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VET 401 Basic Foundations > VET 406 Toxic Plants > Flashcards

VET 406 Toxic Plants Flashcards

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1
Q

When are grazing animals more likely to eat toxic plants?

A

When stressed e.g. driven through pastures with poisonous plants, thirsty, hungry, handled

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2
Q

How to diagnose plant poisonings?

A

History, evidence of ingestion, identifying plant on farm visit, clinical signs, consistent gross and histologic findings, response to therapy, confirmation in the analytical toxicology lab
-diagnosis can be difficult bc signs can be non-specific or plant may be gone when signs manifest

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3
Q

Plants affecting the nervous system

A

poison hemlock, lupine, tobacco, yellow star thistle (1st 3 are neurotoxic and teratogenic), cyanide containing plants

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4
Q

Poison hemlock scientific name

A

Conium maculatum

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5
Q

Lupine scientific name

A

Lupinus spp.

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6
Q

Tobacco scientific name

A

nicotiana spp.

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7
Q

Yellow Star Thistle scientific name

A

Centaurea spp

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8
Q

Poison Hemlock Characteristics

A

4-6 ft tall, hollow stems with purple spots, root is like a carrot, leaves are coarsely toothed with a fernlike appearance, flowers in compound umbels small and white, strong odor (like mouse urine)

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9
Q

Tobacco characteristics

A

N. gluaca= tree tobacco: tubular/yellow flowers, shrub/small tree, bluish green alternate leaves, leaves/stems have white powder that rubs off easily,

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10
Q

Lupine Characteristics

A

many species, 3 feet tall, white or purplish flowers around main axis, fruit is multi-seeded pod, palmately compounded leaves

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11
Q

Neurotoxic/teratogenic toxic principle (poison hemlock, tree tobacco, lupine)

A

-Alkaloids act on autonomic nervous system by mimicking the action of acetylcholine

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12
Q

Neurotoxic/teratogenic symptoms (poison hemlock, tree tobacco, lupine)

A

-neurotoxic: shaking, twitching, staggering, paralysis, convulsion, heavy breathing, coma, death
-teratogenic: immobilization of fetus, cleft palate, scoliosis, other congenital defects

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13
Q

Poison hemlock toxin, toxicity, species affected

A

coniine (alkaloid)
-toxic in fresh plant, hay and seeds
-cattle and pigs mainly (and other grazing animals)

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14
Q

Nicotiana spp. toxin, toxicity and species affected

A

anabasine (alkaloid)
-toxic when dried or fresh
- cattle, sheep, goats, pigs

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15
Q

Lupinus spp. toxin, toxicity, and species affected

A

ammodendrine
-dried and fresh toxic, seeds are most toxic
-cattle (teratogenesis), sheep (acute poisoning)

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16
Q

What is the lab diagnosis for poison hemolock, nicotiana spp., and lupinus spp.?

A

alkaloids in urine or GI contents

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17
Q

When are teratogenic effects seen in gestating animals for poison hemlock, tree tobacco, lupine?

A

Varies based on species in what gestation period (ex pigs 30-60 are very susceptible to poison hemlock)

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18
Q

Poison Hemlock, Tree Tobacco, Lupine Treatment

A
  • no specific treatment
  • in acute poisoning: activated charcoal, cathartics, careful monitoring
  • if survive acute poisoning full recovery is possible
  • prevent by removing these plants from pastures
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19
Q

Heteromeles asbutifolia (Toyon, tollon, christmas holly, christmas berry) type of toxin

A

Cyanide

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20
Q

Cyanide containing plants

A

-sorghum species: sudan grass, etc
-prunus spp.: chocke cherries
- triglochin spp.: arrow grass
- malus spp.: crab apple leaves
- eucalyptus cladocalyx: sugar gum
- amelanchier alinifolia: service berry

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21
Q

Where are cyanogenic glycosides found (glycosides)?

A
  • leaves, fruit, seeds of mature fruit
  • newly developing leaves
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22
Q

Cyanogenic glycosides (cyanide) mechanisms

A

-hydrolysis of beta-glucosidase yields hydrogen cyanide
- this happens in the GI tract and can happen in plant when stress (frost, wilting, etc)
- free hydrogen cyanide is highly poisonous to all animals
- absorbed free cyanide binds to iron in cytochrome oxidase preventing normal enzymatic action and inactivates cellular respiration
- oxygen saturated hemoglobin can’t release oxygen so get cherry red blood

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23
Q

Cyanide clinical signs and diagnosis

A

-death within 1-2 hours after lethal dose
- labored breathing, frothing, ataxia, muscle tremors, convulsions
- bright red MM initially then turn blue terminally
-Diagnose: check color of blood, test blood/tissue for cyanide (protect sample from heat because cyanide can volatize)

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24
Q

Cyanide treatment

A

-Antidote available: sodium nitrate and sodium thiosulfate
- traps cyanide before can make methemoglobin

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25
Yellow Star Thistle (Centaurea solstitialis) and Russian Knapweed (Centaurea repens) toxicity
- both only affect horses and require large intakes over weeks to months -fresh and dried plants are toxic - toxins are not definitely determined (lactones) -destroys dopaminergic neurons resulting in "Equine nigropallidal encephalomalacia" (ENE)
26
Yellow Star Thistle (Centaurea solstitialis) and Russian Knapweed (Centaurea repens) clinical signs
- "chewing disease": continuous chewing, frothing, difficulty swallowing food -open mouth, frequent yawning -drinking dip whole head in bucket and then tip head back -ulceration of mouth - dies of starvation - diagnosed by MRI
27
Plants affecting the Cardiovascular System
-Nerium oleander: oleander (top toxicant of large animals in California) - rhododendron spp.: Azalea - persea americana: avocado - taxus spp.: Yews (similar to Oleander: Foxglove, summer pheasant's eye, cardiotoxic milkweed, Lilly of the valley)
28
Diagnosis of Oleander Poisoning
- identification of leaves in ingesta (often mistaken for eucalyptus) - test for oleandrin
29
Oleander Toxicity and Clinical Signs
-toxic in pretty much all animals -all parts dried and fresh are toxic -minimum lethal dose about 5 leaves - clinical signs happen with a few hours: diarrhea, depression, anorexia, excess salivation, bradycardia, tachycardia, arrhythmias, sudden death, kidney failure (necrosis in kidneys)
30
Oleander Treatment
-No specific treatment - active charcoal - maybe atropine or other meds for the arrhythmias (depends on type of arrhythmia) -avoid calcium and potassium containing fluids - guarded prognosis
31
Mechanisms of cardiac glycosides
- many different types but generally inhibits sodium- potassium pumps in the heart and skeletal muscle, and as sodium accumulates fail to pump out calcium and get mineralization in the heart - toads have similar mechanisms
32
Grayanotoxins (cardiovascular toxin) are found in
- the heath family (ex rhododendron, azalea, rosebay and many more) -highest concentrations in the leaves but also in flowers, nectar and stems
33
Grayanotoxins Toxicity and Clinical Signs, and Diagnosis
- animals and humans susceptible but most often in goats -clinical signs: vomiting, salivation, colic, depression, tachycardia, tachypnea, recumbency, elevated body temperature, seizures -test urine, serum, GI contents for grayanotoxins, or identify the plant
34
Grayanotoxins treament
-no antidote available -decontamination: activated charcoal, cathartics -supportive therapy with fluids -antibiotics in animals that may have aspirated -antiarrhythmics -prognosis: good with supportive care full recovery within 3-5 days
35
Taxus spp. (yew) toxin, toxicity, diagnosis, treatment
-cardiotoxic toxin: taxine alkaloids -toxicity: toxic green and dry, 6-8 oz -diagnosis: taxine alkaloids in GI contents -treatment: activated charcoal, and atropine
36
Avocado (Persea americana) clinical signs
-acute death/cardiac signs in birds, rabbits, goats -mastitis and agalactia in cattle, horses, goats, rabbits -colic, diarrhea, neck edema: horses
37
Avocado (persea americana) toxin, toxicity, diagnosis, treatment
-toxin: persin (unknown mechanism) - toxicity: all parts of plant is toxic - diagnosis: post mortem lesions -treatment: supportive
38
Plants affecting the digestive system
-diffenbachia sequine: Dumbcane -Hordeum jubatum: Foxtail barley -Setaria spp: Bristle grass -Arbus precatoriusL precatory bean -ricinus communis: castor bean -Robinia pseudoacacia: Black locust -Datura spp. Jimsonweed -plants with insoluble calcium oxalates
39
Dumbcane (diffenbachia sp.) toxin and clinical signs
-toxin: insoluble calcium oxalates (needle like projections contained in mesophils) -clinical signs: rapid within 2 hours of ingestion, hypersalivation, head shaking, chewing, pawing at mouth
40
Grasses that cause trauma, signs, and treatment
-exposure to sharp grass, barbed bristles, or prickly plant parts results in injury to oral mucosa, ear canal, or skin -livestock and horses: mainly oral exposure, excessive salivation, ulceration, granulation tissue in ulcer, anorexia - dogs: sneezing, limping and licking, head shaking/ear scratching, lacrimation -Treatment: remove plant, general care for infections
41
Setaria glauca common name
yellow foxtail
42
Hordeum jubatum
foxtail barley
43
Plants with lectins (toxalbumins, ex ricin)
-robinia pseudoacacia: black locust - abrus precatorius: rosary pea, precatory bean - ricinus communis: castor bean -mistletoe
44
Robinia pseudoacacia: black locust toxicity
-bark and seeds have the highest concentrations of lectins, but in leaves as well
45
Albus precatorius: Precatory bean plant and toxin
-established in Florida -fruit= legume pod - seeds: glossy red with jet black eye -toxin= abrin (highly toxic in small concentration)
46
ADF and NDF
-acid detergent fiber -neutral detergent fiber
47
Ricinus communis: castor beans plant and toxin
-toxin= ricin (a lectin) -seeds: shiny with gray and brown mottling -beans are very toxic in small doses -all parts of the plant are toxic but especially the seeds -the seeds must be broken or crushed to release toxin - castor oil does not have ricin
48
Toxic principles of lectin, mechanisms and signs
-proteins with higher affinity for sugar molecules, very toxic -mechanism: bind to certain cell receptor sites, inhibit cell protein cell synthesis, cell death over several days -clinical signs: GI irritation hours to days after exposure -colic -increased heart rate -hypovolemic shock -treatment: supportive and symptomatic, GI decontamination, activated charcoal, fluids
49
Ricinus communis: castor beans mechanism of action
-two glycoprotein chains (A and B) - B chain: binds to galactoside-containing proteins on cell surface facilitating internalization -A chain: enters ER and depurinates an rRNA so inhibits protein synthesis resulting in cell death
50
Ricinus communis: castor beans diagnosis, therapy, prevention
-leukocytosis, increased ALT, detection of alkaloids in gastric contents -no specific antidote, supportive care, poor prognosis if large dose -prevention: moist heat destroys ricin
51
Tropane alkaloid containing plants
-Datura spp: Angel's trumpet -brugmansia spp.: thorn apple -both contain tropane alkaloids (hyoscine, hyoscyamine) and have highest concentration in seeds and leaves -think "atropine"
52
Tropane alkaloid clinical signs
- anticholinergic toxidrome -increased respiratory rate, heart rate, dry mouth, incoordination, dialation of pupils, and decreased digestive tract motility -race horses test positive for atropine
53
Toxicants affecting skin and liver often result in
-increased susceptibility of skin to damage to UV radiation -requires photodynamic agent in the bloodstream and its excitement by UV light -in non pigmented skin: erythema, edema and pruritis -clinical signs: photophobia, hyperesthesia, exudation, ulceration, blindness
54
Type 1: Primary photosensitization
-from ingestion of plants with photodynamic agents ex. Hypericum perforatum: St. John's wort (the toxin in this is hypericin)
55
Type 3: Secondary photosensitization
-hepatogenous: associated with liver or bile injury -causes photosensitization on light parts of the body and mucosal surfaces -phylloerythrin is the photosensitizing compound, becomes toxic after break down of cholorphyll in GIT, usually removed by the liver but problem when get accumulation in the liver
56
Toxin resulting in photosensitization and plants with this, and species affected
-pyrrolizidine-alkaloid containing plants - senecio vulgaris: common groundsel - senecio jacobaea: Tansy ragwort -cattle and horses -sheep are more resistant
57
Pyrrolizidine-alkaloid toxicity and mechanism
-from liver action of PAs to toxic pyrroles resulting in hepatic disease -cattle and horses are more susceptible -can result in acute liver disease if eaten 5-10% bodyweight in a few days or weeks -most common: small amounts over several months to reach total dosage of 25-50% bodyweight resulting in chronic liver disease -animals are reluctant to eat these plants but may be in hay and pellets
58
Pyrrolizidine-alkaloid clinical signs
-acute: icterus, edema -chronic: firm nodular liver (cirrhosis), icterus, +/- photosensitivity -can have microscopic lesions too -CNS involvement: wandering, chewing, head pressing
59
Plants affecting the blood
-Acer rubrum: red maple -allium spp: onion
60
Acer rubrum: red maple plant appearance
-large tree -3-5 lobes with palmately arranged veins - the fruit is red in color and has 2 wings
61
Acer rubrum: red maple toxin and mechanism
-unidentified toxin in wilted and dried leaves - green leaves are apparently not toxic -all acer species should be considered toxic -animals affected: horses, ponies, zebras, alpacas -oxidant damage to RBC resulting in hemolytic anemia
62
Acer rubrum: red maple toxicity and clinical signs
-ingestion of 1.5 g/kg bw is lethal in ponies -clinical signs: appear several days after exposure, acute hemolytic anemia, red-brown urine, oliguria, anuria, weakness, tachypnea, depression, cyanosis, icterus -low PCV, heinz bodies, hyperbilirubinemia, hemoglobinuria, proteinuria -lesions: icterus, splenomegaly, severe diffuse congestion of kidneys
63
Acer rubrum: red maple treatment
-symptomatic and supportive -mainly fluids to maintain kidney function so hemoglobin won't accumulate -activated charcoal, dexamethasone, ascorbic acid, blood transfusion -prevent by removing leaves/branches and not planting maples around enclosures
64
Allium spp. common plants, toxic principle and mechanism
-allium cepa (onion) -allium sativum (garlic) -n-propyl disulfides, present in all forms even cooked -cats are more sensitive -mechanism: increased free radical formation, direct erythrocyte membrane damage and denatured hemoglobin, heinz bodies and cute hemolysis
65
Allium spp. toxicity and clinical signs
-most susceptible dogs, cats, and cattle -clinical signs: inappetence, lethargy, tachycardia, tachypnea, pale mucous membranes, abortions possible -treatment: avoid stress and blood transfusions -in blood smear can see heinz bodies and eccentrocyte
66
Plants affecting the kidneys
-plants with soluble oxalates like pigweed (amaranthus retroflexus) -quercus spp.: oak -grapes/raisins, and lillies
67
Amaranthus retroflexus: Redroot pigweed species and toxic principle
-affects pigs primarily but other large animal also affected -season of risk: mid june to late summer, also toxic when dried - has 3 toxins: first one is unknown but causes acture renal tubular necrosis, but can also accumulate nitrates and soluble oxalants
68
Amaranthus retroflexus: Redroot pigweed clinical signs
- typically 5-10 days after ingesting large amounts -posterior weakness, incoordination, and sternal recumbency -gross lesions: perirenal edema +/- hemorrhage and ascites -histologically: acute tubular necrosis
69
Soluble oxalates system affected and mechanism
-kidneys -mainly a problem in grazing animals without adaptation (cattle, sheep, goats) -highest concentrations of soluble oxalates are in the leaves -if large quantities ingested form insoluble Ca and Mg oxalates resulting in hypocalcemia and crystallization of Ca-oxalate in the kidneys
70
Plants with soluble oxalates
-rumex spp: dock -rheum: rhubarb
71
soluble oxalates treatment
-no specific treatment -treat symptoms with fluids to flush crystals out
72
Quercus spp. Oak toxic prinicple
-fruit is the acorn -hydrolyzable tannins= polyphenolic complexes (tannins result in phenolic acids) -phenolic acids of concern: gallic acid, pyrogallol, resorcinol -astringent effect on gut mucosa, get GI irritation -react with cell proteins, denature and cell death -tissue destruction: kidney (severe in cattle), and liver
73
How toxic are oak tannins
-tannins found in leaves, bark and acorns (especially young leaves/ flower buds) -need to eat large amounts preceded period of feed restriction
74
Oak clinical signs
-cattle typically affected -abrupt onset, diarrhea or constipation with bloody or mucoid feces, anorexia, listlessness, rumen stasis, oliguria (acute renal failure), weakness and recumbancy -goats and deers can browse oak effectively because have tannin binding proteins in saliva/GIT -horses: diarrhea, colic, tenesmus, fewer renal effects
75
Quercus spp. treatment/prevention
- remove access to oak -if unavoidable mix 10% calcium hydroxide may help bind to tannins -activated charcoal or mineral oil -fluids
76
Plants affecting the reproductive system and congenital defects
-veratrum californicum: skunk cabbage, corn lilly -pinus ponderosa: ponderosa pine - also in poison hemlock, lupine, tree tobacco
77
Veratrum spp. toxic principle
-all parts of plant are toxic -many types of alkaloids -cevanine alkaloids are neurotoxic -jervanine alkaloids: teratogenic (cyclopamine, cycoposine, and jervine) -cyclopamine is believed most important due to high concentration in plants: interferes with intercellular signaling and patterning during embryo/organogenesis
78
Veratrum spp: Corn Lily
-teratogenic and neurotxic in all species - usually not enough ingested to be neurotoxic, unknown mechanism -frost results in loss of toxicity -different teratogenic effects based on when it is ingested (if on 14th day results in cyclops
79
Pine Needle Abortion
-associated with pinus ponderosa and some other pinus, Juniper communis: common juniper -toxin: isocupressic acid, results in reduction in uterine blood flow then abortion -in bark/needles, needles have greatest risk -abortion 2-21 days after exposure -in cattle greatest risk after 3 months of pregnancy, need to eat 2.2-2.7 kg of pine needles per day for more than 3 days
80
Plants affecting Musculoskeletal System
-juglans nigra: black walnut -some other in supplemental info
81
Black walnut species
-primarily affects horses -used in hardwood and used to be used as bedding -has dark brown shavings -toxin can be absorbed through skin or ingested
82
Juglans nigra: black walnut clinical signs
-can happen in outbreaks as large groups of horses are exposed to new bedding -reluctance to move within 24 hours -depression -increased: temp, heart and respiration rate, digital pulses, hoof temp -lower limb edema more indicative sign -severe laminitis with continued exposure

VET 401 Basic Foundations (2 decks)

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