Unit 2 - Toxic Plants in Large Animals I Flashcards
1
Q
What species are affected by Yellow Star thistle/Russian knapweed toxicosis?
A
Horses only
2
Q
T/F: Fresh or dried Yellow Star Thistle is toxic.
A
True
3
Q
What is the indicated toxic principle of Yellow Star Thistle?
A
Sequiterpine lactones
4
Q
What do sesquiterpine lactones do?
A
Depletes glutathione which results in oxidative damage, mitochondrial dysfunction and neuronal death
5
Q
What clinical signs are associated with Yellow Star thistle toxicosis?
A
Involuntary chewing moments, food falling from mouth
Depression
Inability to eat
6
Q
How is Yellow Star thistle toxicosis diagnosed?
A
Clinical signs
History of exposure
7
Q
What is necessary for horses to get Yellow Star thistle toxicosis?
A
They need to have an extended period of consumption - high intake over 30+ days
8
Q
What lesion does Yellow Star thistle cause?
A
Nigropallidal encephalomalacia
9
Q
How is Yellow Star thistle toxicosis treated?
A
There is no treatment - euthanasia is recommended
10
Q
When do perennials grow?
A
In spring/summer
11
Q
T/F: Locoweed or milkvetch is typically eaten when other forages are not present.
A
False - it is palatable and nutritious and may be eaten even when other forages are present
12
Q
What is the toxic principle of locoweeds?
A
Indolizidine alkaloid -Swainsonine
13
Q
Where is swainsonine located in locoweeds?
A
In all parts of the plant - it is highest in leaves, flowers, and seedpods
14
Q
Swainsonine is ______ absorbed, crosses the _____, is secreted in _____, and excreted _______ in ________.
A
Rapidly placenta milk unchanged urine
15
Q
What is the MOA of swainsonine?
A
- Inhibits alpha-D-mannosidase and Golgi mannosidase II
- Accumulation of oligosaccharides in lysosomes of cells in the brain and other tissues
- Generalized lysosomal storage disease ensues
16
Q
What species are affected by locoweed toxicosis?
A
Cattle, horses, sheep, goats, and elk
17
Q
When do clinical signs due to Locoweed toxicosis occur?
A
After several weeks of consumption
18
Q
How do sheep with Locoweed toxicosis typically appear?
A
Blind with stargazing behavior
19
Q
What clinical signs are associated with Locoweed toxicosis in horses?
A
Neurologic signs - depression, procioceptive deficits, circling, ataxia, and falling over backwards
20
Q
What clinical signs are associated with Locoweed toxicosis in cattle and sheep?
A
Reproductive problems - abortions, fetal resorption, skeletal malformations, testicular atrophy, and decreased spermatogenesis
21
Q
What lesions are associated with Locoweed toxicosis?
A
Vacuolation of neurons, renal tubular epithelia, and macrophages
22
Q
What species are affected by Jimson weed?
A
All species - pigs and horses are worse
23
Q
What do Jimson weed plants look like?
A
2-5 feed high with simple irregular toothed leaves
Tubular flowers with 2-4
24
Q
T/F: Jimson weed is normally palatable
A
True
25
What part of Jimson weed is toxic?
The entire plant - but it is concentrated in seeds
26
What is the toxic principle of Jimson weed?
Tropane alkaloid
27
What is the MOA of tropane alkaloid?
Anticholinergic effects at muscarinic receptors in the CNS
28
Jimson weed appears like an ______ overdose.
Atropine
29
What clinical signs are associated with Jimson weed toxicosis?
Reduced secretions
Mydriasis/blindness
Muscle twitching, incoordination, paralysis
GI stasis, tachycardia, urine retention
30
How is Jimson weed toxicosis treated?
Physostigmine
31
What other plants have similar effects to Jimson weed?
Mandrake and deadly nightshade
32
What do lupine and bluebonnet look like?
Flowers are generally blue, but yellow or white in some species
33
What are the toxic principles of lupine?
Quinolizidine alkaloids - Lupanine and anagyrine
34
What does Lupanine do?
Bind nicotinic and muscarinic receptors
35
What does Anagyrine do?
Teratogenic alkaloid in cattle
36
When do clinical signs due to Lupine/Blue bonnet toxicosis occur?
Within 1-3 hours post ingestion
37
What clinical signs are associated with Lupine/Blue bonnet toxicosis in sheep?
```
Labored breathing pattern
Depression, salivation, ataxia
Clonic spasms, head pressing, tremors, seizures and coma
Death due to respiratory paralysis
+/- transient excitement/aggression
```
38
What clinical signs are associated with lupine/blue bonnet toxicosis in cattle?
Salivation/bruxism
| Congenital defects
39
When during gestation does eating lupine/blue bonnet toxicosis result in congenital defects in cattle?
38-70 days
40
What congenital defects are associated with Lupine/blue bonnet toxicosis?
Misaligned joints/arthrogryposis
| Neck, back, and cleft palate
41
What are the features of poison hemlock?
Hollow stems and parsely-like alternate, dissected leaves
| Flowers occur in small, white, umbrella-shaped clustures
42
What is the toxic principle for poison hemlock?
Piperidine alkaloids
43
What do piperidine alkaloids do?
Initial stimulation followed by severe depression of neuromuscular junctions and autonomic ganglia
44
What components of the poison hemlock plant are toxic?
Toxins are highest in root, vegetative parts in spring, and decrease in summer
45
When do clinical signs due to poison hemlock occur?
Within 1 hour of consumption
46
What clinical signs are associated with poison hemlock toxicosis?
Death from respiratory failure
Salivation, abdominal pain, muscle tremors, and incoordination
Dilated pupils, prolapse of nictitating membrane
Weak pulse
Frequent urination and defecation
Coma without convulsions
47
How is poison hemlock toxicosis diagnosed?
Detection of alkaloid in stomach content, serum, and urine
48
How is poison hemlock toxicosis treated?
Emetics/cathartics early are important
Mineral oil or charcoal
Maintain airway. respiratory support
49
What species are susceptible to water hemlock toxicosis?
Cattle, horses, sheep, and people
50
What does water hemlock look like?
Two to eight, thick, tuberous roots
Alternate leaves with toothed edges
White flowers
51
What is the toxic principle of water hemlock?
Aliphatic alcohol
52
What is the MOA of aliphatic alcohol?
Blocks GABA receptors
53
What parts of water hemlock are toxic?
Roots, young leaves
54
What clinical signs are associated with water hemlock toxicosis?
Chewing, teeth grinding, ataxia
Progress to violent seizures
Rapid death
55
How is water hemlock toxicosis diagnosed?
plant ID and confirmed consumption
56
How is water hemlock toxicosis treated?
Generally not feasible
57
What is the toxic principle of Larkspur?
Diterpene alkaloids
58
What species are susceptible to Larkspur toxicosis? Resistant?
Susceptible - cattle, rarely horses
| Resistant - sheep/goats
59
Tall larkspur has (low/high) toxicity when young, but (low/high) palatability. When it is mature it is the exact opposite.
high; low
60
What is the MOA of Larkspur toxicosis?
Blocks the action of nicotinic acetylcholine receptors within CNS and NM junctions
61
When is the greatest risk of Larkspur toxicosis?
During flowering and fruit formation
62
What clinical signs are associated with Larkspur toxicosis?
Sudden death
Stiffness, weakness, staggering, ataxia, paralysis, tremors, recumbence
Impaired eructation
63
How is Larkspur toxicosis treated?
With a cholinesterase inhibitor - Physostigmine
| Manage bloat
64
How is Larkspur toxicosis managed/prevented?
Large flocks of sheep can be used to trample
| or eat larkspur before bringing in cattle to graze
65
What species are affected by milkweed?
Cattle, horses, and small ruminants
66
What is the toxic principle of milkweed?
Cardiac glycosides
67
What is the MOA of cardiac glycosides?
They inhibit Na/K ATPase pumps affecting myocardial conduction and contractility
Certain species produce a neurotoxin
68
What part of the milkweed is toxic?
All parts, green or dry
69
What clinical signs are associated with milkweed toxicosis?
Staggering, weakness, muscle fasciculation, SEIZURES
Colic/bloat, excess salivation, dyspnea, mydriasis
Rapid, weak pulse
Coma, death
70
How is milkweed toxicosis diagnosed?
Identifying plants in the rumen
71
What does white snakeroot look like?
2-4 feet tall
heart-shaped, 3-6 inch serrated leaves
crowned with composite flowers
72
What is the toxic principle of white snakeroot?
Tremetone
73
Tremetone is toxic when ______, secreted in ______, and induces _______.
Dried
milk
myonecrosis
74
T/F: Toxic effects of white snakeroot are cumulative
True
75
What clinical signs are associated with white snakeroot toxicosis?
```
Reluctance to move/sluggish behavior
Muscle tremors
CRT >3 sec
Dark urine: myoglobin
Acetone odor to breath
```
76
What additional clinical signs do horses show with white snakeroot toxicosis?
Sweating, jugular pulses, arrythmia
77
What laboratory findings are associated with snakeroot toxicosis?
Myoglobinuria, elevated CK, elevated liver enzymes (AST and ALT)
78
How is white snakeroot toxicosis treated?
```
Detox with charcoal and cathartics
Good nursing care and nutrition
Treat cattle for ketosis
Avoid consumption of milk
Monitor EKG in horses
```
79
What species are susceptible to the Yew plant?
All
80
What does the Yew plant look like?
Common ornamental evergreen shrub - small, flat lanceolate leaves and seed cones with a fleshy red covering
81
What is the toxic agent of the Yew plant?
Taxine alkaloids
82
Where are taxine alkaloids located in the Yew plant?
Bark, leaves, and seeds
| It is higher in older leaves
83
What part of the Yew is highly toxic if chewed?
The seeds
84
What is the suspected MOA of Yew?
Depress conduction or depolarization - direct action on cardiac myocyte ion channels
85
Most cases of Yew toxicosis occur due to what?
Clippings from bushes
86
When is the onset of clinical signs do to Yew toxicosis?
Onset 2-4 hours post ingestion in ruminants
87
What may be the only sign of Yew toxicosis?
Sudden death may be the only sign
88
What clinical signs, if they occur, are associated with Yew toxicosis?
Nervous signs including trembling, dyspnea, incoordination, reluctance to move, and collapse
Acute cardiac failure - bradycardia and jugular pulses
Gastroenteritis and diarrhea
89
How is yew toxicosis diagnosed?
Presence of yew leaves in rumen or stomach
Microscopic exam of stomach contents
Chemical assay
90
What is the prognosis for yew toxicosis?
Guarded to grave
91
How is yew toxicosis treated?
Activated charcoal +/- cathartic
Rumen lavage or rumenotomy and removal of rumen content
Atropine for bradycardia
92
What species are affected by Red maple toxicosis?
Horses
93
What is the toxic principle of red maple?
Tannic acid
94
Where is tannic acid found?
In wilted or dried red maple leaves
95
What is the MOA of tannic acid?
It is converted into gallic acid into the ileum and then to pyrogallol
Pyrogallol is absorbed into the blood stream causing methemoglobinemia
96
What does red maple toxicosis induce?
Heinz body formation
Methemoglobinemia
Intravascular hemolysis
97
What clinical signs are associated with red maple toxicosis?
```
Weakness
Tachypnea
Tachycardia
Icterus
Cyanosis
Hemoglobinuria
```
98
How is red maple toxicosis treated?
History of exposure
Clinical signs
Laboratory findings
99
How is red maple toxicosis treated?
IV fluids
Oxygen
Blood transfusion
100
What is the toxic principle of rapeseed and kale?
Dimethyl disulfide
101
What species are affected by rapeseed or kale toxicosis?
cows
102
What is the MOA of dimethyl disulfide?
1. Oxidizes hemoglobin
2. Heinz body formatino
3. Hemolytic anemia
103
What clinical signs are associated with kale or rapeseed toxicosis?
The same as Red maple or allium
Diagnostics and treatment is the same
104
What species are affected by sorghum and sudan grass toxicosis?
Ruminants
105
What is the toxic prinicple of Sorghum and sudan grass?
Dhurrin
106
What is the amount of Dhurrin dependent on?
Climate, stage of growth, speed of growth, and fertility of plant
107
Where is the highest concentration of Dhurrin?
In leaves
108
What is the MOA of dhurrin?
1. Damage to plant cells
2. Enzymes convert non-toxic dhurrin to toxic prussic acid
3. Prussic acid is absorbed into the blood stream
4. Cells cannot utilize oxygen
109
What clinical signs are associated with Sorghum and Sudan grass toxicosis?
Tachypnea, tachycardia, dyspnea, and arrhythmia
Collapse, bright red mucus membrane
Trembling, spasms, convulsions, death from respiratory paralyssi
110
How is Sorghum and Sudan grass toxicosis diagnosed?
History of recent exposure and clinical signs
Detection of cyanide in rumen/blood/feed
Detection of thiocyanate in urine
111
How is Sorghum and sudan grass toxicosis treated?
Amyl nitrate (inhaled) + Sodium nitrite (IV, fast) + sodium thiosulfate (IV, slow) + sodium thiosulfate (oral
112
What are some other options for Sorghum and Sudan grass toxicosis treatment?
Hydroxycobalamin, 4-DMAP, EDTA, and Methylene blue
113
What species are susceptible to bracken fern toxicosis?
Cattle and sheep
| Pigs, horses, and other species are also susceptible
114
When does bracken fern toxicosis typically occur?
In times of drought where better forages are not available
115
Disease due to bracken fern is dependent on _____, _____, and the _____ affected.
Dose, duration, species
116
What are the forms of disease caused by bracken fern toxicosis?
```
Bone marrow aplasia/anemia
Enzootic hematuria
Bracken staggers
Bright blindness
Chronic low-level exposure
```
117
What laboratory findings are associated with bracken fern bone marrow aplasia/anemia?
Thrombocytopenia, anemia, and neutropenia
118
Bracken fern bone marrow aplasia/anemia mostly affects ______ that have had _______ consumption in a _____ period of time.
Cattle
Heavy
short
119
What is the toxic principle for all forms of bracken fern toxicois?
Ptaquiloside
120
What species are affected by enzootic hematuria?
Cattle and sheep
121
T/F: Enzootic hematuria due to bracken fern toxicosis is rapid and due to little exposure
False - it requires prolonged exposure
122
Bracken staggers is basically _____ deficiency that affects ______ and _____. It requires consumption of approximately _____% of their diet for 2-3 weeks.
thiamine
horses
pigs
25%
123
What clinical signs are associated with bracken disease?
Neuro disease - uncoordinated, wide stance, unable to treat
124
What is the lesion that causes bright blindness?
Progressive retinal degeneration
125
Chronic low-level exposure of Bracken fern occurs over ___ to ____ years. It is a ______ agent that causes neoplasia in ruminants. It is excreted in _____.
2-4
carcinogenic
milk
126
What is the toxic principle of sweet clover?
Melilotoside
127
Melilotoside + fungi =
dicoumarol
128
What is the MOA of dicoumarol?
It is a vitamin K antagonist that inhibits epoxide reductase - reduced coag factors II, VII, IX, and X
129
When is the onset of clinical signs due to sweet clover toxicosis?
Several days
130
What clinical signs are associated with sweet clover toxicosis?
Large hematomas, anemia, weakness, pallor, prolonged hemorrhage
131
How is sweet clover toxicosis diagnosed?
Elevated PT and PTT
| Platelet numbers are normal
132
How is sweet clover toxicosis treated?
Fresh blood or plasma
| Vitamin K1
