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CHOKECHERRY - Prunus species

CHOKECHERRY PLANT

CHOKECHERRY PLANT

CHOKECHERRY PLANT

CHOKECHERRY PLANT

(106K) (115K) (110K) (85K)

CHOKECHERRY PLANT

CHOKECHERRY PLANT

CHOKECHERRY PLANT

CHOKECHERRY PLANT

(104K) (67K) (146K) (115K)

Prunus serotine

Prunus serotine

(59K)

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Distinguishing Features

Shrubs or trees with smooth bark marked by lines (lenticels running around the stem; leaves glossy, simple, alternate, lanceolate, usually with a few glands (raised spots) on the petiole (leaf stalk) or on the base of the blade; flowers in clusters, showy and fragrant, appearing in spring; fruit fleshy, usually blue to black (except in peach and apricot) enclosing a pit or stone. 

Toxic principle: cyanogenic glycosides or cyanogens (amygdalin, prunasin, dhurrin, linamarin)

 Hydrogen cyanide (HCN) is formed when the glycosides are hydrolyzed by enzymes in plants or by rumen microorganisms:

β - glucosidase

 

Cyanogenic glycosides   ®  sugar + aglycone

Aglycone   ®   HCN + aldehyde or ketone

 

Hydroxynitrile lyase

The glycosides occur in vacuoles in plant tissue while the enzymes are found in the cytosol.  Damage to the plant from wilting, trampling, mastication, frost, drought, bruising etc. results in the enzymes and glycosides coming together causing hydrogen cyanide to be formed.  b-glycosideases are also produced by rumen microorganisms.  The optimal pH for enzyme activity is near neutrality, so release of HCN is more rapid in the rumen than in the highly acid stomach of monogastrics.  For this reason, ruminants are more sensitive to cyanogens than nonruminants.

Toxicity: Cyanide is lethal at dosages of 0.5 to 3 mg/kg b.w.  Ingestion of 100 g of wild cherry leaves with ~ 200 mg CN per 100 grams would be lethal to a 100 lb. animal.
MOTA: Once free cyanide is released from the plant tissue and is absorbed it reacts with ferric iron (+3) in cytochrome oxidase which halts cellular respiration.  Oxyhemoglobin cannot release oxygen for electron transport in the cytochrome system since the cyanide – cytochrome oxidase will not function in electron transport.
Diagnosis

  Clinical signs: 

ü      Animals are commonly found dead due to rapidity of cyanide’s effects

ü      When observed, signs may include excitement, general muscle tremors, dyspnea, salivation, defecation, urination followed by clonic convulsions and death.

  Laboratory diagnosis:  Measurement of cyanide in GI contents.

Lesions:  bright red color to blood and mucous membranes, detection of plant material in GI tract.

Treatment:

General: remove from source

Specific:  sodium nitrite at 10 to 20 mg/kg with 500 mg/kg sodium thiosulfate as needed.  The treatment is directed at breaking the cyanide – cytochrome bond with the nitrite forming methemoglobin.  Methemoglobin has a greater affinity for cyanide than does cytochrome oxidase, so it strips cyanide from the enzyme.  The thiosulfate then reacts with the cyanide via the enzyme rhodanase forming thiocyanate which is readily excreted in the urine.

Prevention:  Test forage prior to feeding.  Cyanide is volatile, so opening bales of  hay 24 hours before feeding allows the cyanide to dissipate.
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Copyright © 2002

University of Pennsylvania
Created by:    Alexander Chan (2003), Daphne Downs (2002), Chris Tsai (2001), Brett Begley (2000), Janet Triplett (1997)
Faculty Advisor:  Dr. Robert Poppenga