Toxic Flashcards
What is the name of the endophyte that infects fescue grass and that causes “summer slumps”?
Tall fescue is infected with Neotyphodium coenophialum endophyte
What toxin does the endophyte Neotyphodium coenophialum contains and what does it causes in cattle?
It contains vasoactive ergopeptine alkaloids that cause vasoconstriction and reduced blood flow to the skin of ruminants. It also induces bronchoconstriction and pulmonary vasoconstriction, (compromising their ability to lose heat, especially during hot seasons).
What infests perennial ryegrass in western US that can also cause hyperthermia in ruminants?
Claviceps purpurea
How do chlorophenols and nitrophenols cause hyperthermia?
Chlorophenols and nitrophenols are used as herbicides and wood preservatives. They cause uncoupling of oxidative phosphorylation within mitochondria and lead to rapid extreme rises in body temperature.
Mention what is the toxin contained in Larkspur (Delphinium spp.), what is the mechanism of action of this toxin, the species affected and most common clinical signs.
Contains toxic diterpenoid alkaloids. Tall larkspur (Delphinium barbeyi) is considered the most problematic. The alkaloids cause a curare-like blockade of neuromuscular junctions, by reversibly binding to nicotinic acetylcholine receptors. Death may result in as little as 3 hours after consumption. Affects horses, cattle and ovine (less sensitive). Clinical signs include excitability, muscle tremors, stiffness, staggering, and a basewide stance. Cattle may assume a kneeling position before collapsing and develop boat, regurgitation (ruminants), and constipation.
What are the species susceptible and the most common clinical signs of cyanogenic plant toxicity?
Cyanide blocks molecular oxygen transfer in cytochrome oxidase systems in mitochondria, causing anoxia. Species affected are ovine, caprine, equine, bovine and porcine. Clinical signs include respiratory distress, rapid breathing, bloat, salivation, muscle twitching, staggering, mydriasis, cardiac arrhythmias, and convulsions. Ruminants are more susceptible because rumen microorganisms release cyanide from the cyanogenic glycosides. Chronic toxicity may lead to neurologic damage to the brain and spinal cord resulting in weakness, ataxia, and urinary incontinence. It has been associated with sorghum consumption in pregnant horses and cattle. Foals and calves are born with arthrogryposis. In low doses can be goitrogenic.
Mention some examples of plants containing cyanide toxins.
Acacia, African star grass, apple, arrow grass, Bahia grass, bamboo, Bermuda grass, birdsfoot trefoil, bracken fern, cassava, chokecherry, Christmas berry vetch, corn, elderberry, eucalyptus, ax, owering quince, hydrangea, Indian grass, Johnson grass, lima bean, mountain mahogany, poison suckleya, reed canary grass, service berry, sorghum, South African daisy, star grass, Sudan grass, tall manna grass, Texas queen’s delight, and white clover. Seeds of apples and crabapples (Malus spp.). Seeds, and leaves of the Prunus spp. (bitter almond, cherry, chokecherry, apricot, peach, nectarine, plum, mock orange)
What is the tx for acute cyanide intoxication?
IV or intraperitoneal injection of 20 mL of a 10% solution of sodium thiosulfate mixed with 10 mL of a 10% solution of sodium nitrite (not approved for food animals). Alternative treatment for ruminants - thiosulfate alone using a 30% to 40% solution IV at a dose of 25 to 50 g/100 kg of body weight. Administration of a gallon of vinegar diluted in 3 to 5 gallons of water by stomach tube to help acidify the rumen.
What predisposes some plants to accumulate nitrates?
Drought, frost, hail, and herbicide application
Mention some if the clinical signs of nitrate intoxication in ruminants
Nitrates are converted into nitrites and ammonium in the forestomachs, triggering oxidation of the ferrous iron in hemoglobin, producing methemoglobin. Vasodilation and hypotension may result, leading to hypoxia, dyspnea, exercise intolerance, death, fetal stress and abortion, stillbirths, and/or weak neonates. In bulls, sperm abnormalities and degenerative changes within the testes have been reported. If the animals are anemic or hypoxic for any other reason, methemoglobinemia will have even greater consequence.
What toxic plants in western US can cause many different toxic syndromes? From sudden death (methemoglobinemia and nitro compounds) and neurologic signs, to respiratory syndrome with emphysema, and selenium toxicosis.
Locoweed and milkvetch (Astragalus spp. and Oxytropis spp.)
What is the toxin that causes the neurological signs with locoweed or milkvetch ingestion? How is it diagnosed?
Swainsonine It can be diagnosed by measuring swainsonine or α-mannosidase in serum. Swainsonine creates a lysosomal storage disease in which α-mannosidase is inhibited (this results in swelling of axonal hillocks, growth of new dendrites and synapses in severe locoweed cases)
What is the toxin identified in box elder seeds?
Hypoglycin A, a branched chain amino acid metabolized to methylene cyclopropyl acetic acid (MCPA), a potent inhibitor of multiple acyl-CoA dehydrogenases (MADD).
What are the clinical signs in atypical myopathy?
Muscle weakness, recumbency, and myoglobinuria. Other signs include dysphagia, esophageal obstruction, or colic-like signs. Myocardial damage may be detected with electrocardiography (ventricular premature depolarizations, prolonged QT intervals); echocardiography (abnormal ventricular wall motion); and elevated serum troponin concentrations.
Ingestion of what plant causes atypical myopathy or summer pasture-associated myositis?
Box elder (Acer negundo) Some outbreaks have been observed after ingestion of maple leaves (Acer pseudoplantanus) covered with European tar spot (Rhytisma acerinum)
What species are more commonly affected by cardiac glycosides? Mention some examples of plants that contain them.
Cattle is more commonly affected. Plants containing them include: In pasture milkweed (Asclepias spp.), dogbane or Indian hemp (Apocynum cannabinum), and blue-eyed grasses (Sisyrinchium spp.) More likely to be found in gardens than pastures foxglove (Digitalis spp.), hellebores (Helleborus spp.), hyacinth (Hyacinthium spp.), kalanchoe (Bryophyllum spp.), lily of the valley (Convallaria majalis), oleander (Nerium spp.), periwinkle (Vinca major), pheasant’s eye (Adonis microcarpa), spindle tree (Euonymus spp.), squill (Drimia or Urginea spp.), and star of Bethlehem (Ornithogalum spp.)
Mention the 4 of the most important plants causing damage of the myocardium and high mortality in large animals.
Yew (Taxus spp.), avocado (Persea americana), death camas (Zigodenus spp.), and summer pheasant eye (Adonis spp.)
What does Cassia occidentalis cause in horses when ingested with ground corn?
Also called coffeeweed, Cassia spp., in particular the seeds, are very toxic to multiple species. It contains N-methylmorpholin and anthraquinone glycoside, it’s found in eastern and southern U.S.Clinical signs include diarrhea, anorexia, staggering gait, myoglobinuria, renal failure and liver failure. Sixty percent of a herd of broodmares died with signs of hepatic encephalopathy, histologic lesions included pericentrolobular necrosis.
What is and what causes crooked calf disease?
It is a syndrome that includes skeletal deformities such as arthryogryposis, kyphosis, scoliosis, torticollis, and cleft palate that can result of lupine ingestion during early to midgestation in ruminants.
What are the clinical signs associated y what is the active toxin associated with Perilla mint (Perilla frutescens) ingestion?
It causes significant morbidity and mortality in ruminants. Perilla contains ketones and related furan compounds that are bioactivated in the lung and cause atypical interstitial pneumonia and acute respiratory distress.
Wha clinical signs are associated with ruminant consumption of sweet potato? What particularity does it need to cause the clinical signs?
Sweet potatoes (Ipomoea batatas) need to be damaged by Fusarium spp. molds to cause the clinical signs. It causes atypical interstitial pneumonia and acute respiratory distress.
What are the clinical signs of oxalate toxicity?
Signs of muscle tetany or flaccid paralysis may be observed (secondary to hypocalcemia and hypomagnesemia). Other reported signs include anorexia, ruminal stasis, mouth froth, weakness, stiffness, tachypnea, ataxia with jerky extensor rigidity, coma, and death. Necropsy - severe rumenitis, pale kidneys, edematous, and enlarged. Calcium oxalate crystals in the rumen wall and kidneys.
