A common shrub or small tree 10-20 feet high growing along waterways in mountain valleys and occassionally in drier areas.
Cattle, sheep, goats
Cyanogenic glycosides (prunasin,and amydalin) which are readily hydrolysed by rumen microorganisms to free hydrogen cyanide (HCN). All parts of the plant contain cyanogenic glycosides except the ripe berries. The wilted leaves are more toxic than when fresh. Cyanide blocks the action of the enzyme cytochrome oxidase preventing the utilization of oxygen in the tissues and leaving the oxygen bound to hemoglobin. Death results rapidly from anoxia.
All members of the Prunus family including cherries, apricots, almonds, peaches and their hybrids contain cyanogenic glycosides in their stems, leaves and seeds. The concentrations of the cyanide glycosides increases when the plant is stressed by drought or frost. The cyanide potential is highest in the new growth of the plants.
Shrub or small tree with greyish bark marked by lenticels. Leaves are simple, glossy, alternate, ovate with serrate margins. The white flowers are produced in cylindrical racemes that are fragrant. The berries turn purple when ripe and are not toxic except for the seeds. Similar species include Prunus pennsylvanica (pin cherrry) and P. serotina (black cherry).
Excessive salivation, nervousness and weakness precede death.
Without stressing the animal, sodium thiosulfate and sodium nitrite should be given intravenously. A mixture of 1ml 20% sodium nitrite and 3ml of 20% thiosulfate should be prepared and given at the rate of 4 ml of the mixture per 100lbs body weight. In ruminants Sodium thiosulfate may also be given orally via stomach by dissolving 30gm in a gallon of water.
Sudden death. Mucous membranes appear pink and redder than normal. Venous blood is cherry red in color. Stressing the animal rapidly leads to collapse and death.
Initially animals show difficulty in breathing. Open-mouth breathing is common as the animal becomes oxygen deprived. Death occurs rapidly.
Sudden death with evidence of animal eating cyanogenic plants. Severe respiratory difficulty, cherry-red mucous membranes are highly suggestive of cyanide poisoning. Plant material or fresh rumen contents can be submitted for detection of cyanide (Picrate test).
Ruminants are most susceptible to plant-induced cyanide
poisoning because their rumen bacteria and alkaline pH of
the rumen quickly hydrolyze the glycosides to free cyanide,
which is absorbed to cause poisoning. In simple stomached
animals, including the horse, the acid pH of the stomach
and the fact that horses do not have a lot of bacteria in their stomach's to
breakdown the cyanogenic glycosides, means that they are not
likely to develop cyanide poisoning from eating the leaves
of cherries and apricots etc. Under rare situations where a
horse might eat large amounts (10 lbs) of wilted cherry/apricot leaves, there may be enough cyanide present to cause poisoning. However, if a horse is fed a normal balanced ration, or if there is plenty of normal grass present, it is very unlikely that apricots etc. would pose any risk to horses.
------The mare reproductive loss (MRLS) syndrome that caused significant fetal losses in Kentucky in 2001 was initially attributed to mares eating black cherry trees (Prunus serotina), and the effects of cyanide on the fetus. However, cyanide intoxication was found not to be the cause of MRLS. Numerous research reports now indicate that the MRLS is related to the Eastern Tent caterpillar that was contaminating the food and water of the pregnant mares. Further research indicates that it is the hairs from the caterpillars damage the intestinal lining of the mare and thereby allow bacteria and/or a toxin into the circulation of the mare and ultimately the developing fetus.
Ref: Bernard WV, LeBlanc MM, Webb BA, Stromberg AJ. Evaluation of early fetal loss induced by gavage with eastern tent caterpillars in pregnant mares. J Am Vet Med Assoc. 2004, 225:717-721.
Ref: Levent Dirikolu et al. The Toxicokinetics of Cyanide and Mandelonitrile
in the Horse and Their Relevance to the Mare Reproductive Loss Syndrome.
Toxicology Mechanisms and Methods, 13: 199-211,2003.