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Toxicology > Toxic Plants > Flashcards

Toxic Plants Flashcards

1
Q

Larkspur (Delphinium spp) spp susceptibility

A

Cattle most susceptible

Sheep and horses also affected

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2
Q

Larkspur (Delphinium spp) Toxic pathogenesis

A

Curare-like blockade of neuromuscular junctions— reversibly binding to nictonic acetylcholine receptors

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3
Q

Larkspur consumption can also enhance the toxicity of another range plant

A

Death camas (Zigadenus spp)

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4
Q

Larkspur (delphinium spp) clinical signs

A

Sudden death—3 hours post consumption
—> excitability, mm tremors, stiffness, staggerings & basewide stance or kneeling position (cattle), bloat regurge (ruminants) constipation, mmild GI irritation, venous congestion & aspiration pneumonia

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5
Q

Larkspur toxicosis diagnosis

A

Identify pieces of larkspur in the upper GI tract

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6
Q

Larkspur toxicosis treatment

A

-relieve bloat
-IV physostigmine
—> neostigmine not as effective

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7
Q

Larkspur ingestion/toxicosis prevention

A
  • sheep most tolerant and can reduce plant density
  • lithium chloride administration
  • insect control with larkspur myrid (hoplamachus affiguratus)
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8
Q

Cyanogenic plants clinical signs

A

SUDDEN DEATH
Rarely: resp distress, rapid breathing, bloat, salivation, mm twitching, staggering, mydriasis, cardiac arrythmias, convulsions

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9
Q

Cyanogenic plants pathogenesis

A

Cyanide blocks molecular oxygen transfer in cytochrome oxidase systems in mitochondria causing tissue anoxia

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10
Q

Ruminants are more susceptible to cyanogenic plants because

A

Rumen microorganisms readily release cyanide from the cyanogenic glycosides

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11
Q

Cyanogenic plants post mortem findings

A
  • cherry red venous blood
  • bitter almond odor— rumen contents
  • hemorrhages in multiple organs
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12
Q

Cyanide detection post mortem

A

Heart, brain, skeletal mm or rumen contents

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13
Q

Factors that increase the cyanogenic potential for toxicity

A

Wilting
Frost
Drought
Other damgage to plant

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14
Q

Cyanogenic plant tox treatment

A
  • sodium thiosulfate/sodium nitrate mixture (not approved in food animals)
  • vinegar orally
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15
Q

Examples of CROPS with the potential to accumulate nitrates

A 
Barley (Hordeum spp)
Beets (Beta vulagris)
Corn (Zea mays)
Flax (Linum spp.)
Kale (brassica oleracea)
Oats (Avena spp)
Pearl millet (Pennisetum typhoides)
Rape (Brassica napus)
Rye (Secale cereale)
Soybeans (Glycine max)
Sunflower (Helianthus annuus)
Turnips Triticum aestivum)
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16
Q

Examples of FORAGES with potential to accumulate nitrates

A 
Alfalfa (Medicago sativa)
Barnyard grass (Echinochloa spp)
Buttong rass (Dactyloctenium radulans)
Johnson grass (Sorghum halepense)
Sudan grass (Sorghum vulgare)
Sweet clover (Melilotus spp.)
Tall fescue (Lolium arundinaceum)
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17
Q

Examples of WEEDS that can accumulate Nitrates

A 
Canada thistle (Circsium arvense)
Cheese weed, mallow (Malva spp)
Dock (rumex spp.)
Field bindweed (Convolvulus arvensis)
Fireweed (Kochia spp.)
Goldenrod (Solidago spp.)
Jimsonweed (Datura stramonium)
Kochia (summer cypress) *Kochia scoparia)
Lambsquarters (Chenopodium spp)
Nightshades (solanum spp)
Pigweed (Amaranthus spp)
Ragweed (ambrosia spp.)
Russian thistle (salsola kali)
Smart weed (Polygonum spp.)
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18
Q

Triggers for NITRATE accumulation in plants

A 
— photosynthesis impaired by shade or prolonged cloudiness or excessive nitrogen applied to plants (fertilizers)
Others:
-drought
-frost
-hail
-herbicide application
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19
Q

Characteristic clinical signs of NITRATE toxicity

A

Chocolate brown mucous membranes & blood

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20
Q

What is the cause of chocolate brown mucous membranes in nitrate toxicosis?

A

Ruminants— ingested nitrates converted to nitrites & ammonium in forestomaches
—>absorbed nitrites trigger oxidation of ferrous irone in hemoglobin— produces METHEMOGLOBIN

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21
Q

Methemoglobinemia in nitrate toxicity results in pathogenesis that leads to what clinical signs

A

Vasodilation & hypotension

—> hypoxia, dyspnea, exercise intolerance, death, fetal stress, subsequent abortion, stillbirths &/or weak neonates

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22
Q

Mares with nitrate toxicity

A

Produce neonates with congenital hypothyroidism
OR abortion
OR dysmature foal after prolonged gestation
(Mandibular prognathism, flexural deformities of forelimbs, secondary rupture of common digital extensor tendon just above the carpus, poorly ossified cuboidal bones, poor immune function)

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23
Q

Treatment of nitrate toxicity

A 
Methylene blue (prohibited in food animals)
Mineral oil/vinegar— NGT
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24
Q

Locoweed and milkvetch can cause 4 different toxic syndromes

A
  1. Sudden death (from methemoglobinemia)
  2. Respiratory syndrome w/ emphysema like signs (most commonly sheep)
  3. Neurologic signs
  4. Selenium toxicosis
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25
Q

The toxin swainsonine is produced by

A

Endophyte (Undilum oxytropis)

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26
Q

Swainsonine is produced in what part of the plant (seed/plant)

A

seeds

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27
Q

Swainsonine pathogenesis

A

Creates lysosomal storage disease
—> alpha mannosidase is inhibited resulting in swelling of axonal hillocks & grwoth of new dendrites & synapses in severe locoweed cases (nonreversible change)

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28
Q

Clinical neurological signs of locoweed intoxication

A

Depression, incoordination & progress to aberrant behavior, aggression, circling, weight loss & eventually death

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29
Q

Bracken fern toxic principle

A

Ptaquiloside

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30
Q

Jimsonweed thornapple toxic principle

A

Tropane alkaloids

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31
Q

Johnson grass toxic principle

A

Hydrocyanide

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32
Q

Lupines toxic principles

A

Piperidine, quinolizidine

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33
Q

Milkvetches toxic principle

A

Miserotoxicin

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34
Q

Ryegrass toxic principle

A

Lolitrem B

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35
Q

Sudan grass toxic principle

A

Hydrocyanide, nitrates

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36
Q

Milkvetch spp: Astragalus toxic pathogenesis

A

Beta-D-glycosides converted to 3-nitro-1-propanol (miserotoxin) nit eh rumen and subsequently changed to the toxic compound 3-nitropropionic acid in liver

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37
Q

Diagnosis of locoism

A

Based on:

  • clinical signs
  • swainsonine and/or alpha mannosidase in serum
  • vacuolation of peripheral lymphocytes
  • vacuolation of many tissues— esp. brain and liver
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38
Q

Day blooming jasmine (cestrum diurnum) induces what pathogenesis in ruminants/cattle

A

Calcinosis in horses and cattle by calcinogenic glycosides converted to vitamin D-like compounds

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39
Q

Cestrum diurnum location

A

Southeastern US & tropical countries

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40
Q

White snake root effects which age of cattle and why?

A

Does not affect adult cattle, but causes clinical signs in mild-fed calves
(C/S of msk disease)

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41
Q

Summer Pasture-Associated Myositis and Equine Atypical Myopathy caused by ingestion of which plant

A

Box elder seeds from female trees (Acer negundo)

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42
Q

Toxic principle in box elder seeds

A

Hypoglycin A

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43
Q

Pathogenesis of Box elder

A

Hypoglycin A metabolized to methylene cyclopropyl acetic acid (MCPA)— potent inhibtor of multiplle acyl-CoA dehydrogenases.
Lack of these enzymes causes:
*damages mitochondria
*impairs lipid meatbolism w/in mm cells
Cell death

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44
Q

4 important plants with toxins that damage the myocardium and cause mortality in large animals

A
  • yew (Taxus spp.)
  • avocado ( Persea americana)
  • death camas (Zigadenus spp. )
  • summer pheasant eye (Adonis spp.)
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45
Q

Pathogenesis of Red Maple leaf toxicosis

A

Oxidative damage to erythrocytes & acute Heinz body anemia or methemoglobinemia

46
Q

Clinical signs of red maple leaf toxicosis

A 
Weakness
Tachycardia
Tachypnea
Icterus
Hemoglobinuria
47
Q

Plants that cause a thiamine deficiency the cause neurological signs in horses

A
  • Thiaminase enzymes in bracken fern (Pteridium aquilinum)

* horse tail (Equisetum spp)

48
Q

Plant that causes enzootic hematuria in cattle

A 
Bracken fern (Pteridium aquilinum)
** causes cancerous the changes in urinary tract
49
Q

Ptaquiloside in bracken fern through what mechanism, causes what consequently

A

Sesquiterpene glycoside responsible for detrimental effects on bone marrow and neoplastic changes in the bladder and upper GIT

50
Q

What plant is associated with upper digestive tract squamous cell carcinoma and bovine papillomavirus type 4

A

Bracke fern (P. Quilinum)

51
Q

Alsike clover produces what 2 syndromes in horses:

A
  1. Hepatic encephalopathy

2. Photosensitization

52
Q

Examples of plants that cause damage to biliary cells leading to secondary photosensitization as the primary clinical sign

A 
Agave (Agave lechuguilla)
Bear grass or sacahuista (nolina texana)
Bos asphodel (Narthecium ossifragum)
Kleingrass and switch grass (Panicum spp.)
Puncture vine (Tribulus terrestris)
53
Q

Examples of plants that contain Pyrrolizidine alkaloids

A 
Groundsel (Senecio spp)
Heliotrope (Heliotropium spp)
Houndstongue (cynoglossum officinale)
Kochia (Kochia scoparia)
Paterson’s cursse (Echium platnagineum)
Rattlebox, rattlepod
Tansy ragwort (Senecio jacobaea)
Tarweed, fiddleneck (Amsinckia spp.)
Viper’s bugloss (Echium vulgare)
54
Q

Which spp are most susceptible to pyrrolizidine alkaloids?

A

Cattle

Horses

55
Q

Crotolaria spp causes what in horses

Pyrrolizidine alkaloids

A

Liver failure & fibrosing pulmonary alveolitis

56
Q

Ponderosa pine (Pinus ponderosa) needles and bark, when consumed in which term in pregnancy & cause what?

A

— third trimester

—abortion & premature delivery in cattle in western USA/canada

57
Q

Pathogenesis of Ponderosa pine ingestion

A

Isocupressic acid, abortifacient compound, rapidly metabolized to agathic acid in rumen

—>vasoconstrictive ffect on uterine vessels leads to uterine inertia, abortion & freq dystocia and/or retained placenta

58
Q

Examples of phytoestrogens

A

Alfalfa
Clovers (some types, produce coumestrol)
Soybeans (isoflavones)

59
Q

Cause of crooked calf disease (problem in range cattle)

A

Lupine ingestion during early gestation to midgestation in ruminants

60
Q

Lupine ingestion in mid to late gestation causes what musculoskeletal deformities

A 
Arthrogryposis
Kyphosis
Scoliosis
Roticollis
Clefft palate
61
Q

Teratogens identified in lupine

A

Anagyrine ( a quinolizidine alkaloid)

Ammondendrine (piperadine alkaloid)

62
Q

Teratogenic effects of poison hemlock are greatest in which spp:

A

Cattle

Pigs

63
Q

Ingestion of which plants in early gestation result in abortion and birth of cyclopic lambs:

A 
False hellebore
Skunk cabbage (Veratrum spp)
64
Q

Goitrogenic effects may be observed from plants containing:

A

Excessive iodine (ie: seaweed)
Thiocyanates (white clover)
Glucosinolates (brassic spp., kale, turnips, canola seeds)

65
Q

Congenital hypothyroidism in equine neonates can be caused by ingestion of

A

High nitrate forages

Or plants with goitrogenic effects

66
Q

Many grass spp can be infected with endophytes such as

the most economically important

A

Fescue (lolium spp) infected with Neotyphodium coenophialum

67
Q

Ergot (Claviceps spp) infected forages and grains produces what appearance of the plants:

A

Dark fungal sclerotia (ergot bodies) shaped like seeds readily visible in the plants seed head in pasture, hay or contaminated grains

68
Q

What is the most economically important endophyte?

A

Fescue (Lolium spp) infected with Neotyhpodium coenophialum)

69
Q

What is the most prevalent ergopeptine in endophyte infected tall fescue that is responsible for the most signs associiated with fescue toxicosis?

A

Ergovaline

70
Q

Endophyte infection of fescue provides what advantages

A

Increased resistance to drought, insects, parasitic nematodes & herbivores

71
Q

Species susceptibility to Ergot alkaloids

A 
Horses (highest)
Cattle
Sheep
Goats
Camelids
72
Q

Pathogenesis of Ergot alkaloids (ergovaline)

A

Vasoconstrictive effects (alpha 2 adrenergic agonist) &/or depress secretion of prolactin via effects on lactotropic dopamine (D2) receptrs in the adenohypophysis of the pituitary—> resulting in decreased steroid genesis= decreased progresterone production by the corpora lutea & relaxin

73
Q

Ruminants are less susceptible to ergot alkaloids because:

A

Ruminants placenta produces relaxin (less impact on readiness for parturition)

74
Q

Grasses infected with Claviceps paspali produces neurologic signs associated with

A

Gamma-aminobutyric acid inhibition

75
Q

Clinical abnormalities attributable to ergot and endophyte infections of grasses detected in which regions of the US

A

Warm, wet climates of Southern US— endophytes

Cool, wet springs of NW US—- ergot

76
Q

Ergot alkaloid and endophyte toxicity can result in what clinical sign in the Winter

A

Gangrene of distal extremities & amness

77
Q

Ergot alkaloid and endophyte toxicosis can result in what clinicla signs in summer/heat

A

Heat stress
Hyperthermia

failure of heat dissipation in through the skin

78
Q

Ergot alkaloid clinical signs in pigs

A

Agalactia

Abortion

79
Q

Clinical signs of Ergot alkaloids/endophyte tox in mares

A 
Faluire of udder development
Agalactia
Prolonged gestation
Placental abnormalities
Dystocia
Decreased milk production
Subfertility
80
Q

Diagnosis of Ergot alkaloids & endophytes tox

A

C/s and consumption of infected feed

High performance liquid chromatography (HPLC)

81
Q

Examples of plants that cause predominantly respiratory signs in large animals

A 
Perilla mint (Perila frutescens)
Sweet potatoes (Ipomoea batatas) damaged by fusarium spp molds
82
Q

Pathogenesis of Perilla mint (perilla frutscens)

A

Perilla contains ketones & related furan compounds—> bioactivated in the lung

—> atypical interstitial pneumonia & acute respiratory distress

83
Q

Toxins that cause atypical interstitial pneumonia & acute respiratory distress

A 
Sweet potatoes ( Ipomoea batatas) damaged by Fusarium spp 
Perilla mint (Perilla frutescens)
84
Q

Acute bovine pulmonary emphysema & edema may occur following ingestion of forages high in:

A

Tryptophan

—> typically immature summer grasses

85
Q

Acute bovine pulmonary emphysema and edema pathogenesis

A

Forages high in tryptophan

—> rumen bacteria convert tryptophan to 3-methylindole—> further metabolized to a lung toxicant

86
Q

Prevention of acute bovine pulmonary emphysema and edema

A
  • gradually introduce cattle to grasses high in tryptophytan
  • monensin or tetracycline in feed for a week before & 2 weeks after turnout on pasture (refer to regulations in veterinary feed directive)
87
Q

Pathogenesis of photosensitization

A

-sunlight triggers an oxidative reaction with photoreactive, polyphenolic compounds absorbed form the digestive trac tin areas of unpigmented skin
—>leading to inflammation, cellular necrosis & sloughing of skin

88
Q

Common plant sources of primary photosensitization

A 
St. John’s Wort (Hypericum perforatum)
Buckwheat (Fagopyrum esculentum)
Dutchman’s breeches (Thamnosma texana)
Bischops weed (Amni majus)
Rain lily (Cooperia pedunculata)
Spring parsley (Cymopterus watsonii)
Giant hog weed (Heracleum mantegazzanium)
Cow parsnup (Heracleum spp)
89
Q

Plants that commonly accumulate selenium

A

Milkvetch (Astraglus spp)
Wood aster (Machaeranthera, section Xylorrhiza)
Goldenweed (Haplopappus, section Conopsis)
Princes plume (Stanleya pinnata)

90
Q

Three syndromes of excessive selenium intake

A

Acute toxicosis
Blind staggers
Chronic alkali disease

91
Q

Effects of oak toxicity on the urinary system

A

Nephritis with necrosis
Renal tubular casts
**possibly leading to acute renal failure

92
Q

Common plant toxicities that are harmful to the urinary system

A 
Bracken fern (P. Aquilinum)
Cocklebur (Xanthium spp.)
Inkweed (P. Octandra)
Oak (Quercus spp.)
Pigweed (amaranthus retrflexus)
93
Q

Where are cyanobacteria found?

A

Suspended in water column

— easily visible or attache dot surfaces of stones & sediments along bottom of lakes or rivers

94
Q

What is the most common cyanotoxin poisoning in large animals?

A

Acute hepatotoxicosis subsequent to microcystin exposure

95
Q

Fungal sources of alfatoxins

A

**corn & corn-byproducts
Nuts
Cotton seed

96
Q

Primary toxic effects of alfatoxins

A

Macromolecular binding enzymatic inhibition

DNA adducts formed—> hepatic insult/failure cancer (primary ehpatic)

97
Q

Major alfatoxins found in contaminated grains include

A

B1, B2, G1 & G2

98
Q

Conditions leading to alfatoxin production by Aspergillus spp

A

Drought &/or insect damage to corn or other susceptible plants followed by warm, humid (>70% humidity), ambient weather conditions

99
Q

Mycotoxin: Deoxynivalenol (DON/vomitoxin) produced by:

A 
Fusarium graminearum (formerly Fusarium roseum)
-corn, wheat, barley
100
Q

Primarily toxic effects of Deoxynivalenol (DON/Vomitoxin)

A

Decreased protein synthesis
GI irritation
INC vomiting
—>feed refusal, DEC nutrient absorption, DEC immunity

101
Q

Mycotoxin Zearalenone is produced by

A

F. Graminearum (formerly F. Roseum)

Corn, wheat, barley

102
Q

Primary toxic effects of zearlaenone

A

Hyperestrogenism—> productive tract changes
Pseudopregnancy
Early embryonic death

103
Q

Mycotoxin Fumonisins produced by

A 
Fusarium verticillioides (formerly Fusarium monilforme)
**primary corn
104
Q

Primary toxic effects of Fumonisins

A 
Shingolipid changes—> leukoencephalomalacia
*** Horses
Pulmonary edema 
***swine
—hepatic disease in both
105
Q

Zearalenone pathogenesis

A

Nonsteroidal xenoestrogen that binds to both alpha and beta estrogen receptors

106
Q

Fumonisin toxin that is the most comon and clinically important fumonisin

A

FB1

107
Q

What ist eh primary toxic mechanism of action proposed for fumonisins

A

Inhibition of conversion of sphinganine to sphingosine—> results in disruption of sphingolilpid biosyntehsis

108
Q

Which spps are most susceptible to fumonisin intoxication

A

Horses & swine

109
Q

Clinical signs of equine luekoencephalomalacia

A

Alterted mentation (depression— to neuroexcitation)
Head pressing
Incoordination & apparent blindness
Recumbency & death w/in 5-7 days

110
Q

Equine leukoencephalomalacia pathognomonic lesion

A

Degeneration of white matter of the brain

** grossly visible involving one or both cerebral hemispheres

111
Q

What is the primary clinical abnormalities associated with FB1 exposure in swine

A

Porcine pulmonary edema (PPE)

Toxic insult to liver

Toxicology (5 decks)

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