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Toxicology > Range Plants (Western Canada) > Flashcards

Range Plants (Western Canada) Flashcards

1
Q

What is the most poisonous plant in western canada?

A

western water hemlock

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2
Q

Where is water hemlock and whats the toxic principle? what part?

A

obligate aquatic plant (marsh)
cicutoxin (long chain unsaturated diol)

young leaves, esp roots and tubers
yellow liquid ("carrot like odor")
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3
Q

What is the MOA of water hemlock? (cicutoxin)?

A

uncertain

- directly acting neurotoxin

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4
Q

what are the conditions of poisoning of water hemlock?

A

mistaken for wild carrot/parsnip
early spring
cattle most at risk but all species
toxin active when dry (hay)

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5
Q

What are the clinical signs of water hemlock?

A 
rapid onset (10-15mins)
violent
found dead
salivation, apprehension, muscle twitching, jaw clamping/teeth grinding
CNS stim
- spasmodic jerking, running fits
- horse will "back up weird"
clonic/tonic seizures --> coma
resp paralysis within 45-90min
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6
Q

What is the Dx of water hemlock?

A 
found dead with struggle
history
clin path and histopathology
rumen contents
mouse bioassay of root extract
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7
Q

What is the treatment of water hemlock?

A 
impractical in field but anesthetic dose of barbituates (control seizures) Diazapam not enough
avoid exposure (grazing management
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8
Q

Where is yellow star thistle found and whats the toxic principle? what parts of the plant?

A 
aggressive weed (dry conditions)
California and interior BC
unidentified (in all parts)
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9
Q

What is the MOA of yellow star?

A

may be dopaminergic neurotoxin

  • acts to destory the dopaminergic nigrostriatal pathway (cerebral cortical pathway) involving CN 5, 7, 9
  • loss of neural connections
  • ischemic necrosis of substantia nigra and globus pallidus in brain
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10
Q

what is the toxicity and conditions of yellow star?

A 
signs after continuous grazing for 30d
- consumption of BW over weeks/month
ONLY EQUIDS
- usually forced but can aquire it
- toxic when dry (hay)
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11
Q

What are clinical signs of yellow star?

A

“equine parkinsons”
“chewing disease”

sudden onset after prolonged exposure
reflect necrosis of nuclei in brain
- hypertonicity of facial muscles, lower lip hand, paralysis of tongue (not flaccid) , yawning, head tossing, walk with head down
- chewing movements but cant chew food
- feed drops out
- cant drink (lip muscles)
emaciation, starvation, death
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12
Q

What is the Dx for yellow star?

A

clinical signs, history, pathology

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13
Q

what is the Tx for yellow star?

A 
S&Scare
avoid exposure (grazing managment)
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14
Q

Where is St Johnswort found? whats the toxic principle? significant feature?

A

roadside/pastures
dry gravel soils

hypericin (fluorescent photodynamic pigment)
in pigmented granules in leaves and flowers
“looks like holes”

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15
Q

Which plant acts in the same way as St Johnswort?

A

buckweat

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16
Q

What is the MOA of St johnswort (hypericin)?

A 
primary photosensitization (goes to capillaries in skin)
lightly pigmented skin (UVA exposure + oxygen = reaction)
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17
Q

What is the toxicity/conditions of St Johnswort?

A

low levels are toxic (high in young plants, mature foliage, new growth palatable)
- decreases with drying (still toxic)
many species at risk (unpigmented skin)

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18
Q

What are the clinical signs of St Johnswort?

A

appear within 24h
erythema of non-pigmented skin –> edema –> vesicles –> necrosis
tachycardia, tachypnea, pyrexia, salivation, diarrhea
erythema of conjuctival and buccal MM (blindness, feed refusal)
Shock, hypotension, convulsions, death

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19
Q

What is the Dx of St Johnwort?

A

clinical signs
history
rule out liver problems

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20
Q

What is the Tx or St Johnswort?

A

remove, GI decontam, terminate UV exposure
treat skin leasions like burns (antibiotics
antihistamines

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21
Q

What is secondary photosensitization and what plants cause it?

A

coal oil brush, lupin, flix weed, rape

agent is based on metablism of chlorophyl

  • converted to polyurethrine in the liver
  • liver damage can build up toxin
  • common in cattle
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22
Q

What is the toxic principe in Fiddleneck/tansy ragwort? where is it found? what part of plant?

A

pyrrolizidine alkaloids
in foliage and seeds

invaders in pasture (grain/hay fields)

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23
Q

What is the MOA of Fiddleneck/tansy ragwort?

A

toxin enters portal circ –> metabolized by P1 enzymes to pyrrole derivatives which bind cellular macromolecules DNA adducts –> impaired cell division –> hepatocytomegaly cell death –> hepatic necrosis, bile duct proliferation –> decreased liver function/failure

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24
Q

What is the toxicity and conditions of fiddleneck/tansy ragwort?

A

acute toxicity, chronic more common

cattle and horses
contam of grain, hay or silage
overgrazing risk

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25
Q

what are the clinical signs of fiddleneck/tansy ragwort?

A

hepatic insufficiency suddenly

horses: cachexia +/- icterus, sleepy staggers “hepatic coma”, delirium death

Cattle: nervousness, mania, colic, diarrhea, tenesmus, rectal prolapse, hepatogenous photosensitization, death

high doses –> hepatic necrosis and acute death

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26
Q

what is the Dx and Tx for fiddleneck/tansy ragwort?

A

clinical signs
Hx
alkaloid screen
pathology

S&S care
prevent

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27
Q

What is the toxic principle of horsetail? where can you find it?

A

moist meadows, flood plains

thiaminase in non-rum
unknown in rum

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28
Q

What is the MOA of horsetail?

A

thiaminase splits thiamin into pyrimidine and thiazole rings

- inactivating the vitamin

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29
Q

What is the toxicity and conditions of horse tail?

A 
significant exposure required
young horses most at risk
ruminants less sensitive
pigs also
toxic when dry (hay contam)
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30
Q

What are the clinical signs of horsetail?

A

progressive weight loss, ataxia, staggering, general peresis
progressive rigidity, dyspnea, weak pulse, tremors –> convulsions
recumbancy –> coma –> death

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31
Q

what is the Dx for horsetail?

A

clinical signs response from treatment
Hx
clin path and histopath

32
Q

what is the Tx for horsetail?

A

remove from source

thiamine hydrochloride treatment

33
Q

What is the toxic principle in bracken fern? where is it found?

A

eastern manitoba, riding mountains and BC
upland or old burns

Thiaminase in non rum
in rum:
- aplastic anaemia factor
- enzootic hematuria factor
- cyanogenic glycoside
34
Q

what is the MOA of bracken fern?

A

thiaminase induced thiamine deficiency in non-rum
non-thiaminase in cattle
- toxin acts on bone marrow –> aplastic anemia
- converted to carcinogen in bladder

35
Q

What is the toxicity/conditions of bracken fern?

A

prolonged exposure (hay contam)
horses or rum
many species
grazing risk in late summer (thiaminase levels peak)

36
Q

What are the clinical signs of bracken fern?

A

monogastrics
- progressive cahcexia and neuro signs (ataxia, stance, knuckling, tremors, recumbancy, convulsions, death)

Ruminants:

  • aplastic anemia/acute hemorrhage syndrome
  • depression pyrexia, anorexia, emaciation, widespread hemorrhage
  • death 4-8d later
  • neoplastic syndrome/enzootic hematuria (latent months years) - bladder transitional cell carcinoma (bleed)
37
Q

What is the Dx of bracken fern?

A

clinical signs
history of prolonged exposure
clin path
histopath

38
Q

What is the Tx of bracken fern?

A

remove source
horses: thiamine hydrochloride treatment
Cattle: S&S care

39
Q

What is the toxic agent of lupine? Where is it found? defining feature?

A

teratogenic alkaloid anagyrine

mountain slopes

finger-like leaflets

40
Q

what is the MOA of lupines?

A

nicotinic like alkaloids = CNS stim or depres
teratogen anagyrine = arthrogryposis (“crooked calf”)
- sedates them in utero

41
Q

What causes crooked calf disease?

A

lupine

teratogen anagyrine

42
Q

What is the toxicity and conditions of lupines?

A 
sheep
- foliage prolonged exposure
- seeds very toxic
cows
- little needed
- teratogenic

sheep most often
variation in season
hay contam
seed pods in fall

43
Q

What are the clinical signs of lupines?

A

vary

CNS depress
- dyspnea, depression, coma, death from resp paralysis
CNS stim
- trembling, headpressing, teeth grinding, falling, convulsions, death
crooked calf syndrome

44
Q

what is the Dx for lupines?

A

clinical signs
Hx
pathology

45
Q

What is the Tx for lupines?

A

decontam
S&S care
avoid cattle exposure during peak period (fall)
grazing managment

46
Q

What is the toxic principle of False Hellebore? where is it found?

A

rockymountains in wet meadows

steroidal alkaloids
teratogenic alkaloids (cycloposine)
47
Q

What is the MOA of False Hellebore?

A

MOA for acute uncertain
teratogenic alkaloid
- selective inhibtion of mitosis during cell division (facial or limb deformities

48
Q

What is the toxicity/condition of False Hellebore?

A

toxic
teratogenic dose much less

sheep generally only species at risk

  • acute greatest risk in spring
  • when ewes graze mountain meadows
49
Q

what are the clinical signs of False Hellebore?

A

acute syndrome
- 2-3h
- salivation, vomiting, diarrhea, weakness, ataxia, bradycardia, cyanosis, recumbancy, convulsions, paralysis
- death in 6-18h
Teratogenic
- cyclopean malformations + fetal pituitary gland –> prolonged gestation (24-30d)
- cleft palate (25-36d)
- hypoplasia of metacarpals and metatarsals
- tracheal stenosis

50
Q

What is the Dx of False Hellebore?

A

clinical signs
Hx
path
congenital defects

51
Q

What is the Tx of False Hellebore?

A

GI decontam
S&S care
avoid exposure during spring

52
Q

What is the toxic principle in ponderosa/western yellow pine? where are they found? what parts?

A

labdane resic acids isocupressic acid
acetly-ICA
succinyl-ICA
- ICA = abortifacient

rockies and foothills

needles, new growth tips, bark

53
Q

What is the MOA of ponderosa?

A

uncertain

54
Q

What is the toxicity and conditions of ponderosa?

A

for 3 days in last trimester = abortion
cattle may abort after single feeding

cattle, bison, llamas sensitive during last trimester
horses and other rum resistant

risk in late winter/spring = forces cattle to eat
dried or green

55
Q

what are the clinical signs of ponderosa?

A

abortion 48h to 2w after exposure

  • depression, edema of vulva and udder, bloody discharge, weak uterine contractions, incomplete cervical dilation
  • aborted fetus may be autolyzed
  • retained placenta and metritis common
  • live calves born weak will die
56
Q

What is the Dx of ponderosa?

A

clin signs (late term abortion)
history
pathology

57
Q

What is the Tx of ponderosa?

A

S&S care with cows

avoid exposure during latespring/winter

58
Q

What is the toxic principle of group 2 astragalus (loco)? where is it found? what part?

A

dry plains/hill country with alkaline soils

may be indolizidine alkaloid (swainsonine)

foliage

59
Q

What is the MOA of loco?

A

swainsonine inhbits saccaride metabolism

  • accumulation of oligosaccharides in cells of brain and other organs
  • lysosomal storage disease (build up)
60
Q

What is the toxicity and conditions of loco?

A

varies
typically prolonged exposure (but not high doses)
sheep it takes a lot
horses most sensitive

can get habituated, young animals (passed in milk, affects maturing neurons)

61
Q

What are the clinical signs of loco?

A

depression, anorexia, weightloss, trembling, ataxia, excitability
loss of sense of direction and herding instinct (circling, wandering off, attitude/behavioural changes)
abortions and congenital defects

62
Q

What is the Dx for loco?

A 
clinical signs
hx
clin path
- leukopenia/lymphopenia
histopath
63
Q

What is the treatment for loco?

A

remove from source
mild cases resolve in 1-2w
chronic never recover

64
Q

What is the toxic principle of Death Camas? where is it found? what parts?

A

steroidal alkaloids (all parts)

hillsides to 8000ft
AK and AB

65
Q

What is the MOA of Death Camas?

A

inducing arteriole dilation = hypotension
constricts venules
slowing of HR

66
Q

What is the toxicity/conditions of Death Camas?

A

interspecies variation
seeds more toxic
bulb highly toxic

confused with wild onion
early spring risk
sheep especially susceptible
toxic when dry

67
Q

What are the clinical signs of Death Camas?

A

often found dead
signs within 1-2h
salivation, colic, vomiting, tachypnea, trembling, ataxia, pulse weak, rapid, irregular hypothermia
weakness > depression > recumbancy > coma
agonal struggling/jaw clamping

68
Q

What is the Dx of Death Camas?

A

clin signs (signs of struggle, foaming)
Hx
alkaloid screen of rumen
path

69
Q

What is the Tx of Death Camas?

A

impractical in field
S&S
avoid (grazing managment)

70
Q

What is the toxic principle in Larkspur? where is it found? what parts?

A

multiple polycyclic diterpene alkaloids

tall larkspur
- foothills, rockies and interior BC
low larkspur
- S AB and BC

all parts

71
Q

What is the MOA of Larkspur?

A

curare-like neuromuscular blocking agent

post synaptic nicotonic cholinergic receptors at NMJ

72
Q

What is the toxicity/conditions of Larkspur?

A

varies with species/environ
cattle low dose (tall more common)

sheep and horses less sensitive
risk in hay

73
Q

What are the clinical signs of Larkspur?

A

rapid course often dead

nervous signs
- excitability, nervousness, disorientation, stiffness, muscle tremors, loss of motor control, convulsions, fall downhill

resp depression, bradycardia, hypotension, death from resp paralysis or bloat (within 3-4h)

milder cases = GI signs and bloat

74
Q

What is the Dx of Larkspur?

A

clin signs
Hx
alkaloid screen
path

75
Q

What is the Tx of Larkspur?

A

impractical in field
S&S
avoid exposure

Toxicology (27 decks)

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