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VET 401 Basic Foundations > VET 406 Toxic Plants > Flashcards

VET 406 Toxic Plants Flashcards

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
Q

Yellow Star Thistle (Centaurea solstitialis) and Russian Knapweed (Centaurea repens) toxicity

A
  • 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)
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26
Q

Yellow Star Thistle (Centaurea solstitialis) and Russian Knapweed (Centaurea repens) clinical signs

A
  • “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
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27
Q

Plants affecting the Cardiovascular System

A

-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)

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28
Q

Diagnosis of Oleander Poisoning

A
  • identification of leaves in ingesta (often mistaken for eucalyptus)
  • test for oleandrin
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29
Q

Oleander Toxicity and Clinical Signs

A

-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)

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30
Q

Oleander Treatment

A

-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

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31
Q

Mechanisms of cardiac glycosides

A
  • 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
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32
Q

Grayanotoxins (cardiovascular toxin) are found in

A
  • the heath family (ex rhododendron, azalea, rosebay and many more)
    -highest concentrations in the leaves but also in flowers, nectar and stems
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33
Q

Grayanotoxins Toxicity and Clinical Signs, and Diagnosis

A
  • 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
Q

Grayanotoxins treament

A

-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
Q

Taxus spp. (yew) toxin, toxicity, diagnosis, treatment

A

-cardiotoxic toxin: taxine alkaloids
-toxicity: toxic green and dry, 6-8 oz
-diagnosis: taxine alkaloids in GI contents
-treatment: activated charcoal, and atropine

36
Q

Avocado (Persea americana) clinical signs

A

-acute death/cardiac signs in birds, rabbits, goats
-mastitis and agalactia in cattle, horses, goats, rabbits
-colic, diarrhea, neck edema: horses

37
Q

Avocado (persea americana) toxin, toxicity, diagnosis, treatment

A

-toxin: persin (unknown mechanism)
- toxicity: all parts of plant is toxic
- diagnosis: post mortem lesions
-treatment: supportive

38
Q

Plants affecting the digestive system

A

-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
Q

Dumbcane (diffenbachia sp.) toxin and clinical signs

A

-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
Q

Grasses that cause trauma, signs, and treatment

A

-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
Q

Setaria glauca common name

A

yellow foxtail

42
Q

Hordeum jubatum

A

foxtail barley

43
Q

Plants with lectins (toxalbumins, ex ricin)

A

-robinia pseudoacacia: black locust
- abrus precatorius: rosary pea, precatory bean
- ricinus communis: castor bean
-mistletoe

44
Q

Robinia pseudoacacia: black locust toxicity

A

-bark and seeds have the highest concentrations of lectins, but in leaves as well

45
Q

Albus precatorius: Precatory bean plant and toxin

A

-established in Florida
-fruit= legume pod
- seeds: glossy red with jet black eye
-toxin= abrin (highly toxic in small concentration)

46
Q

ADF and NDF

A

-acid detergent fiber
-neutral detergent fiber

47
Q

Ricinus communis: castor beans plant and toxin

A

-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
Q

Toxic principles of lectin, mechanisms and signs

A

-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
Q

Ricinus communis: castor beans mechanism of action

A

-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
Q

Ricinus communis: castor beans diagnosis, therapy, prevention

A

-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
Q

Tropane alkaloid containing plants

A

-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
Q

Tropane alkaloid clinical signs

A
  • 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
Q

Toxicants affecting skin and liver often result in

A

-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
Q

Type 1: Primary photosensitization

A

-from ingestion of plants with photodynamic agents ex. Hypericum perforatum: St. John’s wort (the toxin in this is hypericin)

55
Q

Type 3: Secondary photosensitization

A

-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
Q

Toxin resulting in photosensitization and plants with this, and species affected

A

-pyrrolizidine-alkaloid containing plants
- senecio vulgaris: common groundsel
- senecio jacobaea: Tansy ragwort
-cattle and horses
-sheep are more resistant

57
Q

Pyrrolizidine-alkaloid toxicity and mechanism

A

-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
Q

Pyrrolizidine-alkaloid clinical signs

A

-acute: icterus, edema
-chronic: firm nodular liver (cirrhosis), icterus, +/- photosensitivity
-can have microscopic lesions too
-CNS involvement: wandering, chewing, head pressing

59
Q

Plants affecting the blood

A

-Acer rubrum: red maple
-allium spp: onion

60
Q

Acer rubrum: red maple plant appearance

A

-large tree
-3-5 lobes with palmately arranged veins
- the fruit is red in color and has 2 wings

61
Q

Acer rubrum: red maple toxin and mechanism

A

-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
Q

Acer rubrum: red maple toxicity and clinical signs

A

-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
Q

Acer rubrum: red maple treatment

A

-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
Q

Allium spp. common plants, toxic principle and mechanism

A

-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
Q

Allium spp. toxicity and clinical signs

A

-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
Q

Plants affecting the kidneys

A

-plants with soluble oxalates like pigweed (amaranthus retroflexus)
-quercus spp.: oak
-grapes/raisins, and lillies

67
Q

Amaranthus retroflexus: Redroot pigweed species and toxic principle

A

-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
Q

Amaranthus retroflexus: Redroot pigweed clinical signs

A
  • 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
Q

Soluble oxalates system affected and mechanism

A

-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
Q

Plants with soluble oxalates

A

-rumex spp: dock
-rheum: rhubarb

71
Q

soluble oxalates treatment

A

-no specific treatment
-treat symptoms with fluids to flush crystals out

72
Q

Quercus spp. Oak toxic prinicple

A

-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
Q

How toxic are oak tannins

A

-tannins found in leaves, bark and acorns (especially young leaves/ flower buds)
-need to eat large amounts preceded period of feed restriction

74
Q

Oak clinical signs

A

-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
Q

Quercus spp. treatment/prevention

A
  • remove access to oak
    -if unavoidable mix 10% calcium hydroxide may help bind to tannins
    -activated charcoal or mineral oil
    -fluids
76
Q

Plants affecting the reproductive system and congenital defects

A

-veratrum californicum: skunk cabbage, corn lilly
-pinus ponderosa: ponderosa pine
- also in poison hemlock, lupine, tree tobacco

77
Q

Veratrum spp. toxic principle

A

-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
Q

Veratrum spp: Corn Lily

A

-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
Q

Pine Needle Abortion

A

-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
Q

Plants affecting Musculoskeletal System

A

-juglans nigra: black walnut
-some other in supplemental info

81
Q

Black walnut species

A

-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
Q

Juglans nigra: black walnut clinical signs

A

-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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