspecific symptoms of numerous disorders and are not a reliable diagnosis of nitrate poisoning. Low nitrate levels can cause abortion without
any other noticeable symptoms. Acute toxicity usually is not apparent until approaches lethal concentrations of methemoglobin.
Symptoms include bluish color of mucus membranes, labored breathing, muscular tremors, which follows with coma and death
within two to three hours.
Nearly all plants contain nitrate, however some plants are more prone to nitrate accumulation than others. Plants such as forage
sorghum, grain sorghum, sudangrass, sudan-sorghum hybrids, and pearl millet are notorious nitrate accumulators. Other species
such as kochia, lambsquarters, sunflower, and pigweed also are routinely high in nitrate.
Generally nitrate content is highest in young plant growth and decreases with maturity. However, sorghums and sudangrasses
are an exception because concentrations usually remain high in mature plants. If plants are stressed at any stage of growth, nitrates can accumulate. Nitrates normally accumulate in stems and conductive tissues. The highest levels occur in the lower onethird of the plant stalk. Concentrations tend to be low in leaves because nitrate reductase enzymes levels are high there.
Nitrates accumulate in plants during moderate drought. During a severe drought, lack of moisture prevents nitrate absorption by
plant roots. However, following a rain, the roots rapidly absorb nitrate and accumulate high levels. After a drought-ending rain, it
requires 7 to 14 days before the nitrates will be metabolized to low levels, provide environmental conditions are optimum. Extended periods of cloudy weather can increase nitrate content. Conditions such as frost, hail, or disease can damage leaf area
which can inhibit the nitrate reduction process and nitrates accumulate in plant. Nitrogen fertilization increases soil nitrate levels
and the subsequent uptake by plant roots. Weeds damaged but not killed by a herbicide will have high nitrate levels because of
depressed enzyme activity and reduced leaf area.
If forages are harvested as hay, nitrate concentrations remain virtually unchanged over time. If plants are fed as green chops, the
harvested forage should be fed immediately after cutting, not allow to heat up. As the plants respire, nitrates are converted to
nitrites, which are about 10 times more toxic than nitrates. Have representative samples of suspect forage analyzed before feeding.
Prussic Acid Toxicity
Prussic acid (also known as hydrocyanic acid or hydrogen cyanide (HCN)) is caused by cyanide production in several types of
plants under certain growing conditions. These plants possess a cyanogenic molecule called dhurrin in their epidermal cells. In
healthy intact leaf tissue, dhurrin is non-toxic. However, mesophyll cells located beneath the epidermis have an enzyme that
removes HCN from dhurrin. If the leaf becomes damaged, dhurrin and its hydrolyzing enzyme will intermix and release cyanide.
Once consumed, cyanide is absorbed into the bloodstream and binds to enzymes in the cell. This cyanide complex prevents hemoglobin from transferring oxygen to individual cells and the animal dies from asphyxiation. Cyanide poisoning is related to the
amount of forage and the animal’s condition. On a dry matter basis, forages with more than 500 ppm HCN should be considered
potentially toxic.
Prussic acid acts rapidly and frequently killing the animal within a few minutes. The clinical signs of prussic acid poisoning are
similar to nitrate toxicity, but animals with cyanide poisoning have a bright red blood that clots slowly, whereas animals poisoned with nitrate have dark, chocolate-colored blood which will change to dark red within a few hours after death. The smell
of bitter almonds is often detected in animals poisoned with cyanide. Because it occurs quickly, the symptoms are usually observed too late for effective treatment.
Crop forages most commonly involved with prussic acid poisoning are sorghums, johnsongrass, and sudangrass. Grain sorghums
are potentially more toxic than forage sorghums or sudangrass. However, potential cyanide production can vary widely among
summer annual forages.
Cyanide is more concentrated in young leaves than in older leaves or stems. Young, rapidly growing plants are likely to contain
high levels of prussic acid. Pure stands of indiangrass that are grazed when the plants are less than 8 inches tall can possess lethal concentrations of cyanide. Generally, any stress condition that retards plant growth may increase prussic acid content. Hydrogen cyanide is released when plant leaves are physically damaged. During drought and a frost, stunted plants accumulate
cyanide and can possess toxic levels at maturity. Freezing ruptures the plant cells and releases cyanide. After a killing frost, wait
at least 4 days before grazing to allow the released HCN to dissipate.
Prussic acid poisoning is most commonly associated with regrowth following a drought-ending rain or the first autumn frost.
New growth from frosted or drought-stressed plants is palatable but dangerously high in cyanide. Most losses occur when hungry or stressed animals graze young sorghum growth. Ruminants are particularly susceptible to prussic acid poisoning because
cud chewing and rumen bacteria both contribute to releasing cyanide. However, the enzyme responsible for hydrolyzing HCN
from dhurrin is destroyed in stomach acid, which allows monogastric animals, such as horses and swine, to be more tolerant of
cyanide than ruminants.
Prussic acid concentrations are higher in fresh forage than in silage or hay because HCN is volatile and dissipates as the forage
dries. However, if the forage had extremely high cyanide content before cutting, or if the hay was not cured properly, hazardous
concentrations of prussic acid could remain.