Range Plants (Western Canada) Flashcards
What is the most poisonous plant in western canada?
western water hemlock
Where is water hemlock and whats the toxic principle? what part?
obligate aquatic plant (marsh)
cicutoxin (long chain unsaturated diol)
young leaves, esp roots and tubers
yellow liquid ("carrot like odor")
What is the MOA of water hemlock? (cicutoxin)?
uncertain
- directly acting neurotoxin
what are the conditions of poisoning of water hemlock?
mistaken for wild carrot/parsnip
early spring
cattle most at risk but all species
toxin active when dry (hay)
What are the clinical signs of water hemlock?
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
What is the Dx of water hemlock?
found dead with struggle history clin path and histopathology rumen contents mouse bioassay of root extract
What is the treatment of water hemlock?
impractical in field but anesthetic dose of barbituates (control seizures) Diazapam not enough avoid exposure (grazing management
Where is yellow star thistle found and whats the toxic principle? what parts of the plant?
aggressive weed (dry conditions) California and interior BC unidentified (in all parts)
What is the MOA of yellow star?
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
what is the toxicity and conditions of yellow star?
signs after continuous grazing for 30d - consumption of BW over weeks/month ONLY EQUIDS - usually forced but can aquire it - toxic when dry (hay)
What are clinical signs of yellow star?
“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
What is the Dx for yellow star?
clinical signs, history, pathology
what is the Tx for yellow star?
S&Scare avoid exposure (grazing managment)
Where is St Johnswort found? whats the toxic principle? significant feature?
roadside/pastures
dry gravel soils
hypericin (fluorescent photodynamic pigment)
in pigmented granules in leaves and flowers
“looks like holes”
Which plant acts in the same way as St Johnswort?
buckweat
What is the MOA of St johnswort (hypericin)?
primary photosensitization (goes to capillaries in skin) lightly pigmented skin (UVA exposure + oxygen = reaction)
What is the toxicity/conditions of St Johnswort?
low levels are toxic (high in young plants, mature foliage, new growth palatable)
- decreases with drying (still toxic)
many species at risk (unpigmented skin)
What are the clinical signs of St Johnswort?
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
What is the Dx of St Johnwort?
clinical signs
history
rule out liver problems
What is the Tx or St Johnswort?
remove, GI decontam, terminate UV exposure
treat skin leasions like burns (antibiotics
antihistamines
What is secondary photosensitization and what plants cause it?
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
What is the toxic principe in Fiddleneck/tansy ragwort? where is it found? what part of plant?
pyrrolizidine alkaloids
in foliage and seeds
invaders in pasture (grain/hay fields)
What is the MOA of Fiddleneck/tansy ragwort?
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
What is the toxicity and conditions of fiddleneck/tansy ragwort?
acute toxicity, chronic more common
cattle and horses
contam of grain, hay or silage
overgrazing risk
what are the clinical signs of fiddleneck/tansy ragwort?
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
what is the Dx and Tx for fiddleneck/tansy ragwort?
clinical signs
Hx
alkaloid screen
pathology
S&S care
prevent
What is the toxic principle of horsetail? where can you find it?
moist meadows, flood plains
thiaminase in non-rum
unknown in rum
What is the MOA of horsetail?
thiaminase splits thiamin into pyrimidine and thiazole rings
- inactivating the vitamin
What is the toxicity and conditions of horse tail?
significant exposure required young horses most at risk ruminants less sensitive pigs also toxic when dry (hay contam)
What are the clinical signs of horsetail?
progressive weight loss, ataxia, staggering, general peresis
progressive rigidity, dyspnea, weak pulse, tremors –> convulsions
recumbancy –> coma –> death
what is the Dx for horsetail?
clinical signs response from treatment
Hx
clin path and histopath
what is the Tx for horsetail?
remove from source
thiamine hydrochloride treatment
What is the toxic principle in bracken fern? where is it found?
eastern manitoba, riding mountains and BC
upland or old burns
Thiaminase in non rum in rum: - aplastic anaemia factor - enzootic hematuria factor - cyanogenic glycoside
what is the MOA of bracken fern?
thiaminase induced thiamine deficiency in non-rum
non-thiaminase in cattle
- toxin acts on bone marrow –> aplastic anemia
- converted to carcinogen in bladder
What is the toxicity/conditions of bracken fern?
prolonged exposure (hay contam)
horses or rum
many species
grazing risk in late summer (thiaminase levels peak)
What are the clinical signs of bracken fern?
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)
What is the Dx of bracken fern?
clinical signs
history of prolonged exposure
clin path
histopath
What is the Tx of bracken fern?
remove source
horses: thiamine hydrochloride treatment
Cattle: S&S care
What is the toxic agent of lupine? Where is it found? defining feature?
teratogenic alkaloid anagyrine
mountain slopes
finger-like leaflets
what is the MOA of lupines?
nicotinic like alkaloids = CNS stim or depres
teratogen anagyrine = arthrogryposis (“crooked calf”)
- sedates them in utero
What causes crooked calf disease?
lupine
teratogen anagyrine
What is the toxicity and conditions of lupines?
sheep - foliage prolonged exposure - seeds very toxic cows - little needed - teratogenic
sheep most often
variation in season
hay contam
seed pods in fall
What are the clinical signs of lupines?
vary
CNS depress
- dyspnea, depression, coma, death from resp paralysis
CNS stim
- trembling, headpressing, teeth grinding, falling, convulsions, death
crooked calf syndrome
what is the Dx for lupines?
clinical signs
Hx
pathology
What is the Tx for lupines?
decontam
S&S care
avoid cattle exposure during peak period (fall)
grazing managment
What is the toxic principle of False Hellebore? where is it found?
rockymountains in wet meadows
steroidal alkaloids teratogenic alkaloids (cycloposine)
What is the MOA of False Hellebore?
MOA for acute uncertain
teratogenic alkaloid
- selective inhibtion of mitosis during cell division (facial or limb deformities
What is the toxicity/condition of False Hellebore?
toxic
teratogenic dose much less
sheep generally only species at risk
- acute greatest risk in spring
- when ewes graze mountain meadows
what are the clinical signs of False Hellebore?
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
What is the Dx of False Hellebore?
clinical signs
Hx
path
congenital defects
What is the Tx of False Hellebore?
GI decontam
S&S care
avoid exposure during spring
What is the toxic principle in ponderosa/western yellow pine? where are they found? what parts?
labdane resic acids isocupressic acid
acetly-ICA
succinyl-ICA
- ICA = abortifacient
rockies and foothills
needles, new growth tips, bark
What is the MOA of ponderosa?
uncertain
What is the toxicity and conditions of ponderosa?
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
what are the clinical signs of ponderosa?
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
What is the Dx of ponderosa?
clin signs (late term abortion)
history
pathology
What is the Tx of ponderosa?
S&S care with cows
avoid exposure during latespring/winter
What is the toxic principle of group 2 astragalus (loco)? where is it found? what part?
dry plains/hill country with alkaline soils
may be indolizidine alkaloid (swainsonine)
foliage
What is the MOA of loco?
swainsonine inhbits saccaride metabolism
- accumulation of oligosaccharides in cells of brain and other organs
- lysosomal storage disease (build up)
What is the toxicity and conditions of loco?
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)
What are the clinical signs of loco?
depression, anorexia, weightloss, trembling, ataxia, excitability
loss of sense of direction and herding instinct (circling, wandering off, attitude/behavioural changes)
abortions and congenital defects
What is the Dx for loco?
clinical signs hx clin path - leukopenia/lymphopenia histopath
What is the treatment for loco?
remove from source
mild cases resolve in 1-2w
chronic never recover
What is the toxic principle of Death Camas? where is it found? what parts?
steroidal alkaloids (all parts)
hillsides to 8000ft
AK and AB
What is the MOA of Death Camas?
inducing arteriole dilation = hypotension
constricts venules
slowing of HR
What is the toxicity/conditions of Death Camas?
interspecies variation
seeds more toxic
bulb highly toxic
confused with wild onion
early spring risk
sheep especially susceptible
toxic when dry
What are the clinical signs of Death Camas?
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
What is the Dx of Death Camas?
clin signs (signs of struggle, foaming)
Hx
alkaloid screen of rumen
path
What is the Tx of Death Camas?
impractical in field
S&S
avoid (grazing managment)
What is the toxic principle in Larkspur? where is it found? what parts?
multiple polycyclic diterpene alkaloids
tall larkspur
- foothills, rockies and interior BC
low larkspur
- S AB and BC
all parts
What is the MOA of Larkspur?
curare-like neuromuscular blocking agent
post synaptic nicotonic cholinergic receptors at NMJ
What is the toxicity/conditions of Larkspur?
varies with species/environ
cattle low dose (tall more common)
sheep and horses less sensitive
risk in hay
What are the clinical signs of Larkspur?
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
What is the Dx of Larkspur?
clin signs
Hx
alkaloid screen
path
What is the Tx of Larkspur?
impractical in field
S&S
avoid exposure
