Very Common
OTHER DIAGNOSES CONSIDERED
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Diagnosis
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Your vet may diagnose
Cyanide Toxicity from Plants
Synonyms: Poisoning by Plants Containing Cyanogenic Glycosides
Summary
Cyanide toxicity is usually caused by ingestion of cyanogenic glycoside-containing plants of several different plant families. There are many plants, that under certain circumstances, produce cyanogenic glycosides.
Familiar plants producing these glycosides include Johnson Grass, Sudan Grass, Cherry species, Elderberry, Choke-Cherry, Suckleya, Service Berry, Arrow Grass, Blue Flax, Acacia, Mountain Mahogany, some clovers, corn, sorghum and Cassava.
In order to be toxic, the glycoside must be converted to hydrogen cyanide (Prussic Acid). Luckily, unlike ruminants, horses rarely suffer from this problem. During digestion in the rumen, ruminants produce cyanide from the glycosides. This does not happen in horses.
But horses can still be poisoned, usually when eating dying, frozen, or wilting leaves of these plants. During decomposition, the toxic cyanide can be produced.
Drying gradually reduces the amount of toxin in the plant. The mature fruit of these plants has much less toxin in them.
Cyanide interrupts cellular respiration. Hemoglobin, the oxygen containing molecule cannot unload its oxygen into the tissues.
Classic signs of acute toxicity (significant intake of toxin) are rapid breathing, nostrils flaring, with bright red gums. Most horses suffering from acute toxicity are dead within 1-2 hours. Cyanide is said to smell like bitter almond and this can sometimes be detected on the breath of affected animals. More commonly, the horse is simply found dead.
The disease can take a classic form too, i.e. long-term exposure to low levels of these toxins. The signs of this can include birth defects, weakness and neurologic dysfunction.
Diagnosis is made when there is evidence that one of these plants has been consumed, and the clinical signs of cyanide toxicity fit. Lab diagnosis can be performed on blood and tissues, looking for hydrogen cyanide, but it must be performed rapidly in order to find the toxin, which is quickly lost from animal tissues. It also can be found in plant material.
The antidote consists of sodium nitrite and sodium thiosulfate, however this may or may not be effective.
Familiar plants producing these glycosides include Johnson Grass, Sudan Grass, Cherry species, Elderberry, Choke-Cherry, Suckleya, Service Berry, Arrow Grass, Blue Flax, Acacia, Mountain Mahogany, some clovers, corn, sorghum and Cassava.
In order to be toxic, the glycoside must be converted to hydrogen cyanide (Prussic Acid). Luckily, unlike ruminants, horses rarely suffer from this problem. During digestion in the rumen, ruminants produce cyanide from the glycosides. This does not happen in horses.
But horses can still be poisoned, usually when eating dying, frozen, or wilting leaves of these plants. During decomposition, the toxic cyanide can be produced.
Drying gradually reduces the amount of toxin in the plant. The mature fruit of these plants has much less toxin in them.
Cyanide interrupts cellular respiration. Hemoglobin, the oxygen containing molecule cannot unload its oxygen into the tissues.
Classic signs of acute toxicity (significant intake of toxin) are rapid breathing, nostrils flaring, with bright red gums. Most horses suffering from acute toxicity are dead within 1-2 hours. Cyanide is said to smell like bitter almond and this can sometimes be detected on the breath of affected animals. More commonly, the horse is simply found dead.
The disease can take a classic form too, i.e. long-term exposure to low levels of these toxins. The signs of this can include birth defects, weakness and neurologic dysfunction.
Diagnosis is made when there is evidence that one of these plants has been consumed, and the clinical signs of cyanide toxicity fit. Lab diagnosis can be performed on blood and tissues, looking for hydrogen cyanide, but it must be performed rapidly in order to find the toxin, which is quickly lost from animal tissues. It also can be found in plant material.
The antidote consists of sodium nitrite and sodium thiosulfate, however this may or may not be effective.
my vet's role
Diagnostics Used
These are tests that might be helpful to make this diagnosis or further characterize the condition.
Treatments May Include
These treatments might be used to help resolve or improve this condition.
PROGNOSIS AND RELEVANT FACTORS
Toxicity varies with stage of growth, soil mineral and moisture content. Moist conditions favor the accumulation of the glycosides. Application of herbicides can increase the formation of the toxin.Drying gradually reduces the amount of toxin in the plant, so horses are rarely poisoned from hay. The mature fruit of these plants has much less toxin in them.
Once toxicity occurs, the prognosis is generally poor, especially without early recognition and treatment with the antidote.
my role
I might observe
You might make these observations when a horse has this condition.
Very Common
Less Common
Skills I Might Need
I might need these skills if my horse has this diagnosis.
Questions To Ask Your Vet:
- What is the source of the poisoning?
- What management changes can I make to ensure this never happens again?
Prevention
Remove cherry plants and other dangerous plants from pastures. Ensure that pastured horses are not allowed to overgraze their pastures, leaving these plants as the only accessible green plants.
If horses must be kept on overgrazed pasture, they must be supplied with adequate to excess palatable hay so they are not tempted to try toxic plants. Be aware of the plants in your pasture, and do not let horses graze when potentially toxic plants have higher levels of toxin.
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