Ch 54 Toxins

Question 1

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Larkspur alkaloids?

Answer 1

*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.

Question 2

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for cyanogenic plants?

Answer 2

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.

Question 3

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for nitrate-accumulating plants?

Answer 3

-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

Question 4

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for locoweed?

Answer 4

-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

Question 5

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for milkvetch?

Answer 5

-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.

Question 6

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for white snakeroot, rayless goldenrod, and burrow weed?

Answer 6

-Tremetol
-White snakeroot is passed in milk, adult cows ok
-musculoskeletal signs, Arrhythmias, CHF
-Rayless goldenrod causes myonecrosis and cardiomyopathy
-Mycotoxins may be involved

Question 7

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)?

Answer 7

-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

Question 8

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for cardiac glycosides?

Answer 8

-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.

Question 9

What are the toxic principles, clinical signs, species affected for avocado?

Answer 9

-Myocardial toxin
-horse: edematous head/neck swelling, resp distress, CHF. Noninfectious mastitis

Question 10

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Allium, brassica, and Acer spp?

Answer 10

-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

Question 11

Which toxicities are treatable with Physostigmine?

Answer 11

Solanine alkaloids (nightshade, horse nettle)

Question 12

Which toxicities are treatable with Thiamine?

Answer 12

Kochia, horsetail, bracken fern

Question 13

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for pyrrolizidine alkaloids?

Answer 13

-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

Question 14

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Ponderosa pine, junipers, cypress, and lodgepole pine?

Answer 14

-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

Question 15

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for phytoestrogens?

Answer 15

-Stressed legumes, clovers, soybeans
-Interacts with endogenous estrogen receptors to cause hyperestrogenism
-preputial swelling, early maturity, nymphomania, testicular atrophy, reduced fertility

Question 16

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for ergot alkaloids?
For Fescue specifically?

Answer 16

-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.

Question 17

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for perilla mint or moldy sweet potatoes?

Answer 17

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??

Question 18

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for selenium toxicosis?

Answer 18

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

Question 19

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for hoary alyssum or black walnut?

Answer 19

LAMINITIS.
Limb edema, fever, intravascular hemolysis, endotoxemia, shock, D+, abortion, death. Don’t have to ingest walnut to cause laminitis.
Oxidative stress

Question 20

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Oxalates?

Answer 20

-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.

Question 21

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for cyanobacteria/cyanooxins?

Answer 21

-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

Question 22

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for hepatotoxic microcystins?

Answer 22

They die in a few hours after exposure. elevated liver enzymes. FInd algae in GIT

Question 23

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for aflatoxins?

Answer 23

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?

Question 24

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for Tricothecenes?

Answer 24

Inhibits protein synthesis.
Gastroenteritis, skin necrosis, immune impairment, feed refusal, coagulopathy, die.
Horses and swine most likely.
Test feed. Charcoal?

Question 25

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for fusarium?

Answer 25

Fumonisin B1; inhibit sphingolipid biosynth, block protein synth, apoptosis or stress.
See signs 7-90 days later. High mortality but low morbidity! Neuro, cortical blindness, convulse

centrolobular necrosis, liquefactive necrosis of white matter.

Question 26

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for zearalenone?

Answer 26

In cereal grains.
Hyperestrogenism: repro tract change, pseudopregnancy, embryo death, subfertile
Young gilts most at risk

Question 27

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for deoxynivalenol?

Answer 27

Vomitoxin inhibits protein synthesis, GI irritation, vomiting, anorexia, wt loss, immune system suppression. Worst in swine

Question 28

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for blister beetles?

Answer 28

Cantharidin interferes with phosphoprotein phosphatases.
See GI, renal dz, arrhythmias, stiff gait, “thumps”, hypovolemic shock, death.
Supportive care, GI protectants. Test urine and GI contents.

Question 29

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for arsenic?

Answer 29

Myelodegeneration, GI irritation.
Peripheral nerve damage in monogastrics. Also peracute CV collapse and death. May cause hemorrhagic diarrhea, dehydration, weakness, agalactia.
Treatment: Dimercaprol, lipolic acid, Sodium thiosulfate

Dx: histology, elevated arsenic in liver, kidney, GI, hair (chrc). Abomasitis, pulmonary edema, liver/kidney necrosis

Question 30

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for copper?

Answer 30

-If Cu incr relative to Mb or sulfate, or less Zinc. Can store in liver and sudden damage/stress causes release.
Chronic: bind ceruplasmin and accumulate in liver. Kupffer cell necrosis and release to blood.
Hemolysis, anemia, icterus, MethHb-emia, depression, anorexia.
Esp sheep. Test serum, liver, kidney.
Tx: Ammonium tetrathiobenate, sodium thiosulfate, d-penicillamine

Question 31

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for fluoride toxicity?

Answer 31

-Interferes with mineralization of bones and teeth.
-Wt loss, lame, enamel discolored.
-Worst with volcanic soil. .
See bone cortex thickening, coarse colagenous fibers, more osteoid. no tx

Question 32

What are the clinical signs, species affected, diagnostic of choice, and treatment (if any) for iodine tox?

Answer 32

Goiters in neonates, serous nasal discharge, scaly haircoat, cough, lacrimation. Test serum or milk

Question 33

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for iron toxicity?

Answer 33

See: depression, icterus, neuro (central), liver failure, bruxism, convulse.
Dx: pale tan liver, periportal biliary hyperplasia and necrosis and fibrosis.
Treat with deferoxamine.

Question 34

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for lead tox?

Answer 34

Horses have polyneuritis,
Ruminants have blindness, ataxia, bloat, depressed.
Test blood and tissues. no tx

Question 35

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for mercury tox?

Answer 35

Forms covalent bonds with sulfhydryl groups and forms mercaptides.
See GI ulcers, anorexia, nephrosis.
Test solid organs, blood, urine
Tx with Na thiosulfate, dimercaprol

Question 36

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for chlorinated hydrocarbons?

Answer 36

Inhibits GABA or interferes with sodium channels.
See hypersensitivity, fasciculations, ataxia, hypersalivation, diarrhea. Test brain, fat, liver, and milk.
Dietary restriction?

Question 37

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for ionophore toxicity?

Answer 37

Ex// monensin, lasalocid, alinomycin
-horses most sensitive: weakness, colic, increased RBC fragility, CV failure. ***myocardial damage
Cattle: anorexia, hindlimb ataxia, dyspnea, cardiac failure

Feed analysis. Give charcoal.

Question 38

What are the toxic principles, clinical signs, species affected, diagnostic of choice, and treatment (if any) for organophosphates and carbamates?

Answer 38

-AChE inhibitors, especially at cholinergic nerve synapses and NM junctions, but systemically too
-OP’s bind irreversibly but carbamates do not and can be eventually dislodged
-Also cause glutamate release, activation of N-methyl-d-aspartate and the gamma aminoutergic systems…basically they interfere and can cause seizures

Excreted in urne and feces

Signs: SLUD (salivation, lacrimation, urination, defecation), excessive synaptic NT activity. . Muscarinic signs appear first.

Measure levels in the blood of cholinesterase…< 50% indicates tox.
Treatment is ATROPINE, and reactivate AChE’s with Oximes (2-PAM), best within 24 hours exposure.

Contraindicated: many drugs.