Ch 54 Toxins Flashcards
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Larkspur alkaloids?
*Palatable, in mtn meadows. Produce norditerrpenoid alkaloids. They block nic ACh rec.
See skel muscle paralysis, excitable, bloat, stiff, weak, colic, collapse, aspiration. C, O, E affected. Cattle most.
Treat with Neostigmine. Pre-graze with sheep, give lithium chloride to make cattle averse.
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for cyanogenic plants?
Many plants. Blocks molecular oxygen transfer in cytochrome oxidase mitochondrial systems.
Cx: cherry red blood, resp distress, rapid breathing, bloat, salivation, cardiac arrhythmia, convulse. All species, but especially ruminants. Chronic tox causes arthrogryposis in offspring, neuro damage. Low doses are goitrogenic.
Dx cherry blood, CN in forage and liver or blood. Patchy encephalomalacia, bladder necrosis
Tx. Sodium nitrite to form methHb, sodium thiosulfate.
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for nitrate-accumulating plants?
-Accumulates with impaired photosynthesis or other plant stress (corn, oat, Sorghum, Beet, solanum). Nitrate converts Hb to methHb (Fe3+). Cross placentas, convert to ammonium in rumen.
-Methemoglobinemia, vasodilaton, polypnea, dyspnea, weak, tremor, convulse, abort in 5 d. Chocolatey mm’s and blood. Congenital hypothyroidism.
-Dx. 44 ppm in ocular fluid or serum.
-Don’t allow grazing post-drought. Reduce fertilizers. Methylene blue (180 day withdrawal period) , enteral oil or vinegar to reduce absorption
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for locoweed?
-Swainsonine inhibits cellular alpha-mannosidases
-See emaciation, lethargy, ataxia, hyperesthesia, abortion, high mountain disease. All affected.
-Dx by hx, cx, histopath, neurovisceral vacuolation. Remove access
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for milkvetch?
-3 nitropropanolol and 3-nitropropanoic acid become toxic in the rumen, NPA inhibits succinate dehydrogenase and forms methemoglobin.
-Acute signs: ataxia, distress, dyspnea, cyanosis, weakness, death.
-Chronic signs: resp distress, weakness, knuckling, knocking hinds together
-Cattle sheep are worst
-Dx. Histology, finds pulmonary edema and fibrosis, cerebral hemorrhage, wallerian degeneration of the spinal cord and sciatic, glial edema.
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for white snakeroot, rayless goldenrod, and burrow weed?
-Tremetol
-White snakeroot is passed in milk, adult cows ok
-musculoskeletal signs, Arrhythmias, CHF
-Rayless goldenrod causes myonecrosis and cardiomyopathy
-Mycotoxins may be involved
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Acer spp tree (summer pasture associated myositis and equine atypical myopathy)?
-Box elder, sycamore, maple, tar spot
-Acute, nonexertional, severe - fatal rhabdo.
-Hypoglycin A: metabolized to methylene cyclopropyl acetic acid (MCPA) that inhibits acyl-CoA dehydrogenases
-Lipid metabolism impairment = accumulation, cell death
-Muscle weakness, recumbency, myoglobinuria, dysphagia, choke, colic
-Myocardial damage: VPCs, prolonged QT interval
-Serum troponin elevates
-Myofibril degeneration and lipid accumulation
-Supportive, remove access
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for cardiac glycosides?
-digitalis, oleander, toads, milkweed, hellebore produce many toxins
-Block Na/K ATPase
-Grayanotoxins block fast Na inactivation
-Sudden death, colic, anorexia, tremors, hypertension, QRS widening, ST segment depression, enlarged P waves
-Witness hemorrhagic gastroenteritis and test ingesta
-Treat with activated charcoal, atropine, prevent exposure.
What are the toxic principles, clinical signs, species affected for avocado?
-Myocardial toxin
-horse: edematous head/neck swelling, resp distress, CHF. Noninfectious mastitis
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Allium, brassica, and Acer spp?
-Methhemoglobinemia, hemolysis, thrombocytopenia via oxidative damage to erythrocytes and acute heinz body anemia or methHb-emia.
-Weak, tachycardia, hemoglobinuria, laminitis, colic, abortion
-activated charcoal? prevent exposure
Which toxicities are treatable with Physostigmine?
Solanine alkaloids (nightshade, horse nettle)
Which toxicities are treatable with Thiamine?
Kochia, horsetail, bracken fern
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for pyrrolizidine alkaloids?
-Senecio, amsinckia, heliotrope, rattlebox, tarweed
-Converted to pyrroles and trans-4-hydroxy-2-hexanal; X-link DNA = decr mitosis and incr necrosis
-Liver failure, biliary hyperplasia, megalocytosis, peri-portal bridging fibrosis
-Dx by history, clinpath, liver biopsy
-Horses and cattle more sensitive than sm rum’s
-Remove access, will accumulate effects
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Ponderosa pine, junipers, cypress, and lodgepole pine?
-Isocupressic acid. Rapidly metabolized to agathic acid in the rumen (accelerated when cattle are conditioned to the pines, reducing toxicity)
-Uterine vasoconstriction: abortion, retained FM, edema of vulva and udder, dystocia, weak calves, poor lactation.
-Get cattle used to the pines for a few months before breeding
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for phytoestrogens?
-Stressed legumes, clovers, soybeans
-Interacts with endogenous estrogen receptors to cause hyperestrogenism
-preputial swelling, early maturity, nymphomania, testicular atrophy, reduced fertility
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for ergot alkaloids?
For Fescue specifically?
-Fescue esp. ergovaline is vasoconstrictive (alpha 2) and/or depresses prolactin secretion. Reduced steroidgenesis
-extremities gangrene fat necrosis, reduced milk production, nervous, tachypnea.
Fescue: failure of udder development, placental abnorm, dystocia, agalactia, subfertility. Mares. Dysmature foals.
Diagnosis based on clinical signs, hx, forage testing. Advsere effects when > 100-200 ppb in feed
Tx: remove from pasture, mow, Domperidone in preg mares 10-14 d prior to foaling. Reserpine to lactate.
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for perilla mint or moldy sweet potatoes?
Perilla mint ktones and furans (swt potatoes if damaged by fusarium) are bioactivated in the lungs to cause ARDs and atypical interstitial pneumonia.
High tryptophan is similar, need to slowly adjust to new grasses to prevent overproduction of 3-methylindole in rumen, feed monensin??
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for selenium toxicosis?
3 main syndromes: acute toxicosis, blind staggers, chronic alkali disease.
Oronasal vesicles , hair breakage (horse)
Cattle: unsteady gait, diarrhea, abdominal pain, tachypnea.
Sheep: depression, sudden death
Chronic = rough coat, lameness, dull, cardiac atrophy, hepatic cirrhosis, longbone erosion .
Test liver, hair. Serum tells current bodily Se pool, whole blood tells longterm intake
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for hoary alyssum or black walnut?
LAMINITIS.
Limb edema, fever, intravascular hemolysis, endotoxemia, shock, D+, abortion, death. Don’t have to ingest walnut to cause laminitis.
Oxidative stress
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Oxalates?
-lots of plants
-Raphides = insoluble oxalate crystals
-Bind Ca in GIT, precipitate Ca from the blood to cause hypoCa, damage GI microvasculature, precipitate out into and damage renal tubules and cause ARF, cell death due to inhibited citric acid cycle.
-See signs in 24 hours, sheep most. HypoCa, HypoMg, anorexia, weak, stiff, rumen stasis, extensor rigidity, coma, death.
Horses get nutritional hyperparathyroidism and osteodystrophia fibrosa. Symptomatic tx and slow introduction of sheep to Halogeton weed.
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for cyanobacteria/cyanooxins?
-Hepatic microcystis, nodularia, anabena, etc
-Cyclic peptide hepatotoxins; inhibit protein phosphatase and induce apoptosis; depolarize nicotinic receptors.
-shock, liver failure, hypersalivation, dyspnea, cyanosis, death,
-Increased hepatocellular enzymes and bilirubin
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for hepatotoxic microcystins?
They die in a few hours after exposure. elevated liver enzymes. FInd algae in GIT
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for aflatoxins?
B1 carcinogens, B2 G1 and G2 in grains bind essential enzymes, block RNA polymerase and ribosomal translocation.
Peracute: hemorrhage, bloody D+, death.
Abortion, weak, tremor
Chronic: ill thrift, rough hair coat, liver dmg
Young swine most at risk.
Test feed and liver. Clay prevents absorption?
What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Tricothecenes?
Inhibits protein synthesis.
Gastroenteritis, skin necrosis, immune impairment, feed refusal, coagulopathy, die.
Horses and swine most likely.
Test feed. Charcoal?
