Prunus species: Cherry

Family

Rosaceae

Common Names

Choke cherry (Prunus virginiana), black cherry (P. serotina), cherry laurel (P. laurocerasus), and service berry (Amelanchier species) are of toxicologic significance.

Plant Description

A diverse genus of some 400 species of woody, deciduous shrubs and small trees, Prunus are native to many areas of the Northern Hemisphere. Many species have thorns and smooth bark with obvious lenticels. Leaves are simple, alternate, petiolate, entire or serrate, and glossy green above. Inflorescences are racemes or clusters produced terminally on branches or woody spurs. Flowers have 5 sepals and 5 petals, in white, pink, or red. Fruits are fleshy drupes, each with a hard endocarp or stone, and one round or flattened seed per stone (Fig. 328 and Fig. 329).

Figure 328. Prunus flowers.

Figure 329. Prunus virginiana-choke cherries.

Toxic Principle and Mechanism of Action

Many Prunus species contain cyanogenic glycosides, the primary glycosides being amygdalin (Laetrile) and prunasin [1]. Prunasin is especially high in the new growth and in wilted or frosted leaves, while amygdalin is highest in the seeds. The ripe pulp of the berries surrounding the seeds is not toxic.

At least 2000 plant species, many from the 27 genera represented in the Rosaceae contain cyanogenic glycosides, but relatively few have been associated with poisoning in livestock, and fewer still have affected household pets. The major sources of cyanogenic glycosides responsible for poisoning of ruminants are sorghums such as Johnson and Sudan grasses (Sorghum species), and a number of the Prunus genus. Ruminants are particularly sensitive to plant-induced cyanide poisoning because the cyanogenic glycosides are rapidly hydrolysed in the rumen by plant and bacterial enzyme action to produce the highly toxic hydrogen cyanide (HCN, or prussic acid) [2]. Simple stomached animals such as horses, pigs, and dogs are rarely poisoned by plant cyanogenic glycosides because their digestive systems lack the ability to rapidly hydrolyse the glycosides to HCN. Dogs are very rarely affected by cyanide poisoning from plant origin. There are a few occasions where dogs have eaten quantities of choke cherry leaves and berries and heavenly-bamboo (Nandina domestica) and developed cyanide poisoning [3,4].

Dogs have also been experimentally poisoned with fresh sweet almonds (P. dulcis) containing amygdalin [5]. Since apricot seeds (P. armeniaca) are also high in amygdalin [6], dogs that eat quantities of fallen apricots have the potential for poisoning, especially if the pits are cracked open to expose the seeds to the animals digestive system.

It should be emphasized however that all animals are highly susceptible to HCN [2]. Dogs and cats are quite frequently poisoned by HCN produced in house fires and from eating or drinking chemicals containing sodium or potassium cyanide. It is because plants do not contain free HCN, and it requires enzymatic hydrolysis of the cyanogenic glycosides for the plant to become toxic, that dogs and other simple stomached animals are rarely affected by cyanogenic plants. Ruminants are most susceptible to plant induced cyanide poisoning.

Hydrogen cyanide is rapidly absorbed from the respiratory and digestive tracts and acts primarily by blocking mitochondrial cytochrome oxidase, the critical enzyme essential for oxygen ion transport for cellular energy needs [2,7]. Because the brain has the highest energy needs, HCN rapidly affects brain function, causing anoxia and death.

Risk Assessment

Plant induced cyanide poisoning in dogs and cats is rarely encountered. None the less, it is a wise precaution to avoid exposing household pets unnecessarily to those plants that are known to have high cyanogenic glycoside potential such as choke cherries, service berries, almonds, and apricots. Such plants should not be planted in dog runs where the fruits may fall and be eaten by the dogs.

Other garden plants of the family Rosaceae with cyanogenic glycoside potential include cotoneaster (Cotoneaster spp.), Christmas berry (Heteromeles arbutifolia), crab apples (Malus spp.), Photinia, Japanese photinia (Photinia spp.), firethorn, pyracantha (Pyracantha coccinea), and Spirea (Spirea spp.) [1].

Clinical Signs

Due to the peracute effects of HCN on the oxygen transport system in animals, it is not unusual for the animal to be found in acute respiratory distress or dead within about 30 minutes of ingesting a toxic dose of the plant. Initially mucous membranes are bright red in color due to oxygen saturation of hemoglobin. As the animal becomes severely hypoxic the mucous membranes may appear cyanotic before coma and death occur.

Animals suspected of cyanide poisoning require immediate treatment with as little stress placed on the animal as possible. Intravenous administration of sodium nitrite and sodium thiosulfate is the treatment of choice [8,9]. The nitrite has a great affinity for hemoglobin and forms cyanmethemoglobin thereby removing the cyanide from the cytochrome oxidase [7,9]. Sodium thiosulfate then binds with the cyanide ion to produce thiocyanate that can be excreted by the kidneys. A 20% solution of sodium nitrite should be administered slowly intravenous at a dose of 16mg/kg body weight, followed by a 20% solution of sodium thiosulfate at a dose of 1.65ml/kg body weight [10]. A solution of sodium thiosulfate given via stomach tube may help to reduce further absorption of HCN from the stomach but it has no effect on HCN already absorbed. Hydroxocobalamin, and alpha-ketoglutaric acid hav been shown to be an effective adjunct to treating cyanide poisoning in dogs [11,12].