Unit 2 - Toxic Plants in Large Animals II Flashcards

(85 cards)

1
Q

What plants cause respiratory effects in large animals?

A

Perilla mint and moldy sweet potatoes

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2
Q

What species are susceptible to perilla mint toxicosis?

A

Cattle and horses

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3
Q

When do problems with perilla mint typically occur?

A

In late summer with lack of other forage

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4
Q

What is the toxic principle of perilla mint?

A

Perilla ketone

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5
Q

What does perilla ketone do?

A

It damages endothelial cells and type I pneumocytes

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6
Q

What does perilla mint toxicosis result in?

A

Atypical interstitial pneumonia

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7
Q

When do clinical signs associated with perilla mint toxicosis occur?

A

1-2 days after consumption

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8
Q

What clinical signs are associated with perilla mint toxicosis?

A

Acute onset of dyspnea, extension of head and neck

Froth around the mouth and nose

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9
Q

What clinical signs are associated with severe cases of perilla mint toxicosis?

A

Collapse and death during handling/restraint

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10
Q

How is perilla mint toxicosis treated?

A

Corticosteroids, diuretics, and NSAIDs

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11
Q

What lesions does perilla mint toxicosis cause?

A

Non-collapsing lungs, rib impressions on lung surface, and emphysema

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12
Q

What is the prognosis for perilla mint toxicosis?

A

Good if animals survive past 2-3 days

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13
Q

What is the toxic principle of moldy sweet potatoes?

A

4-ipomeanol

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14
Q

What does 4-ipomeanol do?

A

Damages endothelial cells and type I pneumocytes

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15
Q

T/F: The mechanism, clinical signs, and lesions of Perilla mint and moldy sweet potatoes are the same.

A

True

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16
Q

What is the prognosis of moldy sweet potato toxicosis?

A

Guarded to poor

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17
Q

What are the teratogenic species in sheep that result in cyclopsia?

A

Veratrum californicum, Veratrum viridae, and Veratrum japonicum

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18
Q

What do Veratrum species look like?

A
Coarse erect herb
1-2 meters tall
Stems are unbranched, leafy throughout
Long leaves
Numerous flowers
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19
Q

What parts of the Veratrum plants are toxic?

A

All of them - especially the roots

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20
Q

What are the two toxic components of Veratrum species and what effects are they responsible for?

A

Cevanine alkaloids - neurotoxic

Jervanine alkaloids - teratogenic

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21
Q

What is the MOA of cevanine alkaloids?

A

Bind open voltage-selective Na channels

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22
Q

What is believed to be the most important jervanine alkaloid in Veratrum toxicosis and what is its MOA?

A

Cyclopamine - interferes with intercellular signalling and patterning during embryogenesis and organogenesis

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23
Q

What clinical signs are associated with acute cases of Veratrum poisoning?

A

Onset 2-3 hours post ingestion
Excessive salivation
Ataxia, collapse
Death in severe cases

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24
Q

Teratogenesis occurs when ewes are exposed to Veratrum species from day ___ to ____ of gestation. Cyclops occurs if consumption is on day ____ and limb and tracheal defects occur when consumption is from day ___ to ___. _____ lip and _______, as well as syndactyly are possible.

A
12-30
14
28-33
cleft
palate
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25
What plants are commonly associated with pyrrolizidine alkaloids?
Ragwort, rattlepod, and hound's tongue
26
What species are commonly affected by pyrrolizidine alkaloids? More resistant?
Cattle and horses - young are more susceptible | More resistant
27
When are pyrrolizidine alkaloids generally consumed?
In drought conditions
28
Where are pyrrolizidine alkaloids located in the plant?
In all parts of the plant - highest in flowers
29
What is the MOA of pyrrolizidine alkaloids?
They are converted by mixed function oxidases to toxic pyrroles that are detoxified and rapidly excreted Others are activated and remain in th eliver where they inhibit mitosis
30
What acute gross lesions are associated with pyrrolizidine alkaloids?
Signs of liver failure - icterus and edema
31
What chronic gross lesions are associated with pyrrolizidine alkaloids?
Firm nodular liver, cirrhosis, icterus, +/- photosensitivity
32
What microscopic lesions are associated with pyrrolizidine alkaloid toxicosis?
Heopatocytomegaly Bridging periportal fibrosis Bile duct proliferation
33
How is pyrrolizidine alkaloid toxicosis treated?
Supportive care for liver failure
34
What clinical signs are associated with acute high doses of pyrrolizidine alkaloids?
Hepatic insufficiency Icterus Anorexia Depression
35
What clinical signs are associated with chronic low doses of pyrrolizidine alkaloids?
Chronic hepatopathy - weight loss, emaciation, +/- icterus Hepatic encephalopathy - aimless walking, head pressing, coma Photosensitivity
36
T/F: Pyrrolizidine alkaloids cannot cross the placenta but can pass into milk.
False - it can do both
37
What species are the most often affected by Cocklebur toxicosis? Other species?
Swine are the most often affected | Cattle and sheep are also susceptible
38
What is the toxic principle of Cocklebur toxicosis?
Carboxyatractyloside
39
Where is carboxyatractyloside located in Cocklebur plants?
In seeds and cotyledons
40
What is the MOA of carboxyatractyloside?
1. Competitively inhibits oxidative phosphorylation in mitochondria 2. Block ATP production 3. Cellular damage 4. Hepatocytes and PCTs highly susceptible to damage
41
What clinical signs are associated with cocklebur toxicosis?
Depression, abdominal pain Convulsions/seizures Opisthotonus Apparent blindness
42
What laboratory findings are associated with cocklebur toxicosis?
Elevated liver enzyems | hypoglycemia
43
What gross lesions are associated with cocklebur toxicosis?
Pale liver with enhanced lobular pattern and centrilobular hemorrhages Presence of burs in the stomach/rumen
44
What histologic lesions are associated with cocklebur toxicosis?
Hepatic necrosis and hemorrhage centrilobular to midzonal | Renal tubular degeneration and necrosis
45
How is cocklebur toxicosis diagnosed?
Detection in stomach content
46
How is cocklebur toxicosis treated?
Supportive care and oral detoxification
47
What species are most commonly affected by oak tree toxicosis?
Cattle mainly - spring calves are often poisoned in the fall by acorns There are a few reports in horses
48
What is the toxic principle for oak tree toxicosis?
Metabolites of tannic acid
49
What percentage of a cows diet needs to be oak in order to be toxic?
>50%
50
What are the 3 mechanisms of oak tree toxicosis?
Direct toxicity to GI epithelium Hydrolyzed tannins are absorbed and damage endothelium Metabolites of ingested tannins are toxic to proximal tubular epithelium
51
What clinical signs are associated with early oak tree toxicosis (2 days)?
Anorexia, dullness, rumen atony, constipation, melena
52
What clinical signs are associated with early oak tree toxicosis 3-7 days post exposure?
Weak, prostrate, icterus, hematuria, and dehydration
53
What serum chemistry findings are associated with oak tree toxicosis?
Increased BUN, creatinine, phosphorus
54
What urinalysis findings are associated with oak tree toxicosis?
Hematuria, proteinuria, protein casts
55
What gross lesions are associated with oak tree toxicosis?
Ascites, hydrothorax Perirenal blood tinged edema Hemorrhagic and ulcerative gastroenteritis Acorns in rumen
56
What microscopic lesions are associated with oak tree toxicosis?
Coagulation necrosis of proximal convoluted tubules | Regeneration
57
How is oak tree toxicosis treated?
Remove from access to oak Activated charcoal or mineral oil Fluids to correct dehydration/acidosis
58
What species does redroot pigweed primarily affect?
Pigs Cattle, sheep, and goats are also susceptible
59
What season is Redroot pigweed toxicosis common in?
Mid june to late summer
60
What is the toxic principle and MOA for Redroot pigweed?
Unknown toxic principle | causes acute renal tubular necrosis
61
What clinical signs are associated with Redroot pigweed toxicosis?
Posterior weakness, incoordination, and sternal recumbency (5-10 days post ingestion) Death
62
What gross lesions are associated with Redroot pigweed toxicosis?
Perirenal edema +/- hemorrhage | Ascites
63
What histologic lesions are associated with Redroot pigweed toxicosis?
Acute tubular necrosis affecting both proximal and distal tubules
64
What plants are commonly associated with soluble oxalates?
Halogeton, greasewood, beets, dock, pigweed, lamb's quarters, and rhubarb
65
What species are commonly associated with soluble oxalate toxicosis?
Sheep > cattle | All species are susceptible
66
What are soluble oexalates?
Sodium and potassium
67
What is the MOA of soluble oxalates?
1. Soluble oxalates are rapidly absorbed 2. Complex with serum calcium to form calcium oxalate 3. Excreted in the kidney and crystalize
68
What clinical signs are associated with soluble oxalate toxicosis?
``` Onset: 2-6 hours Dullness, depression Abdominal pain, rumen atony Twitching bruxism Ataxia, prostration, coma ```
69
What gross lesions are associated with soluble oxalate toxicosis?
Ascites, hydrothorax
70
What microscopic lesions are associated with soluble oxalate toxicosis?
Oxalate nephrosis | Crystals within vessel walls
71
What species are affected by black walnut toxicosis?
Primarily horses
72
What is the pathogenesis of black walnut toxicosis?
It is suspected that the wood has a vasoactive effect with ischemia, reperfusion, and reperfusion injury
73
What clinical signs are associated with black walnut toxicosis?
Reluctance to move w/in 24 hours of exposure Depression Increased temperature, heart and respiratory rate, digital pulses and hoof temperature Lower limb edema Severe laminitis with continued exposure
74
How is black walnut toxicosis diagnosed?
History of recent exposure acute clinical disease
75
How is black walnut toxicosis treated?
Nonfatal disease Remove animal from offensive breeding immediately Oral detox Treat limb edema and laminitis
76
What factors are necessary for photosensitization to occur?
1. presence of photodynamic pigment in the skin 2. Exposure to sunlight 3. Areas of susceptible skin
77
What are the two major forms of photosensitization?
Primary - performed photodynamic agent is ingested | Secondary - a photodynamic secondary metabolite is not cleared by the liver
78
What clinical signs are associated with photosensitization?
Photosensitization - photophobia Pruritus and erythema - non pigmented areas are affected most commonly Blindness Sloughing of damaged skin
79
How is photosensitization treated?
Removal from the source Keep animals out of sunlight Antibiotics for secondary bacterial infections Ointments, anti-inflammatories prn for tissue swelling
80
What toxins are involved in the pathogenesis of photosensitization?
Quinones | Phylloerythrin
81
What species are at a higher risk for St. Johns wort toxicosis?
Herbivores > all other species
82
What is the toxic principle of St. Johns wort?
Hypericin - photodynamic pigment
83
What species are affected by buckwheat toxicosis?
All species, but herbivores are at a greater risk
84
What is toxic principle of St. John's wort?
Fagopyrin
85
T/F: The toxic agents of St. John's wort and buckwheat are both slowly eliminated from the body and have cumulative effects
TRUE