Plants Flashcards
(315 cards)
1
Q
Name and main system affected
A
Oleander (Nerium) Heart
2
Q
Name and main system affected
A
Foxglove (Digitalis) Heart
3
Q
Name and main system affected
A
Milkweed (Asclepias) Heart
4
Q
Name and main system affected
A
Rhododendron, azalea, laurel (Rhododendron, Kalmia, Pieris) Heart
5
Q
Name and main system affected
A
Yew (Taxus) Heart
6
Q
Name and main system affected
A
Death Camas (Zigadenus) Heart
7
Q
Name and main system affected
A
Western False Hellebore (Veratrum) Heart
8
Q
Name and main system affected
A
Avocado (Persea) Heart
9
Q
Name and main system affected
A
Kalanchoe (Kalanchoe) Heart
10
Q
Name and main system affected
A
St. Johnswort, Klamath weed, goat weed (Hypericum) Skin - Primary photosensitizer
11
Q
Name and main system affected
A
Allium spp - onions, garlic, chives, shallots Hemolysis
12
Q
Name and main system affected
A
Maple (Acer) Hemolysis
13
Q
Name and main system affected
A
Mustards (Cruciferae) Hemolysis
14
Q
Name and main system affected
A
Sweet Clover (Melilotus) Hemostasis
15
Q
Name and main system affected
A
Bracken Fern (Pteridium) Hemostasis
16
Q
Name and main system affected
A
Pine (pinus), Juniper (Juniperus), (Abies), (Pseudotsuga), (Picea), (Cupressus) Reproductive
17
Q
Name and main system affected
A
Clover (Trifolium), Alfalfa (Medicago) Reproductive
18
Q
Name and main system affected
A
Halogen (halogen), shamrock (oxalis) Kidney
19
Q
Name and main system affected
A
Oak (Quercus) Kidney
20
Q
Name and main system affected
A
Pigweed (Amaranthus) Kidney
21
Q
Name and main system affected
A
Some lilies (lilium, hemerocallus) Kidney
22
Q
Name and main system affected
A
Bleeding heart, Dutchman’s breeches (Dicentra) Nervous system stimulant
23
Q
Name and main system affected
A
Water hemlock (Cicuta) Nervous system stimulant
24
Q
Name and main system affected
A
Yellow star thistle (centauria), Russian knapweed (Acroptilion) Nervous system - mixed effects
25
Name and main system affected
Locoweed (Astragalus) Nervous system - mixed effects
26
Name and main system affected
Morning Glory (Ipomea) Nervous system - mixed effects
27
Name and main system affected
Marijuana (Cannabis) Nervous System depressant
28
Name and main system affected
Jimson weed (Datura) Autonomic Nervous System
29
Name and main system affected
Lupine (Lupinus) Autonomic Nervous System
30
Name and main system affected
Poison Hemlock (Conium) Autonomic Nervous System
31
Name and main system affected
Larkspur (Delphinium) Paralytic
32
Name and main system affected
Horsetail (Equisetum) Thiaminase containing plant
33
Name and main system affected
Cocklebur (Xanthium) Liver (2o photosensitizer)
34
Name and main system affected
Tansy ragwort, groundsel (Senecio), Fiddleneck (Amsinckia), Houndstongue (Cynoglossum) Liver (2o photosensitizer)
35
Name and main system affected
Alsike and red clover (Trillium) Liver (2o photosensitizer)
36
Name and main system affected
Sago palm and cycad (cycas) Liver (2o photosensitizer)
37
Name and main system affected
Buttercup (ranunculus) GI tract
38
Name and main system affected
English Ivy (Hedera) GI tract
39
Name and main system affected
Bulbs (Narcissus, Iris, Hyacinthus, Amaryllis) GI tract
40
Name and main system affected
Nightshade, Potato, Tomatoes (Solanum) GI tract
41
Name and main system affected
Oxalate containing plants (dieffenbachia, philodendron, colocasia, mostera) GI tract
42
Name and main system affected
Castor bean (Ricinus) Gi tract
43
Name and main system affected
Hairy vetch (Vicia villosa) Skin
44
Name and main system affected
Black walnut (Juglans), Hoary alyssum (Berteroa) Skin
45
Name and main system affected
Cyanogenic Glycosides Hypoxia
46
Name and main system affected
Flatweed Musculoskeletal - Stringhalt
47
Name and main system affected
Moldy Sweet Potato Resp - Fog fever
48
Name and main system affected
Perilla mint and mustards Resp - Fog fever
49
Name and main system affected
Lush young green grass Resp - Fog fever
50
Plant characteristics of sweet clover?
Adult is tall and fragrant (3-9 feet)
Leaves are trifoliate and alternate.
Flowers are small and are yellow or white.
51
Toxic principle of Sweet Clover?
Coumarin
52
Mechanism of action of sweet clover?
If sweet clover is put up wet, mold (aspergillus and others) on the clover causes coumarin to become dimeried and oxidized to dicoumarol (only the moldy/dry product is toxic, not fresh plant)
Dicoumarol interferes with vitamin K epoxide reductase
Interferes with clotting factors 2, 7, 9, and 10 and causes bleeding disorders and hemorrhage
53
Animals affected by sweet clover and lesions seen?
Livestock, esp cattle
Bleeding disorders, hemorrhage
Signs, clinpath depend on site of bleeding
54
Treatment for sweet clover toxicity?
Supportive (Vitamin K1, fluids, blood transfusions, etc)
55
6 toxins, MOAs, and clinical signs of mustard (cruciferae) toxicosis?
1. Goitrin/thiocyanate - interfere with thyroid hormone synthesis and iodine uptake - goiter and young born weak and may die.
2. Thiaminase-like activity or high sulfur - polioencephalomalacia and secondary copper deficiencies - lethargy, incoordination, muscle tremors, blindness, recumbancy, convulsion, death.
3. S-methyl cysteine sulfoxide converted to dimethyl disulfide - hemolysis and Heinz bodies - jaundice, hemoglobinuria, anoreixa, splenomegaly, hepatic and renal hemosiderosis and degeneration/necrosis
4. Equine Dysmaturity Syndrome - prolonged gestation but foal still immature with incomplete ossification, tendon ruptures, prognathism, etc.
5. Bloat and other GI issues
6. APEE and nitrate accumulation - reproductive inefficiency and enterotoxemia
56
How much sweet clover does an animal need to eat to see toxicity?
A LOT
Generally a historical problem, not seen much currently
57
How much mustard plants does an animal have to eat to see toxicity
Lots!!!
58
Toxic principle in maple leaves?
Unknown, but whatever it is it is only in the dry not the fresh leaves.
Seems to be most common in Red Maples?
59
Mechanism of action of maple leaves
Acute hemolytic anemia, methemoglobin, Heinz body formation
60
Species affected by maple leaf toxicity and lesions in those animals?
Mostly equine and alpaca
Technically all species susceptible
Hemolysis - icterus, splenomegaly, hepatomegaly (centrilobular degeneration), hemiglobinuric nephrosis.
61
How many dried maple leaves does an animal need to eat to become toxic?
Lots.
62
Toxic principle in allium spp and where is it concentrated in the plant?
Numerous disulfides
Oxidizing agents
Most concentrated in the bulb
63
Mechanism of action of allium spp?
Oxidant damage of the red blood cells leads to Heinz body hemolytic anemia.
64
Clinical signs of allium spp toxicosis?
Hemolysis that begins after a few days and peak at 5 days
Icterus, lethargy, odor to tissues, hemoglobinuric (hypoxic) necrosis chronically, abortions in cattle due to hypoxia.
65
Species most susceptible to allium spp?
Cats, Cattle
Technically all animals susceptible but wide variation in susceptibilities
66
Species most resistant to allium spp?
Sheep and goats
Technically all species susceptible but onions can be fed as 100% of diet to some sheep.
67
Prognosis for animals with allium toxicosis?
Good with supportive care if the animal is not moribund.
68
Of the allium spp, what is the most potent form?
Dried garlic!
69
How much allium spp does an animal have to eat for toxicity?
Depends on the animal
Cat = small amount
Sheep = enormous amount
70
What are the 5 clinical diseases of bracken fern, and what species do these diseases present?
1. Equine - neurotoxicosis from Type I thiaminase - weight loss with good appetite, incoordination, bradycardia, tremors/convulsions, recumbency, death.
2. Bovine - Bone marrow suppression - first of the platelets causing bleeding disorders, last of the red blood cells causing weakness.
3. Bovine - Enzootic hematuria - cyclic inflammation, urinary bladder papillomas, other neoplasms.
4. Sheep - Retinal degeneration - glassy eyed appearance and dilated pupils.
71
What are the toxic principles in bracken fern and where are they located in the plant?
Most toxic principle in young plants (fronds and crizomes) and rhizomes (green or dry) but technically is in all parts of the plant.
Equine diseases: Type I thiaminase
Cattle: Ptaquiloside
72
Treatment for bracken fern toxicosis?
Ruminants: Antibiotics and supportive care
Equine/monogastrics: Thiaminase HCl
73
How much bracken fern does an animal need to eat for a toxic dose?
A lot!
25% of diet composed of fern for 3 weeks or more.
74
How is bracken fern eaten by humans?
Fiddleheads are eaten.
Must cook to get rid of carcinogenic properties.
75
What are some characteristics of the St. Johnswort plant?
Erect perennial found in dry sandy soils.
Leaves have small translucent glands in them.
Leaves are opposite one another.
5-petaled bright yellow flowers with small black dots along flower margins.
76
What is the toxic principle in St. Johnswort?
Hypericin - a primary photodynamic pigment.
77
Which animals are affected by St. Johnswort and how much plant material do the animals have eat?
Any grazing animal.
Have to eat LOTS.
78
Lesions caused by St. Johnswort?
Inflammation of the white areas of the skin, cornea, and conjunctiva.
79
Why do humans take St. Johnswort? What effects can St. Johnswort ingestion have on humans?
Taken as a mood stimulant
Hyperforin inhibits many neurotransmitters including GABA.
Can interfere with the metabolism or excretion of over 50 drugs
80
Cardiotoxins also generally have profound effects on what other bodily system?
The GI tract.
81
What are some characteristics of oleander plant?
Evergreen found mainly in the SW US.
Long, narrow spear like leave with central veins, and very leathery
Flowers are brightly colored (any color but often pink)
82
Toxic principle in oleander?
Cardiac glycosides (specifically oleandrin)
83
Mechanism of action for oleander?
Cardiac glycosides inhibit Na/K ATPase which affects electrolyte distribution and so affects myocardial contractility and conduction.
May also increase vagal tone leading to bradycardia
84
How much oleander does an animal need to eat to see toxicity?
Small amount!
5-10 leaves can be lethal to an adult cow
85
How do grazing animals get access to oleander?
Generally by feeding animals tree clippings, lawn mower clippings, or by material getting into silage or hay
86
Clinical signs of oleander toxicity
Less than 8 hours: salivation, lethargy, diarrhea
Progresses to arrythmias, weakness, hypotension, bradycardia, dyspnea, coma, death.
87
Lesions of oleander toxicity
Myocardial vacuolation, degeneration, and necrosis
Ischemic renal necrosis
88
Diagnosis of oleander toxicity
Oleandrin residue analysis of GI contents and serum
ELISA test for digoxin may cross react with this test
89
Treatment of oleander toxicosis
Toxins excreted slowly, so prolonged treatment (2-3 wks)
Multiple AC doses
Symptomatic care
Digibind: Digoxin specific Fab antibody fragments to bind toxin.
90
How are humans commonly exposed to oleander?
Roasting food on oleander sticks while camping
91
What is more dangerous to dogs: dried oleander or fresh oleander?
Dry
Both have the same toxicity but dry is more palatable (bitter when fresh)
92
Describe foxglove flowers
Bell shaped with dark spots on the inside.
93
Toxic principle of foxglove and where it is found in the plant
Cardiac glycosides (specifically digoxin and digitoxin)
Found in entirety of plant
94
What animals are susceptible to foxglove toxicity?
All species
95
Mechanism of action for foxglove
Cardiac glycosides inhibit Na/K ATPase which affects electrolyte distribution and so affects myocardial contractility and conduction.
May also increase vagal tone causing bradycardia.
96
Diagnosis of Foxglove toxicosis
Can use ELISA test for digoin on serum, blood, GI contents
Histological lesions on the myocardium (vacuolation, degeneration, and necrosis)
97
Treatment of foxglove
Treat for 2-3 wks (toxin excreted slowly)
Multiple activated charcoal doses
Digibind: Digoxin-specific Fab antibody fragments to bind toxin
Symptomatic treatment.
98
Where is foxglove native to?
Western Washington
99
How much foxglove needs to be ingested for toxicosis?
Small amount
100
What is the toxic principle in Rhododendron, azaleas, laurels, and Japanese pieris?
Grayanotoxics
101
Where in rhododendrons is toxin located?
Grayanotoxins in the entire plant but especially the leaves
102
Rhododendrons are toxic to all species, but in what species is toxicity most commonly seen?
Goats - clearing an area they mow down a lot of rhodies.
Toxicities also common if clippings given to other grazing animals.
103
What are the clinical signs of rhododendron toxicity?
PROMINENT GI SIGNS: Vomiting, anorexia, lethargy in 6 hours
24 hours: bradycardia, hypotension, dyspnea, recumbency, convulsions, death.
104
How much rhododendron does an animal have to eat to see toxicosis?
Small amount
105
Lesions for rhododendron toxicity
Gastroenteritis
Renal cortical and tubular necrosis from hypoxia
106
Diagnosis of rhododendron toxicity
History - or leaves easy to see in GI contents
Can test for grayanotoxins in GI contents
107
Treatment for rhododendron toxicosis?
IV lipid therapy
Decontaminate if possible
Supportive care for GI and heart
108
What are the toxic principles in yew?
Taxines (one of ten types of alkaloids in yew)
109
What is the mechanism of action of yew?
Taxines interfere with myocardial conduction by affecting Ca and Na channels and altering intracellular K.
110
How much yew is toxic to an animal?
Small amount
111
Clinical signs and when signs begin to occur?
Monogastrics: 15 minutes - 4 hours
Ruminants: Can be delayed, up to 38 hours
ACUTE CARDIAC FAILURE: trembling, dyspnea, ataxia, collapse, death.
May see some GI issues as well.
112
Lesions for yew toxicity?
None
113
Diagnosis of yew toxicity
GI contents
Test contents for taxine
114
Treatment of yew toxicosis
Activated charcoal and cathartic
Supportive care for GI and heart
115
Which part of the yew plant is toxic?
All except for the fruit of the berry (pink and fleshy, seed is toxic)
116
Describe yew needles
Approximately 1 inch long
Dark on top, light on the bottom
117
Why do people harvest yew bark?
Harvest taxol - has been used therapeutically as a breast cancer treatment
118
Describe death camas
Bulb looks like a wild onion but smells wrong and has a black covering.
Top part of the plant just looks like grass with thick blades and a strong V shape.
119
Toxic principle in death camas?
Steriod alkaloids (zygacine and others)
120
Where in death camas are toxins found?
Steriod alkaloids in all parts of the plant (esp problematic because top part can be grazed or harvested into hay)
121
Mechanism of action of death camas?
Peripheral vasodialtion and vagal stimulation leads to hypotension and bradycardia
122
Clinical signs of death camas
Within 6 hours, vomiting, salivation, muscle tremors, dyspnea, ataxia, weakness, convulsions, and death.
123
Diagnosis of death camas
Test for zygacine in GI contents
124
Treatment of death camas
Supportive care for GI and heart
Activated charcoal
125
Where is death camas commonly found?
Montana and Idaho
126
Why is milkweed called milkweed?
Generally has a milky sap in the stems and leaves that attracts butterflies.
127
What is the toxic principle in milkweed?
Cardiac glycosides and cardenolides.
Two species also have neurotoxins.
128
What is the (main) mechanism of action of milkweed?
Cardiac glycosides inhibit Na/K ATPase which affects electrolyte distribution and so affects myocardial contractility and conduction.
129
What are the clinical signs of milkweed toxicosis?
Heart signs: abrupt death, dyspnea, tachycardia, etc.
Other toxins in the plant may cause GIT, respiratory system, or nervous system signs.
Also causes skin irritation
130
How much milkweed does it take to be toxic to an animal?
Depends on species sensitivity (all animals susceptible)
Moderate amount (about 1 kg) for a horse
Small amount for a sheep.
131
Treatment for milkweed toxicosis
Sedatives, analgesics, other supportive care based on clinical signs.
Control is easy as milkweed tends to grow an obvious, solitary plant.
132
Describe kalanchoe
Houseplant often seen in grocery stores
thick succulent leaves.
Flowers = clusters, bright, long lasting blooms, 4-petalled.
133
Toxic principle in kalanchoe, and where is it found
Cardiac glycosides
Found in all parts of the plant but esp. the flowers
134
How much kalanchoe is toxic to animals?
Pretty large amount
135
Clinical signs of kalanchoe
GIT upset in a few hours
Arrythmias, tacycardia, dyspnea if dose is high enough, cardiac arrest at extreme end.
136
What is the main lesion associated with kalanchoe?
Gastroenteritis
137
Treatment for kalanchoe
Emesis, AC
Supportive care (fluids, antiarrythmic drugs, etc.)
138
What species are susceptible to avocadoes?
BIRDS
All spp technically susceptible but birds are really the only species we see serious toxicosis in.
139
What is the toxic principle of avocado and where in the plant is it found?
Persin
All parts of the plant
140
Clinical signs of avocado toxicosis?
Avian: acute respiratory and cardiac distress
Lactating animals: Non-infectious mastitis and myocardial necrosis.
Horses: Edema of the head and neck which may cause ischemic myopathy / ischemic myelomalacia.
141
Describe the characteristics of western false hellebore
Large alternating leaves with parallel veins
Produce flowers on a thick unbranched stem
Found in very moist areas.
Smells skunky to most people.
142
What is the toxic principle of Western False Hellebore?
Glycoalkaloids and Ester alkaloids
143
Where is toxic principle located in Western False Hellebore?
Concentrated in the young shoots and roots
Decreased concentration in mature leaves
144
What is the mechanism of action of Western False Hellebore?
Heart: Bradycardia from increased vagal tone and Hypotension from peripheral vasodilation.
Teratogenic: 5 alkaloids
145
How much Western False Hellebore does the animal eat to see toxicity?
Teratogenesis: Only a little
Lethality: A lot
146
What are the effects of Western False Hellebore as a teratogen?
Depends on dose and the stage of gestation.
Early embryonic death/Abortions, Cyclopia, Cleft Palate, Arthrogryposis, Tracheal Stenosis, Vertebral column deformities (lordosis, kyphosis, scoliosis)
147
What are the clinical signs of Western False Hellebore as a cardiotoxin?
GI: Salivation, Vomiting/Regurgitation
Cardio: Weakness, incoordintation, bradycardia, hypotension, convulsions, coma, death.
148
Treatment for Western False Hellebore
None
In adult animals, if source is removed should be self-limiting in 3-4 hours.
Only treatment for pregnant animals = prevention
149
What evergreen needle trees have the highest concentration of toxin and how do you recognize them?
Pondarosa pine: long needles in clusters of 3.
Lodgepole pine: long needles in pairs.
Over 25 spp. have toxin but in lower levels and generally unpalatable so not many toxicities seen.
150
Toxic priniciple in pines? Where is it found?
Isocupressic Acid
In bark and needles.
151
Mechanism of action of pines?
Isocupressic acid = TONE GENERATING COMPOUND
Causes uterine vasoconstriction (esp. of the uterine artery)
Fetus releases cortisol causing abortion/premature partruition
Often see retained placentas
152
What stage of gestation are pine needles a biggest problem for?
Risk highest in the last trimester, but fetuses can also be affected in the first or second trimester.
153
How much pine needs to be eaten to see toxicity in animals.
A large amount.
154
What species are most susceptible to pine needle toxicity?
Cattle
155
Lesions from pine needle toxicity?
Vasoconstricution of caruncles with necrosis and hemorrhage.
156
Diagnosis of pine needle toxicity
Test fetal thoracic fluid and fetal GI contents for tetrahydroagathic acid (metabolite of isocupressive acid)
May also be able to test uterine artery
157
Prevention of pine needle toxicity
Don't graze cattle in pine forests
Provide low protein/high energy diet = experimentally produces avoidance
158
For what species can alfalfa and red clover be toxic?
Most signs are mainly in ruminants
Slobbering disease in all species
159
What the toxic principles/clinical syndromes seen with alfalfa/redclover toxicity?
Saponin / proteins can cause bloat
Estrogen / coumesterol can cause infertility or cystic ovaries
Unknown agent can cause photosensitivity
Slaframine can cause slobbering disease
160
Describe halogeton
Reddish stem
Tubular sausage-like fleshy green gray leaves arranged in clumps
Gen in alkaline, dry soil
161
What plant has the same toxic principles as halogeton?
Shamrock (Oxalis)
(4-leaved clover type plant often with a purplish center)
162
Toxic principle of halogeton?
Soluble sodium and potassium oxalates
163
How much halogeton does an animal need to ingest to see toxicity?
Moderate amount
164
In what species is halogeton toxicity most commonly seen in and why?
Grazing animals (esp sheep and cattle) during the winter - dried plants stick up out of the snow and are palatable, and toxin concentrated in the dry plants.
165
Mechanism of action of halogeton
Soluble oxalates are a metabolic poison - interfere with lactate and succinate dehydrogenase
Oxalates bind Ca2+ and so cause hypocalcemia
Formation of calcium oxalate crystals in the renal tubles cause renal necrosis
166
Clinical signs of halogeton?
Generalized hypocalcemic signs early: salivation, lethargy, dyspnea, ataxia, muscle tremors, seizures
Renal signs later
167
Clin Path and Lesions of halogeton
Clin Path: hypocalcemia and azotemia
Renal tubular necrosis due to calcium oxalate crystals
168
Treatment of halogeton?
Give dicalcium phosphate orally so that oxalates will be bound in the gut and not get absorbed as much.
169
Toxic principle of oak and where is it found?
Gallotannins (gallic acid, tannic acid, pyrogallol)
Found in acorns and budding/immature leaves
170
How much oak does an animal need to eat to see toxicity?
Lots and lots
171
Clinical signs of oak toxicity?
GI: bloody, mucoid diarrhea
Renal: weakness, weight loss, lethargy, eventual death.
172
Clinical Pathology of Oak toxicosis
Isosthenuria, proteinuria, azotemia, hyperkalemia, hypoproteinemia, hypocalcemia.
173
Lesions of oak toxicity
Gastroenteritis
Nephritis - multifocal necrosis of proximal renal tubules
+/ edema, ascites, etc.
174
Prognois for oak toxicity?
Generally poor - renal damage irreversible
175
Toxic principle of pigweed
Nitrate accumulator
Also contains soluble oxalates
176
Treatment for pigweed
Renal = supportive
Nitrates = methylene blue
177
What are the two types of lillies that are nephrotoxic?
Lillium and Hemerocallus
(Tiger lily, Easter lily, Day lily, Asiatic hybrid lily, Stargazer lily)
178
What is the toxic principle in nephrotoxic lilies and where is it located?
Unknown but definitely water soluble
All parts of lily
179
How much lily does an animal need to eat to see toxicity
Tiny amount (a bite)
180
In what animals are lilies toxic?
CATS only
(Dogs can have some GI upset from the bulb)
181
Clinical signs of lily toxicity
GI upset
Renal signs in 48-96 hours!
May see facial and paw edema
182
Lesions of lily toxicity
Severe acute renal tubular necrosis
NO oxalate crystals
183
Treatment of lily toxicosis
Decontaminate! Emesis, AC, cathartic, etc.
IV fluid diuresis for 48-72 hours
Monitor renal values
184
What is the toxic principle of bleeding heart and where is it found?
Isoquinoline-like alkaloids
In all parts of the plant
185
Clinical signs of bleeding heart toxicity?
Gastrointestinal signs first
Muscle tremors, prostration, convulsions.
186
Prognosis for bleeding heart toxicity?
Usually good - death is very rare and recovery is rapid.
187
Treatment for bleeding heart toxicosis?
Generally none - animals recover in less than 2 hours in most cases.
188
Describe some characteristics of water hemlock
Bulbous root with yellow resin in very moist areas or in water.
Adult plant can be 3-10 feet tall with a hollow stem.
Umbrella like clusters of white flowers
189
Toxic principle in water hemlock and where it is found
Cicutoxin
Mostly in roots and young shoots
190
How much water hemlock does an animal need to eat to see toxicosis?
Small amt (one root can kill pretty much any animal)
191
Clinical signs of water hemlock toxicosis
Rapid onset in 15-45 minutes: first pre-ictal uneasiness then violent convulsions and death.
192
Diagnosis of water hemlock toxicity?
Generally still see the plants in the GI contents because death is so rapid.
Can also test for cicutoxin in GI contents.
193
Prognosis for water hemlock toxicity?
Grave - fatality so fast.
194
Describe some characteristics of yellow starthistle
1-3 feet tall
Thin, short, narrow leaves that almost look like needles
Stem and leaves covered with cottony hair
Oviod spiny flower base
195
Toxic principle of yellow starthistle and where it is located
Pyrone (hypothesized)
Found only in aerial portions of the plant
196
What species is yellow starthistle a problem?
Horses and other equids
197
What lesion does Yellow Starthistle cause and what nerves does this lesion affect?
Nigropalladial encephalomalacia
Impairs CN: 5, 7, 9, 12. (Trigeminal, Facial, Glossopharyngeal, Hypoglossal)
198
How much yellow starthistle does an animal have to see for toxicity?
A LOT.
199
Mechanism of action of Yellow Starthistle
Binds to dopaminergic receptors and causes necrosis. (Hits same receptors as cocaine does, some young horses seem to be addicted to it)
Dopaminergic areas: Anterior globus palladius, substantia nigra.
200
Clinical signs of yellow starthistle toxicity
Acute presentation of a chronic problem
Lip twitching, involuntary chewing movements.
Trouble eating and drinking = starvation (wasting, death)
201
Prognosis for yellow starthistle toxicity?
Grave. Not reversible.
202
Toxic principles in Locoweed (3)
1. Miserotoxin - in all parts of the plant only when FRESH.
2. Swainsonine/Swainsonine-N-oxide - mainly in the seeds, thought to be a mycotoxin.
3. Selenium accumulator
203
Mechanism of action of locoweed
Miserotoxin: Both neuro and respiratory effects
Swainsonine (and S-N-Oxide) inhibit Golgi mannosidases which leads to the accumulation of mannose in cytoplasma and vacuoles/lysosomes of neurons, hepatocytes, renal tubules, and other tissues.
Selenium: causes skin and abortions.
204
Clinical signs of locoweed
Miserotoxin: ataxia (Wallerian degeneration of peripheral nerves and posterior spinal cord), pulmonary edema and emphysema, death.
Swainsonine: Locoism - ataxia, visual impairment, hyperexcitability or lethargy, emaciation.
Selenium: Hoof and hair problems, abortions, unthriftiness.
205
Diagnosis of locoweed
Can test for swainsonine
Can also evaluate mannoidase activity (for decrease)
206
Histological lesions of locoweed
Vacuolization of many cell types including neurons, renal epithelial cells, hepatocytes
207
Toxic principle in morning glory and where it is located
Lysergic acid derivatives
Only in the seeds
208
How many morning glory seeds does an animal have to eat to see toxicosis?
A LOT.
209
Clinical signs of morning glory toxicosis?
Vomiting, diarrhea, dilated pupils, hallucinations, disorientation, other bizzare behavior
210
Treatment of morning glory toxicosis?
Supportive care +/- sedation.
211
What do you always have to worry about with a pet that came in for eating marijuana?
Dual exposures!! (xylitol, raisins, chocolate, macademia nuts).
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Toxic principle of marijuana?
THC - tetrahydrocannabinols
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Mechanism of action of marijuana
CNS depression and derangement
214
Clinical signs of marijuana toxicosis
Ataxia, lethargy, dilated pupils, easily aroused, inappropriate urination, changes in heart rate, hyperexcitability, inappropriate urination.
215
Prognosis for marijuana toxicity
Good - fatalities very rare and so far only seen with dual toxicities
216
Treatment for marijuana toxicity
IV lipid therapy for very high exposures
Decontamination
Supportive care
217
What does the fruit and leaves of a trumpet vine look like?
Fruit = round, spiny
Leaves = simple, alternating, strong odor.
218
What are the toxic principles in trumpet vine?(3) Where are they?
1. Atropine
2. Hyoscyamine
3. Scopolamine
All parts of the plants toxic but especially the seeds.
219
Clinical signs of trumpet vine toxicity?
Trembling, excitation, colic, dilated pupils, tacky mucous membranes, tachycardia, blurred vision, decreased intestinal motility
220
Treatment for trumpet vine toxicity
Decontamination
Physostigmine should theoretically work but not much clinical success
221
Toxic principles of lupine and which type of plant has most?
Guinolizidine alkaloids
"Bitter" lupines have more alkaloids than "sweet" lupines
222
Lupine mechanism of action
A nicotinic effect - mimicing acetylcholine at both sympathetic and parasympathetic ganglia, NMJs, and CNS.
This acts as an anesthetic for the growing fetus
223
What are the clinical signs of lupine in fetal cattle?
Crooked Calf disease: Arthrogryposis, Vertebral column abnormalities (kypohosis, lordosis, scoliosis), Cleft Palate.
Rarely may kill the calf and cause abortions
224
What is the critical time period for malformations in a cow eating lupine?
Day 40-110 of gestation
225
How much lupine does an animal need to eat for toxicity?
Generally occurs in animals that eat a LOT but in only a short period of time
226
What is the essential characteristics of poison hemlock?
Purple spots! (on the stem)
Otherwise looks very similar to water hemlock except in dry land instead of water.
227
Toxic principle in poison hemlock and where it is located
Piperidine alkaloids
In the whole plant, increasing in concentration as the plant matures.
228
How much poison hemlock does an animal need to eat to see toxicity?
Small amount
229
Mechanism of action of poison hemlock
Nicotinic effects (like lupine) can theoretically cause anesthetic effects and fetal malformations.
230
What animal is most commonly poisoned by poison hemlock?
Humans! Root looks like a carrot.
Then cattle.
231
Clinical signs of poison hemlock?
Muscle tremors, weakness, ataxia and DUMBSLED signs (salivation, lacrimatin, defecation)
Respiratory arrest
Rare: can see arthrogryposis, cleft palate, and vertebral column abnormalities.
232
Toxic principle of larkspur?
Polycyclic diterpene alkaloids
233
When is larkspur most dangerous?
When the plant is the most palatable - from the pre-blooming to the pod-forming stage
234
Mechanism of action of larkspur
Paralysis: Inhibition of the post-synaptic neuromuscular junction by acting as a competative inhibitor of Acetylcholine. Bind more tightly to nicotinic acetylcholine receptors than others.
235
Clinical signs of larkspur
Most commonly, cattle just found dead on pasture (acute death)
May see uneasiness, ataxia, muscle stiffness, muscle twitching, and abdominal pain.
236
Treatment of larkspur
May be able to treat with physostigmine to increase the Ach in the NMJ
Can also use neostigmine for the same reason
237
Prevention of larkspur toxicity?
Graze only when the plant is not palatable (later in the season after pods formed)
Lithim supplements may induce larkspur refusal?
238
Toxic principle in horsetail and where in the plant?
Thiaminase-like compounds (breaks down Vit B1)
All parts of the plant
239
How much horsetail does an animal have to eat to see toxicosis?
Lots!
240
What species are primarily affected by horsetail?
Horses!
241
Clinical signs of horsetail toxicosis?
Like polioencephalomalacia (but no gross lesions!)
Weakness, weight loss despite good appetite, hind limb ataxia or paralysis, convulsions, possibly death.
242
Prognosis for horsetail toxicosis?
Good if animal is not yet recumbant.
243
Treatment for horsetail toxicosis?
Thiamine HCl (aka, Vitamin B1)
244
What do the spines on a cockleburr look like?
Curved and hooked!
245
Toxic principle in cockleburr and where is it found?
Carboxyatractyloside
Found in the seeds within the burr and the dicotyledons (babies) as they grow.
246
How much cockleburr does it take for toxicity?
Moderate amount
247
Clinical signs of cockleburr toxicosis?
12 hours to 2 days: Anorexia, weakness, lethargy, nausea, vomiting, dyspnea, muscle contractions, convulsions, death
Ascites
248
Pathological lesions of cockleburr toxicity?
Mottling of the liver and kidney (due to degeneration/necrosis)
GIT inflammation
IN SWINE ONLY: neuronal degeneration and necrosis
249
Why is cockleburr an uncommon toxicity?
The burrs are so hard that it is often hard for the animals to get to the seeds. Most commonly a problem when the burrs are cut up and then incorporated into silages and hays.
250
Name some of the pyrrolizidine alkaloid containing plants (common names)
Tansy Ragwort
Groundsel
Hound's Tongue
Tarweed
Fiddleneck
251
How much of a plant containing pyrrolizidine alkaloids would an animal have to eat to see a toxicity?
Lots!
TOXICITY IS CUMULATIVE
252
Animals susceptible to pyrrolizidine toxicities
Cattle, horses, pigs, poultry
253
Animals resistant to pyrrolizidine alkaloid toxicities
Sheep and goats (and likely camelids)
254
Mechanism of action of pyrrolizidine alkaloids
Metabolized to highly active pyrroles
Pyrroles alkalate DNA and impairs cell division
Cell continues to grow until critical mass is reached and then necrosis of the cell occurs
255
Lesions of pyrrolizidine alkaloid toxicosis
Grossly liver can be large or small.
Histo: hepatic megalocytosis, centrilobular necrosis, bile duct proliferation, and portal fibrosis
256
Clinical signs of pyrrolizidine alkaloid toxicity
Classic hepatic failure signs + secondary photosensitization and hepatic encephalopathy
257
Diagnosis of pyrrolizidine alkaloid toxicity
This is the primary cause of megalocytosis (though not pathognomonic)
Can test liver and blood in early stages but this is unreliable.
258
What is the toxic principle in alsike/red clover?
Unknown principle can cause liver damage.
Slaframine = slobbering disease
259
Clinical signs of red/alsike clover toxicity
Depending on dose may see secondary photosensitization or hepatic encephalopathy and other liver signs.
Slobbering disease in any animal.
260
Lesions of red/alsike clover toxicity
Hepatomegaly, perilobular fibrosis and bile duct proliferation.
261
Prognosis of red/alsike clover toxicity?
Depends on the amount of liver damage it has caused.
262
In what species is liver damage seen with red/alsike clovers?
Liver damage ONLY in horses
| (slobbering disease in all animals)
263
What are the toxic principles in sago palm? (3) And where are they in the plant?
1. Cycasin (and metabolite methylazoxymethanol) - liver
2. Beta-methylamino-L-alanine - nervous system
3. Unknown
All parts toxic, female parts more so, seeds and nuts are most toxic.
264
Clinical signs of sago palm toxicity and when they occur
15 min: Intense GI signs
2-3 days: hepatic and nervous signs.
265
In what species are sago palm toxicities most commonly seen?
Theoretically can affect all species but 90% of toxicities in dogs.
266
Lesions of sago palm toxicosis?
Focal centrilobular and midzonal necrosis
267
Treatment of sago palm toxicosis
Decontaminate + multiple AC doses
GI and liver protectants
Monitor chemistry panels
Supportive care
268
Toxic principle in buttercup and where is it?
Ranunculin converted to GI irritant, protoanemonin.
In entire plant but only when fresh.
269
How much buttercup does an animal need to ingest to see toxicosis?
A lot
270
Clinical signs of buttercup toxicosis?
Often see dermatitis (esp in humans)
GI issues mainly
In some spp: muscle weakness, difficulty breathing (esp sheep)
271
Toxic principles in English Ivy (3) and where they are?
All parts of the plant, esp the berries
1. Triterpenoid
2. Saponin
3. Hederagenin
272
Clinical signs for English Ivy Toxicity
Severe GI signs: salivation, vomiting, diarrhea.
273
Prognosis for English Ivy toxicosis
Good - fatalities are rare.
274
Which bulbs cause GI symptoms?
Lots - tulips, iris, amaryllis, hyacinth!
275
Toxic principle in tulip bulbs
Alkaloids
276
Clinical signs of tulip bulb toxicity
Oral irritation and mild or severe gastroenteritis
Rarely serious
277
What domestic plants are related to nightshade?
Tomato and potato
278
Toxic principle and mechanism of action in nightshade?
Solanine
This is converted to a sugar or solanidine which affects the purkinje cells of the cerebellum
Some plants contain atropine
279
Clinical signs of nightshade toxicity?
GI signs
Nervous signs: dyspnea, ataxia, paresis or paralysis
DUMBSLED signs if atropine containing plant
280
How much nightshade does an animal have to eat for it to be toxic?
Lots
281
What kind of plants are insoluble oxalate containing plants typically?
House plants
Generally dark green with large broad leaves.
282
What are the toxic principles in insoluble oxalate plants?
Insoluble oxalates and proteolytic enzymes
283
Mechanism of action of insoluble oxalate containing plants?
Oxalate crystals irritate the GI mucosa
Proteolytic enzymes trigger the release of kinins and histamines
284
Clinical signs of insoluble oxalate containing plants?
Salivation, swelling of the oral mucosa
Vomiting and diarrhea
285
Treatment for insoluble oxalate containing plants?
Supportive, esp. rinsing the mouth and giving fluids.
Often includes anti-histamines to quell release.
286
Prognosis for insoluble oxalate plants?
Good
287
If death does occur from insoluble oxalate containing plants, why does it occur?
Hypoxia from swelling of the airways
288
How do pets get castor beans?
Either from gardens or a lot of times found in jewelry.
289
Toxic principle in castor beans and where it is located?
Ricin (water soluble and rapidly absorbed)
In the seed inside of the outer shell
290
How many castor beans are needed to cause toxicity?
Small amount! Just one for a dog.
291
How can castor beans be used as a biological weapon?
If aerosolized and inhaled, ricin will cause pulmonary pathology
292
Clinical signs of castor bean toxicity?
GI distress in 12-48 hours
If high enough does, multi-systemic problems: hypotension, muscle twitching, dyspnea, convulsions, coma, death.
293
Lesions with castor bean toxicosis?
Gastroenteritis
Hepatic, renal, or myocardial necrosis
294
Treatment for castor bean toxicosis?
Only supportive
295
Characteristics of hairy vetch?
Terminal tendrils on the end of each vine
Pea-like flowers and seed pods
296
Toxic principle of hairy vetch?
Unknown
297
Species commonly affected by hairy vetch?
Cattle and horses
298
Clinical disease from hairy vetch?
There are four but most commonly seen is systemic granulomatous disease.
299
How much hairy vetch needed to see toxicity?
A lot!
300
Pathologic lesions associated with hairy vetch
Multiple granulocytic lesions (eosinic, lymphocytic, or plasmacytic infiltrate with multinucleated giant cells)
Dermatitis and conjunctivitis
301
Mechanism of action for hairy vetch?
Granulomas due to a Type IV hypersensitivity reaction.
302
What is the toxic principle for hoary alyssum?
Unknown
303
What plant has the same mechanism of action as hoary alyssum?
Black walnut
304
What animals are affected by hoary alyssum/black walnut toxicity?
Equine
305
Clinical signs of black walnut toxicity?
Limb edema, laminitis, and fever if INGESTED
306
What happens when dogs ingest black walnut WOOD?
Can see neurologic or musculoskeletal signs - vomiting, lethargy, hind limb weakness, tremors, ataxia, disorientation, pain, seizures
307
What are the clinical signs of dogs eating black walnuts themselves or the hulls of black walnuts?
GI signs - salivation, vomiting, anorexia, diarrhea.
308
Should you use fat or water to clean off poison oak/poison ivy lesions?
Both! Toxin is lipid soluble but plant water soluble.
309
What are some examples of cyanogenic glycoside containing plants?
Chokecherries, apple seeds, cherry pits, most other seed fruits.
310
What is the mechanism of action of cyanogenic glycosides?
Cyanogenic glycosides broken down to sugar and aglycone (by beta-glycosidase)
Aglycone converted to hydrocyanic acid (by hydroxynitrile lyase)
Cyanide interacts with ferric iron of cytochrome oxidase, which inhibits electron transport and cellular respiraton.
Blood is fully oxygenated but cannot be utilized by the cells.
311
Clinical signs of cyanogenic glycoside toxicity?
Salivation
Hyperpnea, Dyspnea - death from respiratory paralysis
Weakness and muscle fasciculations, convulsions
Blood may be bright cherry red but rarely observed clinically.
312
Pathologic lesions of cyanogenic glycosides
Bright red mucous membranes
"Bitter almond" smell to GI contents
313
Treatment of cyanogenic glycoside toxicity
Cyanokit - contains hydroxocobalamin (precursor to B12) to bind cyanide and have it be eliminated by the urine.
Other care = supportive
314
What can flatweed cause?
Stringhalt
315
Name four plants that can cause fog fever (pulmonary emphysema and edema), and how each can cause it.
Lush greens in early spring - contains high levels of tryptophan which is converted to 3-methyl indole in the rumen. 3-MI affects the lungs.
Moldy Sweet Potato - produces 4-ipomeanol, affects the lungs.
Perilla mint
Mustards
