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Poisonous Plants > ID and Cyanide Poisoning > Flashcards

ID and Cyanide Poisoning Flashcards

1
Q

Sorghum halepense

A

Sundan grass

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2
Q

Linum lewisii

A

Wild blue flax

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3
Q

Triglochin maritima

A

Arrowgrass

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4
Q

Cercocarpus montanus

A

Mountain mahogany

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5
Q

Trifolium repens

A

White clover

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6
Q

Avena fatua

A

Wild oat grass

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7
Q

Chenopodium album

A

Lambsquarter

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8
Q

Cirsium arvense

A

Canda thistle

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9
Q

Convolulus arvensis

A

Field bindweed

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10
Q

Echinochloa crus-gali

A

Barnyard grass

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11
Q

Kochia scoparia

A

kochia

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12
Q

Salsola tragus

A

Russian thistle

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13
Q

Helianthus annuus

A

common sunflower

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14
Q

Delphinium geyeri delphinium occidentale delphinium barbarbeyi

A

Larkspur spp.

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15
Q

Aconitum columbianum

A

Western monkhood

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16
Q

Conium maculatum

A

poison hemlock

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17
Q

Cicuta douglasii

A

western water hemlock

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18
Q

apocynum cannibinium

A

dogbane or indian hemp

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19
Q

apocynum androsaemifolium

A

spreading dogbane

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20
Q

Asclepias speciosa

A

showy milkweed

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21
Q

asclepias incarnata

A

swamp milkweed

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22
Q

asclepias viridiflora

A

green comet milkweed

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23
Q

zigadenus elegans

A

mountain death camas

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24
Q

zigadenus venenosus

A

meadow death camas

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25
Q
A

Sorghum halpense

Sudan grass

-short grass prairie

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26
Q
A

Prunus virginiana

Western chokecherry

-Dry washbed

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27
Q
A

Amelanchier alnifolia

Western serviceberry

-river bank; sloping sidehill

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28
Q
A

Linum lewisii

Wild blue flax

-rocky or sandy soil

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29
Q
A

Triglochin maritima

Arrowgrass

-along stream through sand dunes

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30
Q
A

Cercocarpus montanus

Mountain mahogany

-abundant in hills

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31
Q
A

Trifolium repens

White clover

-meadow in draw

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32
Q
A

Avena fatua

Wild oat grass

-slope of river and roadside

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33
Q
A

Chenopodium albun

Lambsquarter

-roadside and disturbed areas

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34
Q
A

Cirsium carvense

Canadian thistle

-along wet drainage

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35
Q
A

Convolvulus arvensis

Field bindweed

-sandstone hogbacks and slopes

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36
Q
A

Echinochloa crus-galli

Barnyard grass

-roadside irragation ditch

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37
Q
A

Kochia scoparia

Kochia

-sagebrush slope and streamside

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38
Q
A

Salsola tragus

Russian thistle

-sedintary slopes

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39
Q
A

Helianthus annuus

Common sunflower

-sedintary slopes with wet spots

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40
Q
A

Delphinium

Larkspur spp.

-above treeline in rock skree and alpine turf

41
Q
A

aconitum columbianum

Western monkhood

-along stream

42
Q
A

Conium maculatum

Poison hemlock

  • weedy openings in forest
43
Q
A

Cicuta douglasii

Western water hemlock

-canyon bottom

44
Q
A

Apocynum cannabinum

Indian hemp or Dogbane

-along sandy dry wash

45
Q
A

Apocynum androsaemifolium

Spreading dogbane

-gravely uplands

46
Q
A

Asclepias

Milkweed spp

  • canyon bottom; riparian
47
Q
A

Zigadenus

Death Camas

-beside trail near water

48
Q

SOPs

A
  • “step-by-step instructions for carrying out complex, routine operations”
  • Increase efficiency
  • quality output
  • uniformity of performance
49
Q

Log Sheets

A
  • Long term record-keeping
  • accountability
  • traceability
50
Q

Why are wildlife poisonings overlooked?

A

Not fresh

individuals hard to detect

Don’t care

Lack of toxic recognition

indirect effects

51
Q

What are some metabolic similarities and differences between plants and animals and why is this important?

A
  • Similarities
    • complex biochemical pathways
    • waste production
    • base needs; nutrients, water, shelter, temp control
  • Differences
    • excretion
      • urine, feces
      • accumulates in plants
  • Important because secondary plant chemicals (metabolites)
52
Q

What are some medicines derived from toxins?

A

Aspirin, Taxol, Lidocaine, Morphine,

Atropine

53
Q

What are some benefits of SPC (toxins)?

A
  • herbivory
  • large herbivores/small herbivore physical defenses– thorns spines, etc
  • Insects- toxins for chemical defenses
  • Microbes– bacteria, fungi, viruses
  • attract pollinators
  • drought resistance
  • reproduction
  • communication
54
Q

Looking at insects vs. large herbivores, differentiate their coevolution.

A
  • insects
    • short lifespan
    • high fecundity
    • specialists
    • quickly adapt
  • Large herbivores
    • long life spans
    • few offspring
    • generalists
    • slow adaptation
55
Q

What is the Red Queen Hypothesis?

A

You have to keep running to stay in place

Insects become resistant, plant makes toxin, insects become resistant, etc etc.

56
Q

How do animals cope with injurious plants?

A
  1. Avoidance- learned behavior; genetic; behavior modification
  2. Dilution- eat lots of non-toxic plants; internal mechanisms
  3. Degradation- in GI tract; break down toxin
  4. Detoxification- after absorption from GI
57
Q

What are some ecological impacts of poisonous plants?

A
  • lower fitness, reduce species, reduce predators
  • die offs
  • natural selection, increased fitness
  • plants overgrow
  • restoring populations, expose animals to unfamiliar toxins
58
Q

What are some disadvantages for livestock?

A
  • not native- we move them
  • inability to migrate
  • not apprehensive
  • limited forage supply, lower variety
  • overgraze/degrae rangeland
  • resistance
  • no learned behavior
  • modify their behavior
59
Q

What might cause increased wildlife poisonings?

A
  • degradation of critical habitat
  • disrupted migration
  • translocaational
  • climate change
  • non-native species
60
Q

What is the USDA timeline?

A
  • USDA 1862
  • Local offices- early 1900s
  • USDA poisonous plant research lab 1955
61
Q

What is a natural toxicant?

A

Toxin produced by living things

62
Q

What is acute toxicity?

A

Adverse effects from single or multiple exposures w/in 24 hrs or less

63
Q

What is chronic toxicity?

A

Long term exposure (intermitten or continuous)

64
Q

What is subacute toxicity?

A

adverse effects from single or multiple exposures w/in 24 hrs to 28 days

65
Q

What is subchronic toxicity?

A

Up to 90 days or <10% of lifespan

66
Q

What is LD50?

A

Lethal dose that can kill 50% of test subjects (don’t always know for every substance)

67
Q

What are some direct and indirect impacts of toxicants in agriculture?

A
  • Direct
    • death, abortion, etc
  • indirect
    • Weight loss, withdrawl times, infertility, forage loss (due to avoidance), etc.
68
Q

Cyanogenic glycosides produces what?

A

HCN

Hydrogen cyanide gas

69
Q

Cyanogenic glycosides use what mechanism?

A

Enzymatic hydrolysis

70
Q

Amygdahlin (laetrile) is found in what?

A

Choke cherries, mountain mahogany, service berries

(have prunasin too)

71
Q

Prunasin is found in what?

A

Bracken

72
Q

Dhurrin is found in what?

A

Sorghum spp

Johnson and sudhan grass

73
Q

Triglochinin is found in what?

A

Arrowgrass

74
Q

Linamarin is found in what?

A

Flax (linseed), white clover, cassava

75
Q

What are some toxins that are cyanogenic glycosides?

A
  1. Amygdalin (laetrile)
  2. Prunasin
  3. Dhurrin
  4. Triglochinin
  5. Linamarin
76
Q

Explain how cyanogenic glycoside poisoning works

A

problem happens when process gets overwhelmed and HCN builds up

77
Q

What increases cyanogenic potential?

A

Plant or microbial enzymes, chewing, frost or drought increase cyanogenic potential

78
Q

What is the mechanism of enzymatic hydrolysis?

A
79
Q

Where is the highest content of CN found?

A
  • new shoots
  • new growth
  • regrowth
  • Don’t want to eat these
80
Q

What are some factos that effect concentration of CN in plants?

A
  • stage of growth
  • time of year (winter) early spring
  • soil mineral (high nitrates) and moisture content
  • time of day
81
Q

How can you increase conversion of nitrate to cyanogenic glycosides?

A
  • cool, moist growing conditions
  • Nitrate fertilization
  • Drought/frost
  • herbicides (2, 4-D)
82
Q

If you were a toxin, where would you interupt this process? HCN

A
  • Compete w/ O2 for binding w/hemoglobin
83
Q

What is some differential effects in ruminants vs. non-ruminants of HCN?

A
84
Q

How was HCN used on humans?

A

Nazi’s used on jews

gas chambers

85
Q

Chronic toxicosis for cyanide toxicity is called what? Is there a chance at recovery? What are the symptoms in Horses, Foals/Calves, pregnant ewes? What is affected in animals

A
  • Lathyrism: neurotoxin (sweet pea)
  • Recovery is possible if caught early
  • Symptoms
    • Horses: skeletal defomities, aortic rupture (sweet pea)
    • Foals/Calves: Skeletal deformities, severe degradation of brain and spinal cord (sorghum spp.)
    • Pregnant ewes: goiter
  • Affected animals- posterior alaxia, urinary incontenance, cystitis
86
Q

What are some symptoms of acute cyanide poisoning?

A
  • Sypmtoms in 15-20 min
    • Clinical signs
      • rapid breathing
      • frothing at the mouth
      • dilated pupils
      • ataxia
      • muscle tremors
      • convulsion
      • regurgitation of rumen contents
    • Sudden death in 1-2 hrs
    • Postmortem signs
      • cherry red blood (venous)
      • dark colored musculature
      • hemorrhage in heart and lungs
      • “bitter almond” smell in rumen
87
Q

What is done to treat cyanide poisoning?

A
  • Sodium Nitrite (NaNO2)
    • generate methemoglobin
    • restart ETC
  • Sodium thiosulfate (NaS2O3)
    • cleaves CN off Hb
    • Converts to sodium thiocynate which is easily excreted
88
Q

How can you prevent cyanide poisoning?

A
  • Avoid NEW growth
  • Graze sorghums/sudangrass/hybrids when over 2 ft tall
  • Rotational grazing and heavy stocking
  • Supplement sulfur to reduce toxicity
  • Adequate phosphorus supply in soils
89
Q

What is missing from the chemical structure?

A

Cyanide

90
Q

“65 cows die of fodder poisoning in Kutch”

Miller fodder from outside area

Gvt. assistance during drough

Distributed all over the area

Drinking water after exposure was determined to be deadly

WHY?

A

Hydrolysis

91
Q

Explain what is shown by this graph. Which treatment is most effective? Why?

A
  • Change in blood cyanide concentrations over time following high cyanide dose and treatment with saline (control), glycine, thiosulfate, or glycine/thiosulfate combo
  • Thiosulfate most effective because exploits natural mechanism of HCN conversion
92
Q

What are two cyanide plants that are grasses? What is the toxin found in them?

A
  1. Johnson grass (Sorghum halepense)
    1. drought resistant perennial
  2. Sudan grass (Sorghum sudenense or bicolor)
    1. annual
  3. Toxin
    1. Dhurrin
    2. Can get cyanide free hybrids (cultivars)
      1. cost: nitrite toxicity
93
Q

Describe the cyanide plant Prunis virginiana and what toxin is found in it?

A

Western chokecherry

  1. Rhizomatus shrub/tree –> 16 ft high
  2. Toxin
    1. Seeds –> amygdalin
    2. Leaves, bark, shoots –> prunasin
      1. 368 mg/100 g in fresh leaves
      2. .25% of BW in <1hr
      3. Important for wildlife
94
Q

Describe the cyanide plant Amelanchier alnifolia and its toxin.

A
  1. Western serviceberry
    1. small shrub/tree–> 22ft tall
  2. Toxin: Prunasin
  3. Not very problematic unless nothing else is available
    1. reclamation, wildlife, watershed, shelter belts
95
Q

Describe the cyanide plant linum lewisii and its toxin.

A
  1. Wild blue flax
    1. perennial subshrub
  2. Toxin: Linarmarin
    1. high in seed and seedling tops (910 mg/100g)
  3. Most problematic
    1. usitatissimum
      1. used for linseed production, pressed for oil and linseed cake is leftover which is often fed to cattle, but MUST be boiled first
96
Q

Describe the cyanide plant Triglochin maritima and its toxin.

A
  1. Arrowgrass
    1. perennial forb/herb
  2. Toxin: Triglochinin
    1. really difficult to ID w/o seeds/flowers
    2. most toxic when green or stressed
    3. 0.25-3# can kill a 600# animal
97
Q

Describe the cyanide plant cercocarpus montanus and its toxin.

A
  1. Mountain mahogany
  2. Toxin: Cyanogenic glycoside
    1. common shrub
    2. deer commonly browse
98
Q

Describe the cyanide plant trifolium repens and its toxin.

A
  1. White clover
  2. Toxin: Linamarin
  3. not palatable in summer
  4. low cyanogenic varieties

Poisonous Plants (8 decks)

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