Test 4: 62: plants Flashcards
cicuta douglasii look like
white flowers in umbel
tuberous root
hollow stem
water hemlock- causes acut death
clinical signs of Cicuta douglasii or C maculata exposure
water hemlock
acute death
cicutoxin- all parts of plant- neurotoxin that causes muscle tremors and convulsions
- Hypersalivation, vigorous chewing and teeth grinding, urination, defecation
- Progressing to ataxia, incoordination, seizures, and lateral recumbency → respiratory paralysis and asphyxia in 2-3 hrs
white flowers, tuberous root, hollow stem
if animals do not die right away form Cicuta gouglasii or C. maculata they can develop
myocardial degeneration and skeletal muscle degneration
water hemlock- tuberous, hollow stem, white flowers
treatment of cicuta douglasii and C. maculata ingestion
no antidote
GI decontamination if early
emesis
rumenotomy
vinegar?
pentobarbital to ↓ seizures
water hemlock: white flowers, tuberous root, hollow stem
conium maculatum
posion hemlock
marshy, moist ground
carrot like root with purple spots
fernlike leaves
white flowers
mouse urine smell
conium maculatum look like
conium maculatum
posion hemlock
marshy, moist ground
carrot like root with purple spots
fernlike leaves
white flowers
mouse urine smell
what kind of toxin for conium maculatum
piperidine alkaloid: coniine and G-coniceine
block spinal cord reflexes: first nicotinic muscle activation then paralysis
acute death
conium maculatum
posion hemlock
marshy, moist ground
carrot like root with purple spots
fernlike leaves
white flowers
mouse urine smell
clinical signs of conium maculatum ingestion
salivation, abdominal pain,
muscle tremors and incoordination Followed by dyspnea, dilated pupils, weak pulse, urination, and defecation
Temporary blindness from prolapsed nictitating membrane
muscle activation → paralysis and respiratory failure and coma: death in 2-3 hrs
small amounts can be teratogenic if cows eat day 40-70 of gestation
conium maculatum
posion hemlock
marshy, moist ground
carrot like root with purple spots
fernlike leaves
white flowers
mouse urine smell
aconitum (monkshood)
sudden death
Restlessness, hypersalivation, muscle weakness, hypotension, dyspnea, and collapse
◦ Ruminants may bloat after becoming laterally recumbent
not required plant
delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur
what does delphinium look like
delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur
toxin of delphinium
diterpenoid alkaloids
MLA
The alkaloids reversibly bind to and
competitively block nicotinic acetylcholine receptors at the neuromuscular junction → muscle weakness and paralysis
similar to nicotine and snake bungarotoxin
delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur
what is toxic window of delphinium
cows really like to eat plant when it is growing or after rainstorm when it is most toxic
try not to let cattle graze duing this time
delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur
clinical signs of delphinium
sudden death
Initial signs in cattle include increased excitability, muscle weakness with stiffness, staggering, and a base-wide stance
NM blockage prevents burbing → bloat → pneumonia
delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur
Hydrogen cyanide (HCN) rapidly inactivates — causing —
cellular respiration causing acute death
binds to cytochrome oxidase and inhibits enzymes needed for cellular respiration
cherry red venous blood
prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass
what needs to happen to cyanogenic glycosides to become toxic
damage to plant cells caused by chewing, crushing, drought, wilting, or freezing
rymen microorganism will turn cyanogenic glycosides into HCN
prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass
clinical signs of cyanogenic glycoside
Sudden death
Early signs include rapid labored breathing, frothing at the mouth, dilated pupils, ataxia, muscle tremors, convulsions, tachycardia +/- arrhythmias
Ruminants regurgitate rumen contents when they become recumbent and bloat
Mucous membranes: bright red to cyanotic in the terminal stages as tissues become oxygen depleted
prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass
bitter almonds odor is
cyanogenic glycosides
prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass
treatment for cyanogenic glycosides
sodium nitrite: converts some hemoglobin to methemoglobin: cyanide will bind to met
sodium thiosulfate: binds to cyanide and form nontoxic product
can give ruminants sodium thiosulfate and vinegar
prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass
how to reduce cyanogenic glycoside ingestion
dont let animals graze after plants are growing, drought or frost
* test for cyanide
* curing will kill cyanide
* purchase low cyanide plants (some sorghum plants)
prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass
how do high dose cardiac glycosides work
Cardiac glycosides inhibit cellular membrane sodium-potassium pumps to deplete intracellular
potassium and increase serum potassium → decreased conductivity → arrhythmias and cardiac block, death
low dose cardiac glycosides
Low doses can have the therapeutic effect of increasing
contractility, decreasing heart rate, and increasing cardiac output
high dose: severe arrhythmias and conduction disturbances leading to death
CG inhibit Na/K pump → ↑ potassium = decreased electrical conductivity and arrythmias
clinical signs of cardiac glycosides
acute death from arrythmias
- Early signs include tachypnea, cold extremities, and rapid weak irregular pulses
- Symptoms rarely persist more than 24 hours before death occurs +/- terminal convulsions
Cattle receiving ionophores are more susceptible to cardiac glycosides
Cattle receiving — are more susceptible to cardiac glycosides
ionophores
how to treat cardiac glycosides
GI decontamination: gastric lavage or vomiting, activated charcoal
treat arrhythmias
check potassium levels
digoxin
asclepias speciosa
milkweed
cardiac glycoside
milkweed:; asclepias
thin or thick leaves
umbels of white or red flowers
seed pod has silky hairs
some have milky sap or latex
what does asclepias look like
milkweed:; asclepias
thin or thick leaves
umbels of white or red flowers
seed pod has silky hairs
some have milky sap or latex
cardiac glycoside
asclepias cause —
cardiac glycoside → arrythmia and death
cardenolides
can also effect respiratory, GI, CNS → dyspnea, colic, diarrhea, muscle tremors, seizures, and head pressing
milkweed: asclepias
thin or thick leaves
umbels of white or red flowers
seed pod has silky hairs
some have milky sap or latex
monarch butterflies retain — from — plants
cardenolides: cardiac glycoside
Birds that eat them experience intense emetic effects and avoid eating monarchs in the future
asclepias (milkweed)
milkweed: asclepias
thin or thick leaves
umbels of white or red flowers
seed pod has silky hairs
some have milky sap or latex
clinical signs of asclepias
acute death
cardiac glycoside → arrythmia and death
cardenolides
can also effect respiratory, GI, CNS → dyspnea, colic, diarrhea, muscle tremors, seizures, and head pressing, inability to stand, dilated pupils
recumbent animals: tetany and chewing movements
milkweed: asclepias
thin or thick leaves
umbels of white or red flowers
seed pod has silky hairs
some have milky sap or latex
convallaria
lily of the valley
seeds have high concentrations of cardenolide cardiac glycosides
skin of fruit and flowers- abdominal pain and diarrhea
not requires
digitalis
floxglove
cardiac glycosides are digoxin, digitoxin, and digitonin, found
in all parts of the plant
NOT REQUIRED
nerium oleander
evergreen
white, pink or red flowers with 5 or more petals
cardiac glycoside
what does nerium oleander look like
nerium oleander
evergreen
white, pink or red flowers with 5 or more petals
25 ft tall
cardiac glycoside
zigadenus
death camas
cardiotoxic- steroidal alkaloids with zygacine and zygadenine
↓BP by dilating arteriols and constricting veins and ↓HR
sheep- salivation, nausea,
vomiting, muscular weakness, and staggering, convulsions, coma and death
not required
taxus: Yew
shrub
red to yellow fruits with single seed (fruit not toxic) all other parts are toxic
cardiotoxic: taxine→ arrhythmias
milk and meat withhold times
Taxus toxicity
cardiogenic
taxine: inhibits Na/Ca exhange in myocardiac cells →arrhythmias
milk from poisoned animals
should not be used for at least 48 hours and animals be withheld from slaughter for 35 days
taxus: Yew
shrub
red to yellow fruits with single seed (fruit not toxic) all other parts are toxic
cardiotoxic: taxine→ arrhythmias
careful of milk and meat
clinical signs of taxus ingestion
cardiogenic → Na/Ca → arrhythmias
sudden muscle tremors, incoordination, nervousness, dyspnea, bradycardia, vomiting, diarrhea, convulsions, and death
Death may occur several days after ingestion, however sudden death may sometimes be the only observed sign
taxus: Yew
shrub
red to yellow fruits with single seed (fruit not toxic) all other parts are toxic
cardiotoxic: taxine→ arrhythmias
milk and meat withhold times
persea- avocado
cardiogenic- myocardium and tissue of lactating mammary gland
- horses: edematous swelling of the lips, mouth, eyelids, head, and neck, leading to upper respiratory distress
- Some horses colic
- pulmonary edema due to cardiomyopathy and heart failure
senecio toxicity
pyrrolizidine alkaloid
liver disease → secondary photosensitization
senecio longilobus
scaggily
pyrrolizidine alkaloid
liver disease → secondary photosensitization
pyrrolizidine alkaloids are found in — will build up in the blood and when exposed to UV light will cause
senecio longilobus
liver damage →phylloerythrin accumulates → secondary
photosensitization → Exposure to UV light causes the phylloerythrin to fluoresce and cause oxidative injury to blood vessels and surrounding
skin tissues
how does pyrrolizidine alkaloids work
PAs are converted to toxic pyrroles
affect the endoplasmic reticulum of liver cells, inhibiting mitosis and the
replication of hepatocytes
senecio longilobus
pyrrolizidine alkaloids →pyrroles →liver disease →photosensitization
clinical signs of pyrrolizidine alkaloids
senecio longilobus
pyrrolizidine alkaloids →pyrroles →liver disease →photosensitization
excessive tearing, and swelling, redness, and increased sensitivity of nonpigmented skin
Affected skin rapidly becomes reddened, painful, and raised, with
serum often oozing through to form crusts in the hair
After 2-3 weeks hair and skin slough off leaving ulcerated areas prone to secondary bacterial infections
Lameness may be seen in horses when the skin over joints and the coronet is affected
Signs of liver disease include jaundice, ascites, diarrhea, tenesmus, and rectal prolapse
Hepatic encephalopathy may result in abnormal behaviors such as yawning, aimless wandering, head pressing, and incessant licking
In severe cases, acute liver failure and death may precede photosensitization
pathologic changes of pyrrolizidine alkaloids
◦ Megalocytosis
◦ Bile duct hyperplasia
◦ Fibrosis
senecio longilobus
pyrrolizidine alkaloids →pyrroles →liver disease →photosensitization
path with Megalocytosis, Bile duct hyperplasia and Fibrosis is suggestive of
pyrrolizidine alkaloids
senecio longilobus
pyrrolizidine alkaloids →pyrroles →liver disease →photosensitization
astragalus and oxytropis spp
locoweed
neurotoxic
astragalus and oxytropis toxicity
neurotoxic
Swainsonine inhibits lysosomal enzymes that aid in saccharide metabolism
α-mannosidase inhibition causes cells(brain and organs) to accumulate complex sugars or oligosaccharides
passed through milk
some animals (horses, cattle and sheep) really like the taste
clinical signs of astragalus and ocytropis exposure
locoweed- neuro toxic
swainsonine → oligosacchardie accumulation
can cause repro issues- abortions, testicular atrophy (rams)
weight loss and ill thrift
horses:
- Depression, circling, incoordination, staggering gait, unpredictable behavior
- Especially when animal is stressed or excited
- Can suddenly rear and fall over backward, making them unsafe to ride
Cattle:
- aggressive and difficult to handle
how to diagnose atragalus and oxytropis
locoweed- neuro toxic
swainsonine → oligosacchardie accumulation
cytoplasmic vacuolation
swainsonine in serum
↓ serum α-mannosidase activity
how to prevent atragalus and oxytropis ingestion in cattle
food aversion
feed locoweed then dose with lithium chloride
eupatorium rugosum
white snakeroot
toxin in eupatorium rugosum
neurotoxin
tremetone- requires microsomal activation to become toxic
causes skeletal and mycocardial degeneration
secreted in milk- milk sickness, trembles
pasteurization does NOT detoxify
white snakeroot
eupatorium
clinical signs of eupatorium rugosum ingestion
neurotoxin- tremetone
Initial signs include listlessness, depression, lethargy, and reluctance to move
* Cattle will develop muscle tremors, signs of colic, constipation, bloody feces, and an acetone odor to the breath
* Tremoring animals show stiffness and eventually become recumbent
* Horses may signs of choking due to paralysis of pharyngeal muscles
* Nursing animals may have milk run out the nostrils
* Dark urine may be observed due to myoglobinuria
treatment for eupatorium rugosum
no specific antidote
supportive care
horses have difficulty swallow- fed by NG tube
discard milk
horse chestnut
aesculus
- neurotoxin- aesculin and fraxin → aglycones in rumen which produce neuro signs- twitching, weakness, hopping gait
- monogastrics- vomit and gastroenteritis
- dorsal- medial stabismus
- severe toxicity- hyperglycemia, glucosuria, and proteinuria
NOT required
nicotiana tabacum
ANS- mimic AcH
Small dose: excitement, tachycardia, salivation, vomiting, colic, and diarrhea. Ruminants may bloat
high dose: neuromuscular blockade with weakness, staggering, collapse, and rapid, weak, irregular heart rates
Very large ingestions rapidly cause respiratory paralysis, blindness, prostration, coma, and death
NOT required
bleeding hearts
Dicentra
neuro toxin
Isoquinoline alkaloids
Cattle may exhibit muscle tremors, running back and forth, and incoordination as “spring staggers”
* Projectile vomiting, convulsions, and lateral recumbency with the head extended back and legs in rigid extension may develop depending on the amount of plant consumed
NOT required
yellow star thistle
centaurea solstitialis
neurotoxin- destroys the dopaminergic nigrostriatal pathway that controls prehension and chewing of food → ↑ risk of aspiration pneumonia
Signs do not occur until large quantities have been eaten for 30-60 days
wooden expression, can’t hold food in mouth, frothy saliva and continual chewing
bilateral liquefactive necrosis in the
globus pallidus and substantia nigra
no treatment- euthanize
NOT REQUIRED
acer
red maple
affect blood and bone marrow
horses: acute hemolytic anemia- weakness, tachypnea, tachycardia, cyanosis, icterus, and red-brown urine, methemoglobinemia, and liver lipidosis and necrosis
diagnostics of acer ingestion
red maple
- markedly reduced hematocrit,
methemoglobinemia, Heinz bodies, and depletion of erythrocyte glutathione - Serum AST, SDH, protein, and bilirubin are usually elevated
horses: acute hemolytic anemia- weakness, tachypnea, tachycardia, cyanosis, icterus, and red-brown urine, methemoglobinemia, and liver lipidosis and necrosis
treatment for acer rubrum
red maple → hemolytic anemia in horses
guarded prognosis
Blood transfusions may be needed to address intravascular hemolysis and coagulopathies
IV fluids
methylene blue?
allium
wild onions, garlic, leeks and chives
bulbs, hollow narrow basal leaves, 6 part flower
attack blood and bone marrow
allium toxicity
blood and BM toxic
- N-propyl disulfide affects glucose-6- phosphate dehydrogenase in RBCs, interfering with the hexose monophosphate pathway
- Insufficient phosphate dehydrogenase or glutathione fails to protect the RBCs from oxidative injury
- Oxidized hemoglobin precipitates to form Heinz bodies
- Affected RBCs are removed from the circulation and anemia results
wild onions, garlic, leeks and chives
clinical signs of allium ingestion
- Dark red-brown urine as hemoglobinuria is usually the first noticeable sign of poisoning
- Affected animals have pale mucous membranes and fast weak pulses, and may be observed staggering and collapsing
- Breath, feces, urine, and milk of affected animals may smell like onions
- Heinz bodies may be observed in cattle even if the amount of onion consumed is not enough to induce anemia and hemoglobinuria
wild onions, garlic, leeks, and chives → anemia and heinz bodies
pteridium aquilinum
bracken fern
blood and BM toxic
Thiaminase splits thiamin (vitamin B1) into its two inactive components
↓ thiamin = white brain matter necrosis and CNS depression
Ptaquiloside is carcinogenic and depresses bone marrow →severe blood loss, anemia, thrombocytopenia, and leukopenia
death from anemai or local tumor invasion around the bladder
horse: muscle tremors, uncoordinated gait and paralysis, anorexia → treat by giving thiamin
not required
dieffenbachia bowmannii
dumbcane
toxic to GI tract
calcium oxalate crystals- When plant cells are broken open or
crushed, needlelike calcium oxalate
raphides are released, penetrating
surrounding soft tissues
Calcium oxalate: philodendron and dieffenbachia
dieffenbachia bowmannii toxicity
dumbcane
GI toxic
calcium oxalate crystals- plant damaged and releases needlelike calcium oxalate raphides that penetrating surrounding soft tissues
rapidly occurring oral pain and
swelling of the lips and tongue
kalmia- laurel
grayanotoxin-
- Water-soluble diterpenoids bind cell membranes, affecting sodium channels and causing prolonged depolarization of cells
- Primary effects are on the heart, nervous system, and GI tract
rhododendron, kalmia, pieris all grayanotoxins
pieris - mountain fetter bush
grayanotoxin-
- Water-soluble diterpenoids bind cell membranes, affecting sodium channels and causing prolonged depolarization of cells
- Primary effects are on the heart, nervous system, and GI tract
rhododendron, kalmia, pieris all grayanotoxins
rhododendron
grayanotoxin-
- Water-soluble diterpenoids bind cell membranes, affecting sodium channels and causing prolonged depolarization of cells
- Primary effects are on the heart, nervous system, and GI tract
rhododendron (azalea), kalmia, pieris all grayanotoxins
rhododendron - azalea
grayanotoxin-
- Water-soluble diterpenoids bind cell membranes, affecting sodium channels and causing prolonged depolarization of cells
- Primary effects are on the heart, nervous system, and GI tract
rhododendron (azalea), kalmia, pieris all grayanotoxins
clinical signs of grayanotoxin exposure
grayanotoxin-
- Water-soluble diterpenoids bind cell membranes, affecting sodium channels and causing prolonged depolarization of cells
- Primary effects are on the heart, nervous system, and GI tract
- Initial GI signs include anorexia, hypersalivation, vomiting, colic, and frequent defecation
- Regurgitated rumen contents may cause aspiration pneumonia
- Severely affected animals develop muscle weakness, bradycardia, cardiac arrhythmias, paralysis, and coma before death
rhododendron (azalea), kalmia, pieris all grayanotoxins
how to treat grayanotoxin exposure
grayanotoxin-
- Water-soluble diterpenoids bind cell membranes, affecting sodium channels and causing prolonged depolarization of cells
- Primary effects are on the heart, nervous system, and GI tract
atropine for ↓HR
early decontamination
rhododendron (azalea), kalmia, pieris all grayanotoxins
Philodendron
toxic to GI tract
calcium oxalate crystals- When plant cells are broken open or
crushed, needlelike calcium oxalate
raphides are released, penetrating
surrounding soft tissues
Calcium oxalate crystals: dieffenbachia bowmannii (dumbcane) and philodendron
arisema- jack in the pulpiy
spathephyllum- peace lily
zantedeshia aethiopica- calla lily
which plants produce calcium oxalate crystals when damaged
Calcium oxalate crystals: dieffenbachia bowmannii (dumbcane) and philodendron
arisema- jack in the pulpiy
spathephyllum- peace lily
zantedeshia aethiopica- calla lily
solanum nigrum
black nightshade
tropane alkaloids- competitively inhibit acetylcholine at postganglionic parasympathetic
neuroeffector sites
This results in
* Decreased salivation and intestinal motility → colic, constipation or hemorrhagic diarrhea
* Dilated pupils
* Tachycardia
potato is a type of nightshade!
solanum dulcamera
bittersweet nightshade
tropane alkaloids- competitively inhibit acetylcholine at postganglionic parasympathetic
neuroeffector sites
This results in
* Decreased salivation and intestinal motility → colic, constipation or hemorrhagic diarrhea
* Dilated pupils
* Tachycardia
solanum tuberosum
potato
tropane alkaloids- competitively inhibit acetylcholine at postganglionic parasympathetic
neuroeffector sites
This results in
* Decreased salivation and intestinal motility → colic, constipation or hemorrhagic diarrhea
* Dilated pupils
* Tachycardia
solanum toxicity
night shades- potatoes ?!
tropane alkaloids- competitively inhibit acetylcholine at postganglionic parasympathetic
neuroeffector sites
This results in
* Decreased salivation and intestinal motility → colic, constipation or hemorrhagic diarrhea
* Dilated pupils
* Tachycardia
podophyllum peltatum
mayapple
not required
phytolacca americana
pokeweed
oral irritation, hypersalivation, vomiting, colic, bloody diarrhea, depression, prostration, and death (rare)
not required
juglans nigra
black walnut
toxic to muscles →vasoconstriction of blood vessels in the presence of catecholamines and corticosteroids
laminitis in horses
◦ Depression, edema of the lower legs, lameness, colic, and respiratory distress
walnuts can get moldy and get tremorgenic mycotoxin penitrem A
juglans nigra toxicity
black walnut → muscle toxic
walnuts can get moldy → tremorgenic mycotoxin penitrem A
Wood shavings used as bedding causes laminitis in horses
◦ Depression, edema of the lower legs, lameness, colic, and respiratory distress
vasoconstriction of blood vessels in the presence of catecholamines and corticosteroids
beteroa incana
hoary alyssum
muscle toxic
horse- laminitis and limb edema
abortion
not required
hypericum perforatum
st johns wort
skin and integument toxic
not required
vicia villosa
hairy vetch
skin and integument toxic
not required
— plant makes oxalate poisoning that attacks UT
amaranthus
red rooted pigweed
amaranthus toxicity
attack urinary tract
oxalate poisoning
oxalate crystals rapidly combine with serum calcium and magnesium
* Sudden hypocalcemia in the acute phase of poisoning impairs normal cell membrane
function
* Animals develop muscle tremors and weakness, collapse, and eventually die
* Oxalates also interfere with cellular energy metabolism
* In chronic poisoning, death results from kidney failure due to oxalate nephrosis
Perirenal edema is a characteristic lesion in pigs and cattle consuming —
Amaranthus
oxalate poisoning →urinary system
binds to calcium and magnesium → impairs cell membrane function and cellular metabolism → kidney failure from oxalate nephrosis and death
oxalate poisoning treatment
amaranthus
binds to calcium
giving calcium does not help
oral limewater Ca(OH)2 can prevent further absorption
high levels of dietary calcium in a salt mix or pelleted alfala bind oxalate in the rumen
lilium
kidney toxic in cats-
- Vomiting, anorexia, and depression can first develop within 2 hours of exposure
- Anorexia and depression continue as BUN, creatinine, potassium, and phosphorus rise 24-72 hours after exposure
- Creatinine is often disproportionately higher than
BUN
quercus
oak
effect urinary system
Gallotannins are hydrolyzed in the rumen to smaller compounds that react with cell proteins, denaturing them and causing cell death
not required
symptoms of quercus ingestion
oak
Animals stop eating, become depressed, and develop intestinal stasis
* PU/PD
* Hard dark feces may later turn into black tarry diarrhea
* Teething grinding and hunched back may be an indication of abdominal pain
* Mucoid hemorrhagic gastroenteritis
* Hemorrhages on various organs
* Fluid in peritoneal and pleural spaces
* Pale, swollen kidneys covered with small hemorrhages
* Renal tubular necrosis and liver necrosis are characteristic
treatment for quercus ingestion
oak
attack renal system
fresh food and water
Oral calcium hydroxide can help neutralize residual tannic acid in the rumen
IV fluids
lupinus
repro toxic
quinolizidine( Anagyrine) and piperidine alkaloids in all plant parts
Lupinosis is a severe liver, kidney, and muscle disease associated with a phomopsin-producing fungus
crooked calf disease
lupinus toxicity
repro toxic
quinolizidine( Anagyrine) and piperidine alkaloids in all plant parts
crooked calf disease-
- front leg Limb deformities – arthrogryposis
- Vertebral column malformation – scoliosis, kyphosis, torticollis
- Cleft palate
pinus ponderosa
repro toxic
Isocupressic acid causes premature parturition or abortion in cattle
toxicity of pinus ponderosa
repro toxic
Isocupressic acid causes premature parturition or abortion in cattle
- Marked decrease in uterine blood flow due to vasoconstriction
- Progesterone levels progressively decline due to necrosis of the corpus luteum
- edematous swelling of the
vulva and udder and a mucoid vaginal discharge before premature parturition or abortion → difficult delivery - cow produce little to no colostrum
veratrum californicum
western false hellebore
moutain meadows > 8500 ft
repro toxic
clinical signs of veratrum californicum ingestion
western false hellebore
repro toxic
cyclopia
shortened legs and tracheal agenesis
moutain meadows
robinia toxicity
black locust
lectins in beans
affect GI tract
inhibit cellular protein synthesis in ribosomes
- Anorexia and severe hemorrhagic diarrhea develop within several days of consuming a toxic dose
- Progresses to dehydration and hypovolemic shock
- Horses may develop dilated pupils and cardiac arrhythmias
- Serum chemistry results reflect fluid and electrolyte loss and organ dysfunction
clinical signs of robinia ingestion
black locust
lectins in beans
affect GI tract
inhibit cellular protein synthesis in ribosomes
- Anorexia and severe hemorrhagic diarrhea develop within several days of consuming a toxic dose
- Progresses to dehydration and hypovolemic shock
- Horses may develop dilated pupils and cardiac arrhythmias
- Serum chemistry results reflect fluid and electrolyte loss and organ dysfunction
