Plants Associated with Cyanide Poisoning

Plants Associated with Cyanide Poisoning - Veterinarian's Handbook (Partial Repo.)       A.P. Knight & R.G. Walter College of Veterinary Medicine CO. State Univ.

Botanical Name Common Name Acacia spp. Catclaw, acacia Amelanchier alnifolia Service, June, or Saskatoon berry Bahia oppositifolia Bahia Mannihot esculentum Cassava, manihot, tapioca Cercocarpus montanum Mountain mahogany Chaenomales spp. Flowering quince Cynodon spp. Star grass Eucalyptus spp. Eucalyptus, gum tree Glyceria grandis Tall manna grass Hydrangea spp. Hydrangea Linum spp. Flax Lotus spp. Bird's foot trefoil Malus spp. Crab apple Nandina domestica Heavenly or sacred bamboo Phaseolus lunatus Lima bean Photinia spp. Christmas berry Prunus spp. Choke-cherry, pin cherry Pteridium aquilinum Bracken fern Sambuccus spp. Elderberry Sorghum spp. Johnson, Sudan grass Sorghastrum nutans Indian grass Stillingia texana Texas queen's delight Suckleya suckleyana Poison suckleya Trifolium repens White clover Triglochin maritima Arrow grass Vicia sativa Common vetch Zea mays Corn, maize Mechanism of Acute Cyanide Poisoning - Hydrogen cyanide (HCN) is highly poisonous to all animals because it rapidly inactivates cellular respiration thereby causing death [36-38]. The cyanide ion is readily absorbed from the intestinal and respiratory tracts and has a strong affinity for binding with trivalent iron of the cytochrome oxidase molecule, inhibiting its enzymatic action and preventing cellular respiration [37,39-41]. The characteristic cherry red venous blood seen in acute cyanide poisoning results from the failure of the oxygen-saturated hemoglobin to release its oxygen at the tissues because the enzyme cytochrome oxidase is inhibited by the cyanide. Normally, small quantities of cyanide are detoxified by cellular enzymes and thiosulfates in many tissues to form relatively harmless thiocyanate, which is excreted in the urine. When large quantities of cyanide are rapidly absorbed and the body's detoxification mechanisms are overwhelmed, cyanide poisoning occurs. In most species, the lethal dose of HCN is in the range of 2 to 2.5 mg/kg body weight [36-38]. However, if plenty of other plant material and carbohydrates are present in the stomach, formation and absorption of cyanide may be slowed, allowing animals to tolerate higher doses. Chronic Cyanide Poisoning - In addition to the acute toxic effects of cyanide poisoning, low levels of cyanide will over time cause a variety of chronic effects in humans and animals. Chronic cyanide poisoning is thought to be a form of lathyrism, a neurotoxicity recognized in people in some eastern Asian countries where the seeds of certain peas (Lathyrus spp.) are eaten when other foods are scarce. The neurotoxin in the uncooked peas results in damage to the spinal cord leading to paralysis. Similarly, a chronic neuropathy occurs in people who consume poorly cooked cassava (Manihot esculenta). The perennial sweet pea (Lathyrus latifolius) and the annual sweet pea (L. odoratus) seeds contain neurotoxins (lathyrogens) capable of producing osteolathyrism in animals, especially horses [42]. The primary lathyrogen in the annual sweet pea is b-amino proprionitrile, which causes defective cross-linking of collagen and elastin molecules [42]. This disease in horses is characterized by skeletal deformities and aortic rupture caused by defective synthesis of cartilage and connective tissue [42]. A similar syndrome of musculoskeletal deformities in foals and calves has been associated with pregnant mares and cows chronically eating Sudan grass (Sorghum sudanense) or sorghum hybrids containing low levels of cyanogenic glycosides [43-48]. In addition to limb deformities (arthrogryposis), calves also develop severe degeneration of the spinal cord and brain [44]. Affected animals develop posterior ataxia, urinary incontinence, and cystitis resulting from lower spinal cord degeneration [48]. The cystitis may become complicated by an ascending infection of the kidneys. The underlying problem is the loss of the myelin sheath surrounding peripheral nerves with resulting loss of nerve function. The demyelinization of the nerves is thought to result from the conversion of the cyanide glycoside to T-glutamyl beta-cyanoalanine, a known lathyrogen that interferes with neurotransmitter activity [46]. Neuronal degeneration in the brain associated with chronic cyanide poisoning may be associated with the depletion of hydroxycobalamin [45]. Animals may slowly recover if the source of the toxic aminonitrile is removed before neuronal degeneration becomes severe. Low doses of cyanide are also goitrogenic in humans and animals. Enlargement of the thyroid gland is caused by the formation of thiocyanate, which inhibits the intrathyroidal transfer of iodine and elevates the concentration of thyroid-stimulating hormone [8]. Pregnant ewes grazing star grass (Cynodon spp.) have developed goiter because of the presence of cyanide in the grass [29]. Clinical Signs of Acute Cyanide Poisoning Sudden death is often the presenting sign of acute cyanide poisoning. Affected animals rarely survive more than 1 to 2 hours after consuming lethal quantities of cyanogenic plants and usually die within a few minutes of developing clinical signs of poisoning [29]. If observed early, poisoned animals show rapid labored breathing, frothing at the mouth, dilated pupils, ataxia, muscle tremors, and convulsions. The heart rate is usually increased and cardiac arrhythmias may be present. Regurgitation of rumen contents occurs when ruminants become recumbent and bloating occurs. High blood ammonia levels coupled with increases in neutral and aromatic amino acids may be a significant cause for the loss of consciousness associated with terminal cyanide poisoning [49]. The mucous membranes are bright red in color because oxygen saturates the hemoglobin. Cyanosis of the mucous membranes occurs terminally when the animal’s tissues become depleted of oxygen. Postmortem Findings Animals poisoned by cyanide may have characteristic cherry red venous blood if examined immediately after death. Generalized congestion and cyanosis of the internal organs is often seen at necropsy. The blood clots slowly and the musculature is dark and congested. Hemorrhages occur commonly in the heart, lungs, and various other organs. The smell of bitter almonds reputedly characteristic of cyanide may occasionally be detected in the rumen gas when performing a fresh postmortem examination. Diagnosis Cyanide is rapidly lost from animal tissues unless specimens are collected within a few hours of death and frozen for chemical analysis. Liver, muscle, and rumen contents should be collected and frozen in air-tight containers before shipment to a laboratory capable of doing cyanide analysis. Levels of cyanide in liver or blood exceeding 1 ppm, or in muscle exceeding 0.63 g/mL are considered diagnostic for cyanide poisoning [29,50]. Cyanide poisoning can be confirmed by demonstrating toxic levels of HCN in the rumen contents or the suspect plants (or both) using the sodium picrate paper test [39]. Filter paper strips soaked in yellow sodium picrate and suspended over the suspect plant material in an air-tight jar turn brick red in a few minutes if significant cyanide is present. Commercial test kits are available for testing plants and rumen contents for cyanide. More precise determination of cyanogenic glycoside and cyanide levels is possible through the use of liquid chromatography and colorimetry [41]. Plant material containing more than 20 mg HCN/100 g (200 ppm = 200 mg/kg) is potentially toxic to all animals [36,50]. Liver or blood levels greater than 1 ppm are highly suggestive of cyanide poisoning [50]. Because many factors can alter cyanide determinations in tissues, the most consistent and diagnostically valuable HCN levels can be obtained from the brain and ventricular myocardium. Levels of HCN in excess of 100 g/100 g wet tissue are diagnostic of cyanide poisoning [51]. Treatment Many remedies for cyanide poisoning in man and animals have been evaluated over time. In all cases the successful treatment of acute cyanide poisoning depends on the rapid inactivation and removal of cyanide by metabolizing or complexing it with other compounds to allow its excretion via the kidneys [41,52]. In animals this has been traditionally accomplished by injecting sodium nitrite and sodium thiosulfate intravenously [53]. Sodium nitrite converts some hemoglobin to methemoglobin for which cyanide has a strong affinity, producing cyanmethemaglobin [41]. This complexing of cyanide reactivates the cytochrome oxidase system essential for cellular respiration. Sodium thiosulfate in the presence of the tissue enzyme rhodanese combines rapidly with the cyanide molecule cleaved from cyanmethemaglobin to form relatively nontoxic and excretable sodium thiocyanate [37,54]. A recommended treatment for cyanide poisoning is the intravenous administration of a mixture of 1 mL of 20 percent sodium nitrite and 3 mL of 20 percent sodium thiosulfate. This dose is given intravenously per 100 lb of body weight [53]. The dose may be repeated in a few minutes if the animal does not respond. Additional sodium nitrite should be given cautiously because excess will compound the toxicity by producing, in effect, nitrite poisoning. Better results have been obtained in sheep experimentally poisoned with cyanide by administering 660 mg/kg sodium thiosulfate and 22 mg/kg sodium nitrite intravenously [54]. Thiosulfate is the safest and most effective agent tested for treating cyanide poisoning in dogs. The effectiveness of these compounds given in combination is enhanced if oxygen is given simultaneously [55]. The oral administration of a 5 percent solution of cobaltous chloride at a dose of 10.6 mg/kg body weight further improved the effectiveness of the combination [54]. Alpha-ketoglutaric acid is an effective treatment if administered in conjunction with thiosulfate [56,567]. It is also beneficial to administer orally via stomach tube a solution of sodium thiosulfate (30 g to an adult cow) to detoxify free cyanide still present in the rumen. Animals suspected of consuming cyanogenic plants but that show no clinical signs should also receive oral sodium thiosulfate prophylactically. Administered via stomach tube, 1 gallon of vinegar diluted in 3 to 5 gallons of water will help acidify the rumen and reduce the production of hydrogen cyanide. Prevention of Cyanide Poisoning Appropriate pasture management to avoid exposing livestock to potentially toxic plants will help prevent animal losses. Animals should be prevented from grazing sorghums during early regrowth after the plants have been cut, droughted, or frosted, when they are likely to be most toxic [58]. Allowing sorghum forages to grow at least 2 feet high before allowing animals to graze them significantly reduces the potential for poisoning. Where uncertainty exists about the cyanogenic content of plant crops for animal forage, a sample of the plants should be tested for cyanide content. Properly curing hay and silage destroys the cyanogenic glycosides. Selecting forage sorghums and white clover varieties that have been specifically developed for low cyanogenic glycoside content further reduces the chances for poisoning and allows their safe use as forage crops [59-61]. The selective use of herbicides in localized areas can be used to control dense stands of cyanide-containing plants such as choke-cherry. Whenever herbicides are used as a control measure, it is important to follow manufacturer recommendations for the herbicide and observe local herbicide application ordinances.