Plant Toxicities

Wild Cherry (Prunussp.) - Wild cherry toxicosis can affect all animals, but ruminants are at the greatest risk. All parts of the plant are potentially toxic, however, damaged leaves of the plant are the most toxic.    Clinical signs include anxiety, breathing  difficulties,  staggering,  con­vulsions, collapse, and death. Signs usually develop rapidly.   Wild Cherry contains cyanogenic precursors that release cyanide when leaves are damaged (maceration, frost, drought, wilting). As little as 2 ounces of ingested, damaged leaves can kill an animal. Blood from animals with cyanide toxicosis is often cherry-red because hemoglobin cannot release oxygen to tissue. Cell death occurs because cyanide binds to the ferric (+3) form of cytochromeoxidase, thus halting cellular respiration.   Diagnosis is made by evidence of ingestion of the plant with appropriate clinical signs. Diagnosis is supported by analytical evidence of cyanide in forage and samples from affected animals.   Samples for cyanide analysis should be frozen immediately and held frozen until analyzed. Death is frequently so rapid that treatment is not possible. However, if it is possible, treatment consists of sodium nitrite at 10-20 mg/kg with 500 mg/kg sodium thiosulfate as needed. The treatment is directed at breaking the cytochrome-cyanide bond with the nitrite forming cyanomethemoglobin.   The thio­sulfate then reacts with the cyanide via the enzyme rhodanase forming thiocyanate which is readily excreted in the urine. Other plants that can under the right conditions contain toxic concentrations of cyanide include sorghum/sudan grass and Johnson-grass.

Japanese Yew (Taxussp.)-Japanese Yew is extremely toxic to all animals. This plant has great potential for toxicity because it is so widely used as an ornamental shrub and clippings are often given to livestock. Clinical signs include breathing problems, trembling, weakness, heart problems, stomach upset and fre­quently, sudden death with no other signs. One mouthful of Japanese Yew can kill a horse or cow within minutes. The toxin in Japanese yew is an alkaloid known as taxine which slows down cardiac conduction. Death is due to cardiac and/or respiratory collapse. As little as 0.1 to 0.5% of fresh plant per body weight is lethal. Japanese Yew is toxic, even when it is dry. Diagnosis of toxicity is made at necropsy by observing leaves in the stomach, or by the detection of taxine in rumen/stomach contents.

White   Snakeroot   (Eupatorium rugosum) — White snakeroot also has a high toxicity rating. Mostly grazing animals are at risk. The leaves and stems of the plant are toxic when fresh or dried. Clinical signs include trembling, sweating, depression, stiff gait, heart failure, jaundice, and death. Onset of signs occurs within 2 days to 3 weeks. The toxin in White Snakeroot is believed to be tremetone. Animals start to show signs when 0.5 to 2% of their body weight has been consumed. All livestock are affected, however, the toxin is excreted in the milk; so lactating animals are slower to show signs of toxicosis. Nursing animals are affected by the toxin. This plant toxicity occurs most commonly in late summer and fall on overgrazed pastures.  No specific antidote exists. Diagnosis is made on the history and evidence of grazing on the plant in the pasture. Further diagnosis can be supported by elevated muscle enzymes, skeletal and myocardial degeneration and necrosis, and the presence pf White Snakeroot in the stomach/rumen contents.

Nitrate Toxicity — Nitrates can accumulate in a variety of weeds (pigweed, lambsquarter, dock, nightshade) and several crops (corn, oats, barley, beet tops, wheat). Toxicosis occurs most commonly when cattle graze on cornstalks in the fall after a summer drought because nitrates accumulate in the stalks.    Ruminants are most susceptible to this toxicosis.   Nitrate is converted to nitrite by rumen microbes, and nitrites are 10 times more toxic than nitrate. Nitrate oxidizes the ferrous form of hemoglobin to the ferric form which is called methemoglobin.Methemoglobin has a much lower affinity for oxygen than normal hemoglobin which leads to tissue hypoxia and anoxia. Clinical signs include dyspnea,, sudden death, abortion storms, and methemoglobinemia. Animals may show a muddy red or brown "chocolate" color in the blood, mucous membranes, and tissues. Diagnosis is made from the history, chocolate-colored blood and tissues, and nitrate/nitrite in ocular fluid. Nitrate/nitrite levels can also be measured in rumen contents, but the measurement is not as accurate as fluid from the aqueous humor. Treatment consists of methylene blue at a dosage of 4-15 mg/kg of body weight in a 1% solution. The dosage may need to be repeated. Methylene blue metabolizes to leucomethylene blue which reduces the ferric form of hemoglobin to the ferrous form of hemoglobin so that oxygen transport will increase to normal. To prevent this toxicity, a representative sample of suspect forage should be collected and sent to the ADDL for nitrate analysis. At necropsy, frozen ocular fluid or a frozen eyeball should be submitted.

Blue-green algae (Microcystissp., Anabaena sp.) — Blue-green algae toxicosis affects all species of animals and can kill within 3 to 5 minutes or up to several days depending on the toxin which is produced. Small, stagnant farm ponds in mid to late summer pose the biggest risk. Animals are most commonly affected after a windstorm which blows the algae into their drinking area.   Anabaena blooms can contain a neurotoxin called anatoxin-a. Clinical signs include salivation, lacrimation, urination, and defecation.     Death results from respiratory paralysis. Diagnosis is made on the history, blood cholinesterase levels for anatoxin-a, identification of algae (fix in formalin), and presence of blue-green algae in GI tract. Treatment consists of evacuat­ing the GI tract and administering activated charcoal. Microcystis sp.producehepato-toxins.Signs incluudehepatocyte necrosis with massive intrahepatic hemorrhage, shock and death within hours. Secondary photosensitization can also occur due to the liver damage. Diagnosis is made on history of exposure, elevated liver enzymes, and presence of algae in the GI tract. Note:

Suspect   water   must   be   collected immediately since the "bloom" may not last.

- by Susan Powers, Class of 1998

- edited by Stephen Hooser,DVM,PhD