Toxic Plants in Large Animals Flashcards
1
Q
Which species does yellow star thistle affect?
A
Horses
2
Q
Where is yellow star thistle located?
A
Western/upper midwest
3
Q
What is the clinical onset of signs associated with yellow star thistle like?
A
Abrupt
4
Q
What are the clinical signs associated with yellow star thistle?
A
- Involuntary chewing movements
- Food falling from the mouth
- Twitching of the tongue and lips
5
Q
How does yellow star thistle cause death?
A
Starvation
6
Q
What are the lesions associated with yellow star thistle?
A
- Necrosis of globus pallidus
- Necrosis of substantia nigra
“Nigropallidal encephalomalacia”
7
Q
What is the treatment for yellow star thistle toxicity?
A
None - recommend euthanasia
8
Q
Yellow start thistle requires ____-____% BW for toxicosis.
A
59 - 200% (requires an extended period of consumption)
9
Q
What component of Locoweeds causes the clinical signs?
A
Swainsonine
10
Q
What is the MOA of swainsonine in Locoweeds?
A
Is it an enzyme inhibitor
Inhibits alpha-D mannosidase and golgi mannosidase II –> oligosaccharides buildup in lysosomes of brain cells –> generalized lysosomal storage disease ensues
11
Q
True or False: Swainsonine crosses the placenta, but is absorbed rather slowly.
A
True/False: Swainsonine does cross the placenta, but it is RAPIDLY absorbed.
12
Q
True or False: Swainsonine is secreted in the milk.
A
TRUE
13
Q
True or False: Swainsonine is excreted in the urine unchanged.
A
TRUE
14
Q
Describe the onset of signs associated with locoweed consumption.
A
Signs usually only observed after several weeks of consumption
15
Q
What type of signs would you see in a horse due to locoweed consumption?
A
Neurological signs: ataxia, circling, proprioceptive deficits
16
Q
What type of signs would you see in a cow or sheep due to locoweed consumption?
A
Reproductive problems: abortion, testicular atrophy, decreased spermatogenesis
Sheep: blindness, star gazing
17
Q
What type of lesions would you see with locoism?
A
Vacuolation of neurons, renal tubular epithelia, and macrophages
18
Q
True or False: The vacuolation associated with locoism is IRREVERSIBLE.
A
FALSE: The vacuolation is reversible.
19
Q
Which species are most severely affected by Jimson weed?
A
- Pigs
2. Horses
20
Q
What is the toxic principle of Jimson weed?
A
Tropane alkaloid
21
Q
What is the MOA of Jimson weed?
A
Anticholinergic effects at muscarinic receptors in the CNS
22
Q
What would the clinical signs of Jimson weed consumption be?
A
Similar to an atropine overdose:
- Decreased salivation
- GI stasis
- Mydriasis
- Tachycardia
- Muscle twitching
23
Q
How would you treat a Jimson weed toxicity?
A
- GI detoxification
2. Physostigmine
24
Q
What is the toxic principle of Lupine (Bluebonnet)?
A
Quinolizidine alkaloid
25
Lupanine is a quinolizidine alkaloid. To which receptors does it bind?
1. Nicotinic
| 2. Muscarinic
26
Anagyrine is a quinolizidine alkaloid. How does this affect cattle?
Teratogenic alkaloid in cattle (NOT in sheep however)
27
What are the clinical signs associated with Lupinus spp. in sheep?
1. Labored breathing
2. Salivation
3. Head pressing
4. Ataxia
28
What causes death with Lupinus spp. (Lupine, Bluebonnet)?
Respiratory paralysis
29
What are the clinical signs associated with Lupine/Bluebonnet consumption in the cow?
1. Salivation
| 2. Teeth grinding
30
Consumption at what point during gestation causes problems in calves?
Days 38 - 70 of gestation
31
What causes "crooked calf disease"?
Lupinus spp.
32
What is the toxic principle of Poison hemlock?
Piperidine alkaloids
33
___% BW of poison hemlock is lethal in cattle.
0.5%
34
___% BW of poison hemlock is lethal in sheep.
1%
35
When do clinical signs occur after consumption of poison hemlock?
Within 1 hour
36
When does death occur following consumption of poison hemlock?
Within 2-3 hours
37
What is the cause of death associated with poison hemlock consumption?
Respiratory failure (respiratory paralysis)
38
What type of lesions would you see in adult animals following poison hemlock toxicity?
NONE
39
How would you diagnose a poison hemlock toxicity?
Detect piperidine alkaloids in (1) stomach content, (2) serum, or (3) urine.
40
Where is Larkspur located within the U.S.?
Western U.S.
41
What is the toxic principle of Larkspur?
Diterpene alkaloids
42
What is the MOA of Larkspur?
Blocks action of nicotinic acetylcholine receptors
43
At what point does Larkspur have high toxicity and low palatability?
When young
44
What are the clinical signs associated with Larkspur?
1. Bloat (inability to eructate)
2. Sudden death
3. Stiffness, weakness, staggering, ataxia, paralysis, tremors
45
Which species is more susceptible to Larkspur toxicity, cattle or sheep?
Cattle
46
How would you treat a Larkspur toxicity?
Cholinesterase inhibitor (physostigmine)
47
What is the toxic principle of water hemlock?
Aliphatic alcohol
48
What toxin is found in water hemlock?
Cicutoxin
49
What is the MOA of cicutoxin in water hemlock?
Blocks GABA receptors
50
Which parts of the water hemlock plant are toxic?
1. Roots
2. Young leaves
Mature plant foliage is virtually non-toxic
51
What are the clinical signs associated with water hemlock?
1. Violent seizures
| 2. Rapid death
52
Water hemlock toxicity resembles what other toxicity previously described in class?
Strychnine
53
What is the toxic principle of white snakeroot?
High molecular weight alcohol
54
What plant contains tremetone?
White snakeroot
55
True or False: Tremetone from white snakeroot is not secreted in milk.
FALSE: Tremetone is secreted in milk.
56
What type of necrosis does white snakeroot cause?
Myonecrosis (cardiac > skeletal)
57
What are the clinical signs associated with white snakeroot?
1. Offspring show signs first (as toxin is secreted in milk)
2. Reluctance to move
3. Muscle tremors
4. CRT > 3 sec.
5. Dark urine
6. Acetone breath
58
Why the dark urine with white snakeroot toxicity?
Myonecrosis - break down of myocytes
59
What would you see on lab work with white snakeroot toxicity?
1. Myoglobinuria
2. Elevated CK
3. Elevated liver enzymes
60
What is the toxic principle of the Yew shrub?
Taxine alkaloids
61
What type of toxin is the yew plant (taxine alkaloids)?
Cardiotoxic
62
Which parts of the yew plant are toxic?
All parts, except the aril
63
Taxine alkaloids are not cardiac glycosides. They work directly on cardiac myocyte ion channels to ____ conduction or depolarization.
Depress
64
When would you see onset of clinical signs associated with Yew plants?
Within 2-4 hours
65
What type of gross lesions are associated with Yew plants?
Little to none (minimal lesions)
66
Which specie(s) is(are) affected by red maple?
Horses
67
What is the toxic principle of red maple?
Pyrogallol
68
what is the proposed pathway for red maple toxicosis in the horse?
Tannic acid --> gallic acid --> pyrogallol --> methemoglobinemia once absorbed into the bloodstream
69
When in the body is tannic acid converted to gallic acid and gallic acid converted to pyrogallol?
Ileum
70
What is the toxic principle of rape/kale?
Dimethyl disulfide
71
What is the MOA of dimethyl disulfide (rape/kale)?
Oxidizes hemoglobin --> heinz body formation --> hemolytic anemia
72
Clinical signs of rape/kale toxicosis are similar to clinical signs of what other toxicity?
Red maple
73
What are the 5 forms of disease associated with bracken fern toxicity?
1. Bright blindness (sheep)
2. Enzootic hematuria
3. Bone marrow aplasia
4. Bracken staggers
5. Chronic exposure (carcinogenic)
74
What is the toxic principle of bracken fern?
Ptaquiloside
75
Which species are most affected by the bone marrow aplasia form of bracken fern toxicity?
Cattle
76
Which species are most affected by the enzootic hematuria form of bracken fern toxicity?
Sheep and cattle
77
What is the toxic principle of sweet clover?
Coumarin glycoside
78
What is the MOA of dicoumarol?
Acts as a vitamin K antagonist.
Inhibits epoxide reductase.
Reduces formation of vitamin K-dependent coagulation factors.
79
What are the clinical signs associated with sweet clover toxicity?
1. Hemorrhaging
2. Anemia
3. Pallor
4. Hematomas
80
How would you treat a sweet clover toxicity?
1. Fresh blood
2. Fresh plasma
3. Vitamin K1
81
Describe PT, PTT, and platelet numbers associated with sweet clover toxicity.
Elevated PT
Elevated PTT
Normal platelets
82
True or False: Only the roots of the veratrum spp. are toxic.
FALSE: All parts of the veratrum plant are toxic.
83
Although there are over 50 steroidal alkaloids of the veratrum spp., name 2.
1. Cevanine
| 2. Jervanine
84
Which of the following is a neurotoxin, cevanine or jervanine?
Cevanine
85
Which of the following is teratogenic, cevanine or jervanine?
Jervanine
86
Which of the following is the most important jervanine alkaloid of the vertrum spp., cyclopamine, cycloposine, jervine? Why?
Cyclopamine: interferes with intercellular signaling during embryogenesis and organogenesis.
87
Teratogenesis occurs when ewes are exposed to Veratrum spp. from day ___ to day ___ of gestation.
12 - 30
88
In order for a fetus to develop cyclops, a ewe would have to consume veratrum on what day of gestation?
14
89
Which species is resistant to pyrrolizidine alkaloids?
Sheep
90
What are the acute clinical signs of pyrrolizidine alkaloid toxicity?
1. Hepatic insufficiency
| 2. Icterus
91
What are the chronic clinical signs of pyrrolizidine alkaloid toxicity?
1. Hepatic encephalopathy
2. Emaciation
3. Icterus
4. Photosensitivity
92
What are the microscopic lesions you would see with pyrrolizidine alkaloid toxicity?
1. Bile duct proliferation
2. Hepatocytomegaly
3. Bridging periportal fibrosis
93
What is the treatment for pyrrolizidine alkaloid toxicity?
NONE
94
Which species is most affected by the cocklebur?
Swine
95
What is the toxic principle of the cocklebur?
Carboxyatractyloside
96
What is the MOA of carboxyatractyloside (cocklebur)?
Inhibits oxidative phosphorylation in mitochondria --> block ATP production --> cellular damage of hepatocytes and PCTs
97
Where are cockleburs located?
All over the U.S.
98
What would be the lab findings consistent with cocklebur ingestion?
1. Elevated liver enzymes
| 2. Hypoglycemia
99
What would be gross lesions consistent with cocklebur ingestion?
Pale liver with enhanced lobular pattern and centrilobular hemorrhages
100
What is the main species affected by oak?
Cattle
101
What is the toxic principle of oak?
Metabolites of tannic acid
102
What would you see on lab work (blood work or UA) with oak poisoning?
1. Increased BUN
2. Increased creatinine
3. Increased phosphorous
4. Hematuria
5. Proteinuria
6. Protein casts
103
What type of gross lesions would you expect with oak toxicity?
1. Ascites
2. Hydrothorax
3. Hemorrhagic/ulcerative gastroenteritis
4. Acorns in rumen
104
How would you prevent oak toxicity if cattle have access to oak trees?
Provide grain mix containing 10% calcium hydroxide
105
What type of lesions would you expect with redroot pigweed?
Acute tubular necrosis affecting both proximal and distal tubules
106
What are the clinical signs assocaited with redroot pigweed?
1. Sternal recumbancy
2. Incoordination
3. Weakness
4. Ascites
107
When would clinical signs occur after consumption of redroot pigweed?
Within 5-10 DAYS
108
Which species is most affected by black walnut?
Horses
109
When do clinical signs from black walnut develop?
Within 24 hours of exposure (ingestion)
110
True or False: Black walnut disease is fatal.
FALSE: Nonfatal disease
111
What are the clinical signs associated with black walnuts in horses?
1. Laminitis (rotation of P3)
2. Limb edema
3. Increased temp, HR, digital pulse, and hoof temperature
112
What 3 factors are necessary for photosensitization to occur?
1. Susceptible skin (nonpigmented)
2. Exposure to sun
3. Presence of photodynamic pigment in skin
113
Which species are at greatest risk for St. John's wort toxicity?
Herbivores
114
Which species are at greatest risk for Buckwheat toxicity?
Herbivores
115
What is the photodynamic pigment of st. john's wort?
Hypericin
116
What is the photodynamic pigment of buckwheat?
Fagopyrin
117
What are the clinical signs of photosensitization?
1. Photosensitization
2. Pruritus
3. Erythema
4. Blindness
5. Sloughing of damaged cells
118
What is the MOA of a primary photosensitization?
Toxic quinones are absorbed following ingestion --> circulate to cutaneous vasculature --> activated by light wavelengths of 540-610 nm --> form singlet oxygen --> vascular injury
119
What is the MOA of a secondary photosensitization?
Severe liver damage or biliary obstruction --> phylloerythrin not excreted into bile --> acts as a phtodynamic pigment
