Toxicology - Plant Poisoning

Front 1

How can plant poisoning cause an economic impact?

Back 1

-Direct: death, slow growth, infertility
-Indirect: cost of management and control, decreased land value, loss of fodder

Front 2

What are plant toxins?

Back 2

Biologically active phytochemical precursors and secondary metabolites
-excessive accumulation of "normal" nutrients/phytochemicals
-formation of specialized metabolites

Front 3

Plant toxin production depends on what environmental and biological factors?

Back 3

-climate factors
-Edaphic (soil) factors
-Social interactions
-Life stage/growth phase
-Plant tissue and location

Front 4

Climactic factors that effect toxin production

Back 4

-Macro: rainfall, temp, etc.
-Micro: shadow, wind effects, etc.

Front 5

Soil factors that effect toxin production

Back 5

-depth
-particle size
-nutrient content
-cultivation
-drainage
-etc.

Front 6

Social interactions that effect toxin production

Back 6

-Intra- and interspecies competition/mutualism/commensalism
-herbivory
-infectious (fungal, viral, bacterial)

Front 7

Limitations of Species classification

Back 7

-species-level differentiation involves subjectivity
-hybridization
-genetically isolated populations occur within species leading to unique genomes and possible altered chemistry

Front 8

Major phytochemical classes associated with poisoning

Back 8

-alkaloids
-lectins
-terpenes
-phenolics
-coumarins
-glycosides (hybrids)

Front 9

Cicutoxin
-chemical type

Back 9

-long chain alcohol

Front 10

Cicutoxin
-comes from what plant

Back 10

-water hemlock

Front 11

Cicutoxin
-toxin mechanism

Back 11

-similar to strychnine
-blocks GABA (psychotoxin) --> suppression of Cl- conductance --> uncontrolled depolariztion --> seizures

Front 12

Water hemlock
-geography

Back 12

-all state, mostly east
-close to water

Front 13

Cicutoxin
-highest conc. located where

Back 13

-rootstock and lower stem (yellowy liquid)
-also in young leaves

Front 14

Cicutoxin
-clinical signs

Back 14

-fast acting
-death in 1-8 hrs depending on dose
-muscle tremors
-salivation
-convulsions
-death

Front 15

Cicutoxin
-post-mortem signs

Back 15

-No diagnostic post-mortem lesions due to quick death

-possible skeletal and cardiac muscle degeneration and necrosis
-look for signs of convulsion (scraped skin from ground)
-pieces of chewed rootstock in reticulum/rumen/esophagus

Front 16

Cicutoxin
-treatment

Back 16

-supportive
-emesis/gastric lavage
-activate charcoal
-control convulsions with benzodiazepines/barbituates

Front 17

Cicutoxin
-management

Back 17

-plants are typically avoided if there are other options
-control plants by pulling or herbicides (but plant can become more palatable to animals for a few weeks)
-avoid
-trampled rootstock can poison water

Front 18

Tremetol
-plant

Back 18

-White snakeroot (Ageratina altissima)

Front 19

Tremetol
-effect

Back 19

-liver and/or heart failure depending on the animal species infected

Front 20

Tremetol
-reason for public health hazard

Back 20

-excreted in milk

Front 21

White snakeroot
-found where

Back 21

-forest edge

Front 22

Tremetol
-cause for toxicity

Back 22

-metabolized to a lipid soluble ketone

Front 23

White Snakeroot
-toxic plant part

Back 23

-all vegetative parts
-still toxic when dry

Front 24

Tremetol
-mechanism of toxicity

Back 24

Unknown
-cumulative nerve degeneration
-liver degeneration

Front 25

Tremetol
-clinical picture

Back 25

-mortality in severely affected animals is high
-lactating animals are not as severely effected
-nursing animals at risk (milk sickness)
-muscle tremors (especially after exercise)
-cattle prone to bloat
-aspiration pneumonia

Front 26

Tremetol
-species vs. affected organ system

Back 26

-Sheep and goats: liver
-cattle: liver and heart
-horses: heart

Front 27

Tremetol
-effects of liver syndrome

Back 27

-increased ALT, AST
-depression
-weakness
-CNS abnormalities
-coma
-death

Front 28

Tremetol
-effects of heart syndrome

Back 28

-exercise intolerance
-cardiac arrhythmia (tachycardia)
-jugular pulse
-sweating
-ventral edema

Front 29

Tremetol
-post-mortem findings

Back 29

-leaves in the rumen (peracute & acute cases) with characteristic trichomes
-microscopic lesions resembling nutritional/exertional myopathies

Front 30

Tremetol
-treatment

Back 30

No specific treatment
-remove from contaminated pasture
-activated charcoal
-avoid exercise
-supportive therapy (IV fluid, stomach tube for bloat, antibiotics for aspiration pneumonia)

Front 31

Tremetol
-management

Back 31

-animals develop aversion
-susceptibility in naive goats
-horses more susceptible around young plants
-avoid contact with plant

Front 32

Tannic Acid
-types

Back 32

-Condensed tannins
-hydolyzable tannins

Front 33

Condensed tannins
-characteristics

Back 33

-flavonoid polymers
-wide range of woody species
-astringent (precipitates glycoproteins in saliva)
-anti-nutritive

Front 34

Hydrolyzable tannins
-characterisitcs

Back 34

-restricted to a few spp
-Phenolic compound esterified with a sugar

Front 35

Gallotannins
-come from what plant species

Back 35

-oaks

Front 36

Gallotannin
-effects

Back 36

-renal tubular necrosis
-GI disturbance

Front 37

Defining characteristic of oak trees

Back 37

-acorns

Front 38

Gallotannin
-toxicity

Back 38

gallic acids esterified to glucose

Front 39

Gallotannin
-highest conc. found where

Back 39

-bud
-young leaves and stems
-acorns

-mature leaves not toxic

Front 40

Gallotannin
-mechanism of toxicity

Back 40

-precipitation of protein in the GI tract

Front 41

Gallotannin
-clinical picture

Back 41

Initial:
-anorexia
-rumen stasis
-constipation
-brown urine

Later:
-diarrhea
-dehydrate
-colic
-edema
-PU/PD

Front 42

Gallotannin
-clin path

Back 42

-inc. BUN
-inc. creatinint
-low urine SG, proteinuria, glucosuria, hematuria

Front 43

Gallotannin
-GI signs in monogestrics

Back 43

Horses
-diarrhea
-colic
-tenesmus

Front 44

Gallotannin
-Post-Mortem diagnosis

Back 44

-ascites Hypdrothorax, SC edema
-kidneys swollen, pale, petechiae
-diffuse renal tubular dilation, necrosis of cortical tubular epithelium
-edema of GI mucosa (horse)

Front 45

Gallotannin
-treatment

Back 45

-remove from pasture
-supportive treatment (IV fluid, fresh water, quality hay, activated charcoal)
-recovery if kidney function

Front 46

Gallotannin
-management

Back 46

-avoid hazardous pastures
-supplemental feed to reduce oak intake
-good quality feed to bind tannins
-herbicides

Front 47

Oxalic Acid
-syndromes

Back 47

-hypocalcemia
-renal tubular necrosis

Front 48

Oxalic acid
-levels highest in what plants

Back 48

-rapidly growing

Front 49

Oxalic Acid
-mechanism of toxicity

Back 49

-complexes with Ca to form Ca-oxalate complex which is insoluble
-hypocalcemia
-renal tubular necrosis from crystallization in renal tubules

Front 50

Oxalic Acid
-clinical picture

Back 50

-hypocalcemia (rapid onset, depression , tremors, ataxia, prostration, seizures)
-Sx of kidney failure if animal survives hypocalcemia (weight loss, PU/PD)

Front 51

Oxalic acid toxicity
-prognosis

Back 51

-guarded

Front 52

Oxalic acid
-postmortem

Back 52

-thoracic and abdominal fluid
-petechia in GI and pericardium
-lung emphysema
-oxalate crystals separating renal cortex and medulla
-tubular nephrosis and necrosis
-crystal rosettes in tubules

Front 53

Oxalic Acid
-treament

Back 53

-CaHPO4 2H2O : NaCl (bind oxalates in the GI)
-IV to counteract hypocalcemia
-IV and oral fluid for renal support

Front 54

Oxalic acid
-management

Back 54

-well fed animal have better tolerance
-ruminants adapt to higher levels

Front 55

Ca-oxalate Raphides
-syndromes

Back 55

-upper GI tract irritation

Front 56

Ca-Oxalate Raphide poisoning
-usually due to

Back 56

-pet chewing on ornamental house plants

Front 57

Ca-Oxalate Raphide
-family

Back 57

-Araceae

Front 58

Ca-Oxalate Raphides
-usually stored with

Back 58

-proteolytic enzymes

Front 59

Ca-Oxalate
-mechanism of toxicity

Back 59

-raphides from crushed plant easily penetrate mouth, throat, esophagus
-rapid inflammatory response

Front 60

Ca-Oxalate
-clinical picture

Back 60

-severe inflammatory response (pain swelling, hypersalivation)
-resolves spontaneously in 24 hrs

Front 61

Ca-Oxalate
-treatment

Back 61

-supportive
-rinse mouth w/ water
-offer small amount of milk/yogurt/etc.
-antihistamine
-sucralfate for soothing effect

Front 62

Isocupressic Acid
-aka

Back 62

-Pine Needle Abortion

Front 63

Isocupressic Acid
-animals effected

Back 63

-Cattle during late gestation --> abortion

Front 64

Isocupressic acid
-produced by what plants

Back 64

-Pines

Front 65

Isocupressic acid
-mechanism

Back 65

-reduce uterine blood flow
-release of fetal cortisol induces premature parturition

Front 66

Isocupressic acid
-clinical picture

Back 66

-premature udder development
-vulvar swelling
-vaginal discharge
-premature parturition/abortion

Front 67

Isocupressic Acid
-complications associated

Back 67

-retained placenta
-metritis
-septicemia

Front 68

Isocupressic Acid
-treatment

Back 68

-none for abortion
-treat complications as needed
-supportive care to premature calves

Front 69

Isocupressic Acid
-management

Back 69

-prevent pine needle access during late gestation
-provide alternate nutrition during weather changes

Front 70

Alkaloids
-derived from

Back 70

-amino acids

Front 71

Alkaloid
-structure

Back 71

-nitrogen in a heterocyclic ring

Front 72

Alkaloid
-chemistry

Back 72

-basic
-in plants as water soluble salts

-can't penetrate skin easily

Front 73

Pharmacologic drugs that are used as alkaloids

Back 73

-atropine
-quinine
-cocaine
-morphine
-vincristine

Front 74

Nicotinic alkaloid effects
-effects

Back 74

-receptors at neuromuscular junction that cause transient stimulation with subsequent suppression

Front 75

Nicotinic Alkaloid
-types

Back 75

-Diterpene alkaloids
-Piperdine alkaloids
-Pyridine alkaloids

Front 76

Diterpene Alkaloids
-plants

Back 76

-Delphinum spp.

Front 77

Piperidine alkaloids
-plants

Back 77

-Poison hemlock
-Lupines

Front 78

Pyridine alkaloids
-plants

Back 78

-Nicotina spp.

Front 79

Nicotinic Alkaloids
-found where in the plant

Back 79

-all parts
-highest conc. in growing plants
-dried plants still toxic

Front 80

Nicotinic Alkaloid
-characteristics

Back 80

-potent smell
ibitter taste
-off-flavored milk

Front 81

Nicotinic Alkaloids
-mechanism of action

Back 81

-affect central and peripheral cholinergic and nicotinic receptors
-initial stimulation followed by persistent suppression

Front 82

Nicotinic Alkaloids
-clinical picture

Back 82

Stimulatory phase:
-nervous system effects: excitability, stiff gait, muscle trembling, frequent urination
-GI system effects: salivation, diarrhea, vomiting

Supression phase:
-weakness collapse, respiratory paralysis --> death

Teratogenesis from sub-clinical ingestion by mother
-limb abnormalities, cleft palate

Front 83

Nicotinic Alkaloid
-postmortem signs

Back 83

-non-specific
-congestion and hemorrhage in various organs
-birth defects: contracture-type skeletal defects, cleft palate

Front 84

Nicotinic Alkaloid
-treatment

Back 84

-remove source
-decontamination early (vomit, activated charcoal)
-Atropine to control parasympathetic effects (dose titration)
-limit handling, excitement, disturbance
-prognosis good if no respiratory paralysis

Front 85

Nicotinic Alkaloid
-management

Back 85

-Make sure there is adequate alternate feed (animals will avoid alkaloid plants if have choice)
-Avoid feeding garden waste (some species are popular garden subjects)

Front 86

Tropane alkaloids
-plants

Back 86

-Jimsonweeds (Datura spp.)

Front 87

Tropane Alkaloids
-mechanism of action

Back 87

-parasympatholytic

Front 88

Parasympatholytic
-signs pneumonic

Back 88

-red as a beet
-dry as a bone
-blind as a bat
-mad as a hatter
-hot as a hare

Front 89

Jimsonweeds
-physical characteristics

Back 89

-spiny seedpots
-trumpet-like flowers

Front 90

Tropane alkaloids
-examples

Back 90

-atropine
-scopolamine
-hyoscyamine

Front 91

Tropane alkaloids
-plant toxicity

Back 91

-all parts toxic
-seeds most toxic

-high potency

Front 92

Tropane alkaloids
-mechanism of action

Back 92

-competitive antagonism of central and peripheral muscarinic acetylcholine receptors
-parasympatholytic --> inhibition of res and digest responses

Front 93

Tropane alkaloids
-clinical signs

Back 93

-dilated pupils
-tachycardia (ventricular fibrillation)
-ataxia
-hallucinogenic
-elevated temp
-thirst
-convulsions, coma, death
-colic in horses

Front 94

Tropane alkaloids
-postmortem signs

Back 94

-no specific lesions
-plant may be present in GI tract

Front 95

Tropane alkaloids
-treatment

Back 95

-Benzodiazepines and Barbituates --> control convulsions
-some recovery over several days with supportive care

-Parasymathetic drugs (pilocarpine) are of limited use --> suppress breathing

Front 96

Tropane alkaloids
-management

Back 96

-will be avoided as long as there is alternative feed
-prevent hay contamination

Front 97

Pyrrolizidine alkaloids
-plants

Back 97

-Asteraceae (Senecio sp.)
-Fabaceae (Crotolaria sp.)

Front 98

Pyrrolizidine alkaloids
-effects

Back 98

-liver*, kidney, heart, lungs
-stargazing

Front 99

Pyrrolizidine alkaloids
-reason for public health concern

Back 99

-sometimes found in herbal teas and remedies and can be lethal if combined with acetaminophen

Front 100

Pyrrolizidine alkaloids
-mechanism of toxicity

Back 100

-activated by the liver
-pyrrols (formed by liver) are alkylating agents that cause DNA damage
-liver defenses get overwhelmed and damaged hepatocytes dump pyrrols into system
-some plant pyrrols can transfer to lung fluids

Front 101

Pyrrolizadine alkaloids
-clinical signs

Back 101

acute
-liver failure
-sudden death

chronic
-weight loss
-behavioral change
-urination, rectal prolapse

Front 102

Other toxins found in Crotolaria spp.

Back 102

-monocrotaline --> fibrosing alveolitis in horses
-laminitis (unknown toxin)

Front 103

Pyrrolizadine alkaloids
-lesions

Back 103

Gross
-edematous and congested liver (accentuated lobulation, brittle, fibrosis, cirrhosis)
-icterus
-petchiation
-edema (lungs, perirectal, cecal & colonic)

Micro
-centrilobular hepatic degeneration and necrosis
-fibrotic and cirrhotic liver changes

Front 104

Pyrrolizadine alkaloids
-treatment

Back 104

-none
-poor prognosis

Front 105

Pyrrolizadine alkaloids
-managament

Back 105

-prevent hay contamination (discard contaminated feed)
-control of PA containing plants
-provide alternative feed
-keep young, naive animals away

Front 106

Taxine alkaloids
-plants

Back 106

-yew (Taxus sp.)

Front 107

Taxine alkaloids
-main effect

Back 107

-sudden death due to heart failure

Front 108

Taxine alkaloids
-toxic part of plant

Back 108

-all parts except fleshy fruit

Front 109

Taxine alkaloids
-mechanism of toxicity

Back 109

-inhibition of Ca & Na currents across cardiac muscle membranes --> slow ventricular muscle contraction

Front 110

Taxine alkaloids
-clinical signs

Back 110

-sudden death in animals with recent exposure to garden clippings
-signs of heart failure (hypotension, cardiac arrhythmia)
-death of apparently normal animals if disturbed

Front 111

Taxine alkaloids
-post-mortem findings

Back 111

-no lesions
-leaves/twigs in rumen

Front 112

Taxine alkaloids
-treatment

Back 112

-none
-avoid disturbance
-early removal of stomach contents & activated charcoal

Front 113

Taxine alkaloids
-management

Back 113

-avoid contact with yews
-no garden waste feeding

Front 114

Propyl disulfide & Dimethyl disulfide
-plants

Back 114

-onion/garlic (Allium sp.)
-mustard (brassica sp.)

Front 115

Propyl disulfide & Dimethyl disulfide
-main effect

Back 115

-heinz body anemia

Front 116

Propyl disulfide & Dimethyl disulfide
-chemical derivative of

Back 116

-cysteine

Front 117

Propyl disulfide & Dimethyl disulfide
-kinetics

Back 117

-insoluble in water
-eye and respiratory irritant

Front 118

Propyl disulfide & Dimethyl disulfide
-mechanism of toxicity

Back 118

-occurs with a depletion of glutathione (reduce disulfides)
-free oxygen radical formation in RBCs
-damage to erythrocyte membranes

-fetal hypoxia --> abortion

Front 119

Propyl disulfide & Dimethyl disulfide
-clinical signs

Back 119

-hypoxia
-heinz bodies on RBCs
-hemolysis (pale/jaundice mucous membranes, brown-red urine)
-onion breath
-abortion

Front 120

Propyl disulfide & Dimethyl disulfide
-postmortem lesions

Back 120

Gross
-pale carcass
-onion odor
-congested spleen and kidneys

Micro
-nephrotubular necrosis
-hepatic necrosis
-hemosiderosis (liver, kidneys, spleen)

Front 121

Propyl disulfide & Dimethyl disulfide
-treatment

Back 121

-supportive (blood transfusion, diuretic, IV fluid, oxygen)

Front 122

Propyl disulfide & Dimethyl disulfide
-management

Back 122

-avoid feeding excessive Allium or Brassica to livestock
-avoid feeding onion containing table scraps to pets

Front 123

Glycoside
-why are these commonly found in plants

Back 123

-inc. water solubility of non-polar molecules
-sequesters/stores molecules in water compartments

Front 124

Cardiac glycosides
-plant

Back 124

-oleander (Nerium oleander)

Front 125

Cardiac glycosides
-mechanism of action

Back 125

-inhibition of Na/K ATP-ase
-inc. intracellular Na & extracellular K
-slowed AV conduction --> ventricular arrhythmias
-increased vagal tone --> reduce Heart Rate
-vagal effects on GI

-delayd beta-adrenergic effects

Front 126

Aglycone classes

Back 126

-Cardenolides (acute effects)
-Bufadenolides (cumulative effects)

Front 127

Cardiac glycosides
-clinical signs

Back 127

-animals dead or die when disturbed
-initial bradycardia, then weak, fast pulse and ventricular arrhythmias
-colic, rumen stasis, bloat, vomiting
-ataxia, high-stepping, muscle tremors, hypersensitivity, convulsions, coma

Front 128

Cardiac glycosides
-postmortem effects

Back 128

Gross
-peracute death from high doses --> no lesions
-sub-epicardial hemorrhage
-pulmonary edema
-fluid accumulation
-leaves in ingesta

Histo
-multifocal myocardial inflammation, degeneration, necrosis
-mild renal tubular lesions

Front 129

Cardiac glycosides
-treatment

Back 129

-remove source
-evacuate stomach/rumen early
-activated charcoal
-symptomatic for cardiac arrhythmia (atropine, propranolol)
-anticardiac glycoside Fab antibody

Front 130

Cardiac glycoside
-prognosis

Back 130

-fair with > 2 day survival

Front 131

Cardiac glycoside
-management

Back 131

-prevent exposure
-alternative feed
-avoid contact with garden waste
-avoid oleander hedges

Front 132

Coumarin glycosides
-plant

Back 132

-moldy sweet clover hay/silage (Melilotus sp.)

Front 133

Coumarin glycosides
-mechanism of toxicity

Back 133

-Melilotoside converted by fungal action to dicoumarol
-Inhibits epoxide reductase for Vit K regeneration
-Reduction of prothrombin activation
-depletion of clotting factors II, VII, IX, X
----> uncontrolled hemorrhage

Front 134

Coumarin Glycosides
-clinical signs

Back 134

-prolonged bleeding
-pale mucous membranes, tachycardia
-large hematomas from mild trauma (colic, lameness)
-bleeding from body orafices
-weakness --> downer --> death
-abortion (intra-uterine bleeding)
-weak calves

Front 135

Coumarine Glycosides
-postmortem lesions

Back 135

-hemorrhage and anemia
-icterus

Front 136

Coumarin glycosides
-clin path

Back 136

-inc. PT & aPPT
-dec. Factors IX & X
-dec. PCV

Front 137

Coumarin Glycosides
-treatment

Back 137

-remove source
-prevent trauma
-whole blood transfusions
-Vit K

Front 138

Coumarin Glycosides
-management

Back 138

-avoid feeding moldy hay/silage
-inhibit mold growth (proprionic acid, ammoniation)
-less coumarin in some sweet clover varieties
-avoid feeding before surgery

Front 139

Cyanogenic Glycosides
-plants

Back 139

-Wild plum (Prunus americana)
-Elderberry (Sambucus mexicana)
-Vetch (Vicia sativa)
-Grain Sorghum

Front 140

Cyanogenic Glycosides
-toxic agent

Back 140

-HCN produced by either damaged plant tissues or GI tract

Front 141

Cyanogenic glycosides
-cyanide test

Back 141

-based on discoloration of picric acid-impregnated paper
-use plant material or GI contents

Front 142

Cyanogenic Glycosides
-mechanism of toxicity

Back 142

-cyanide binds to iron in cellular cytochrome oxidase
-blocks electron transfer necessary for cellular respiration
-uncouples oxidative phosphorylation
-Hb can't release oxygen to tissues and the blood becomes supersaturated with oxygen (venous blood bright red)

Front 143

Cyanogenic Glycosides
-clinical signs

Back 143

-animals found dead
-oxygen starvation --> hyperpnea, exercise intolerance, confusion, convulsions, death
-cherry red venous blood

Front 144

Cyanogenic Glycosides
-postmortem lesions

Back 144

-none
-petechiae (abomasum, subendocardium, subepicardium)
-cherry red blood
-almond like odor

Front 145

Cyanogenic Glycosides
-treatment

Back 145

-sodium nitrate/methylene blue --> pulls cyanide from cytochrome oxidase
-sodium thiosulphate --> forms soluble thiocyate

Front 146

Cyanogenic glycosides
-management

Back 146

-risk factors (drought, frost, mechanical damage, regrowth after mowing, caterpillar infestation)
-test before animals feed during hazardous conditions
-prevent feeding on Prunus sp. fruit plants

Front 147

Some of the most potent and lethal plant toxins

Back 147

-Lectins

Front 148

Lectin
-general mechanism of action

Back 148

-blocks protein synthesis

Front 149

Lectins
-plants

Back 149

-Castor bean
-Precatory bean
-Physic nut

Front 150

Lectins
-toxic agent characteristics

Back 150

-protein toxin
-water soluble
-wet heat labile
-not present in properly extracted oil
-poorly absorbed from the Gi tract
-highly potent and lethal

Front 151

Lectins
-Mechanism of Toxicity

Back 151

-B-chain binds to glycoproteins and glycolipids on cell surface
-Protein enters cell via endocytosis
-Endosome fuses with golgi, transports to ER (suicide transport), and A-chain depurinates rRNA

Front 152

Why is ricin so potent?

Back 152

-single ricin molecule can inactivate many ribosomes per minute --> cell death

Front 153

Lectins
-clinical signs (low potency, high potency)

Back 153

Low potency
-reduced growth rate
-diarrhea
-Inc. bacterial infections

High potency
-GI irritation (vomiting, diarrhea)
-hemorrhagic gastroenteritis
-injury to liver, pancreas, muscle when absorbed through GI

Front 154

Lectins
-Post Mortem lesions (gross, micro)

Back 154

Gross
-gastroenteritis

Micro
-intestinal villi disruption
-myocardial necrosis/hemorrhage

Front 155

Lectins
-treatment

Back 155

-remove source
-decontamination (emesis, AC)
-GI tract protectant (kaolin-pectin)
-fluid therapy

Front 156

Lectin
-management

Back 156

-heat-treat lectin-containing feeds
-seeds implicated in pet poisoning

Front 157

Tryptophan
-disease caused

Back 157

-Acute bovine Pulmonary Edema (ABPE)
-fog fever

Front 158

Tryptophan
-poisoning due to

Back 158

-moving cattle from dry to lush pasture

Front 159

Tryptophan
-in order for this poisoning to occur what must be present

Back 159

-functional rumen

Front 160

Tryptophan
-toxic agen

Back 160

-L-tryptophan

Front 161

L-tryptophan
-plants

Back 161

-most plants

Front 162

Tryptophan
-mechanism of action

Back 162

-L-tryptophane converted to 3-methylindole by ruminal Lactobacillus sp.
-oxidases in lung tissues convert 3-methylindole into reactive metabolites
-lung damage --> Edema & Emphysema

Front 163

Tryptophan
-clinical signs

Back 163

-dyspnea
-consolidated lung sounds
-expiratory grunts/wheezes
-nasal discharge
-exercise intolerance
-death

Front 164

Tryptophan
-postmortem lesions (gross, micro)

Back 164

Gross
-heavy, dark, red, firm lungs
-fluid ozzing from cuts
-emphysema &' bullae-formation

Micro
-protein-rich edema
-hyaline membrane formation in alveoli
-large mononuclear cells in alveolar lumens

Front 165

Tryptophan
-treatment

Back 165

-Limited effect
-Try NSAIDs, diuretics, bronchodilators, antihistamines

Front 166

Tryptophan
-management

Back 166

-avoid sudden change to lush pasture
-ionophores provide partial protection

Front 167

Thiaminase
-Plants

Back 167

-Bracken fern (Pteridium aquilinium)
-Horsetail (Equisetum spp.)

Front 168

Thiaminase
-susceptible animals

Back 168

-horses (monogastrics that eat a lot of plants)

Front 169

Thiaminase
-mechanism of toxicity

Back 169

-Thiaminase breaks down Thiamine in the gut before absorbed
-blocks reactions requiring thiamine pyrophosphate
-neurodegeneration

Front 170

Thiaminase
-reason for radiomimetic effects in ruminants

Back 170

-unknown compounds and mechanism
-bone marrow depression

Front 171

Thiaminase
-clinical signs

Back 171

-horses lose weight
-ataxia, posterior paralysis, muscle fasciculation, convulsions, death

Front 172

Bracken fern
-clinical signs in ruminants

Back 172

-bleeding, ulceration, cancer of bladder wall
-susceptible to infection

Front 173

Thiaminase
-treatment

Back 173

-provide Thiamine (Vit B1) early

Front 174

Bracken Fern
-treatment

Back 174

-blood transfusions
-antibiotics

Front 175

Diterpene esters
-plants

Back 175

Spurges (Euphorpbia sp.)
-unisex flowers
-3 chambered capsule fruitd

Front 176

Diterpene agents
-main effects

Back 176

-GI irritants
-blistering agents

Front 177

Diterpene esters
-toxic agents

Back 177

-phobols
-daphanes
-ingenols

Front 178

Diterpene agents
-mechanism of toxicity

Back 178

-mimics diacyleglycerol (DAG) which activates protein kinase C
-inflammation
-tumor production (decreased communication b/n cells)

Front 179

Diterpene agents
-clinical signs (small animals, livestock)

Back 179

Small animals
-GI irritation (salivation, vomiting

Livestock
-blistering of skin and mucous membranes
-salivation, diarrhea
-collapse and death

Front 180

Diterpene agents
-post mortem

Back 180

-no specific lesions
-inflammation, blistering, ulceration

Front 181

Diterpene agents
-treatment

Back 181

-supportive (NSAIDs, fluids, egg white, kaolin
-toxins insoluble in water/milk
-wash away from skin with warm soapy water

Front 182

Diterpene agents
-menegament

Back 182

-mostly unpalatable
-control with herbicides
-avoid in hay
-keep house plants out of reach of young dogs

Front 183

Grayanotoxins
-plant

Back 183

-Heath (Ericaceae)
-acid soils and forested regions

Front 184

Grayanotoxin
-main effect

Back 184

-inc. Na transport across cell membranes --> nerve and muscle depolarization

Front 185

Grayanotoxin
-chemical type

Back 185

-non-ester diterpenes w/ tetracyclic C-skeleton

Front 186

Grayanotoxin
-found in what plant parts

Back 186

-all including nectar & honey

Front 187

Grayanotoxin
-mechanism of toxicity

Back 187

-open voltage-dependent Na-channels on nerve and muscle cells
-maintain excitable cells in a depolarized state
-Inc. intracellular Ca
-uncontrolled muscle contraction

Front 188

Grayanotoxin
-clinical signs

Back 188

-GI (salivation, colic, vomiting, bloat)
-Nervous system (ataxia, recumbence, convulsions)
-Heart (sinus bradycardia, ventricular techycardia, hyperthermia)

Front 189

Grayanotoxin
-postmortem lesions

Back 189

-non-specific
-plant material in ingesta

Front 190

Grayanotoxin
-diagnostic test

Back 190

-qualitative thin layer chromatography
(serum, urine, ingesta, plant tissues, honey)

Front 191

Grayanotoxin
-treatment

Back 191

-decontamination (emesis, AC, laxatives)
-supportive therapy (IV fluid, antibiotics for aspiration pneumonia)
-rumenotomy to remove plant material
-atropine for sinus bradycardia

Front 192

Grayanotoxin
-management

Back 192

-have alternative food
-prevent pet access to ornamental plants
-test unknown plants

Front 193

Meliatoxins
-plant

Back 193

-Chinaberry (Melia azedarach)

Front 194

Meliatoxins
-reason for toxicity

Back 194

-feed on fallen berries when other food is not available

Front 195

Meliatoxin
-found where in the plant

Back 195

-all plant parts
-concentrated in fruit

Front 196

Meliatoxins
-mechanism of action

Back 196

Nicotinic-like affect
-stimulate autonomic NS ganglia ---> blockade
-GI irritation and inflammation

Front 197

Meliatoxins
-clinical signs

Back 197

-nervous system (restless, muscle tremors, cyanosis, paralysis, convulsions, death)
-GI (vomiting, diarrhea)

-need to ingest large quantity

Front 198

Meliatoxins
-Post Mortem lesions

Back 198

-lung contusions, edema
-hemorrhagic enteritis
-berries and woody pips in ingesta

Front 199

Meliatoxins
-treatment

Back 199

-No antidote
-decontaminate
-supportive therapy (diazepam for convulsions)

Front 200

Meliatoxin
-prognosis

Back 200

-poor if nervous system involved

Front 201

Carboxyatractyloside
-plant

Back 201

-Cocklebur (Xanthium strumarium)

Front 202

Carboxyatractyloside
-plant part

Back 202

-cotyledon stage of young plant/seeds
-persists in hay

Front 203

Carboxyatractyloside
-mechanism of toxicity

Back 203

-inhibition of mitochondrial adenine nucleoside carrier
-blocks ATP transport into mitochondria

Front 204

Carboxyatractyloside
-clinical signs

Back 204

-acute death
-CNS (muscle fasciculations, extensor rigidity, convulsions, coma)
-GIT (colic, salivation, vomiting)
-Liver (delayed signs)

Front 205

Carboxyatractyloside
-postmortem lesions

Back 205

-GIT (inflammation, cocklebur seeds/burs)
-Liver (pale, swollen, centrilobular hemorrhage, necrosis)

Front 206

Carboxyatractyloside
-diagnosis

Back 206

-history of plant access
-signs & lesions

Front 207

Carboxyatractyloside
-treatment

Back 207

-AC (early)
-supportive therapy

Front 208

Carboxyatractyloside
-prognosis

Back 208

-guarded/poor

Front 209

Avocado poisoning
-animals affects

Back 209

-caged birds (most)
-mammals

Front 210

Avocado poisoning
-main effects

Back 210

-cardiomyopathy
-sterile mastitis

Front 211

Avocado poisoning
-toxic agent

Back 211

-possibly Persin

Front 212

Avocado poisoning
-plant part

Back 212

-all plant parts
-Hass & Fuerte varieties

Front 213

Avocado poisoning
-mechanism

Back 213

-unknown

Front 214

Avocado poisoning
-signs (birds, mammals)

Back 214

Birds
-CHF
-Sudden death

Mammals
-CHF
-Sudden death
-Sterile mastitis
-Agalactia

Front 215

Avocado poisoning
-treatment

Back 215

-supportive

Front 216

Avocado poisoning
-prognosis

Back 216

-poor w/ cardiomyopathy

-good if limited to mastitis

Front 217

Black Walnut
-main effect

Back 217

-laminitis in horses

Front 218

Black Walnut
-toxic agent

Back 218

Unknown

Juglone
-toxic to fish
-heart, lung, liver affected in mammals

Crude water extract --> laminitis

Front 219

Black Walnut
-cause for laminitis

Back 219

-ingested wood shaving from bedding

Front 220

Black Walnut
-clinical signs

Back 220

-many horses affected in the same area
-laminitis

Front 221

Black Walnut
-treatment

Back 221

-remove contaminated bedding
-supportive (pain relief, foot baths, soft surface, prazosin)

Front 222

Black Walnut
-prognosis

Back 222

-good unless 3rd phalanx rotated

Front 223

Black Walnut
-management

Back 223

Avoid exposure
-check bedding
-remove black walnut branches from paddocks

Front 224

Photosensitivity
-define

Back 224

-abnormally heightened sensitivity to sunlight

Front 225

Primary vs. Secondary Photosensitivity

Back 225

Primary: ingestion of photodynamic agents

Secondary: reduced hepatic elimination of phylloerythrin (bacterial breakdown product of chlorophyll)

Front 226

Primary Photosensitivity
-plants

Back 226

-buckwheat
-St. John's wort
-Bishop's weed
-Spring parsley
-Dutchman's breeches
-Rain lily

Front 227

Primary Photosensitivity
-toxic agents

Back 227

-Polyphenolic pigments; furanocoumarins

Front 228

Polyphenolic pigments
-found where in plant

Back 228

-green plant parts

Front 229

Primary photosensitivity
-mechanism of action

Back 229

-absorb light and produce singlet oxygen (high energy reactive oxygen)
-oxidative tissue damage (apoptosis, necrosis, inflammation)

Front 230

Primary photosensitivity
-clinical signs

Back 230

-photophobia
-excessive tearing
-dermatitis (well vascularized, non pigmented skin areas unprotected with dense hair)

Front 231

Primary photosensitivity
-diagnosis

Back 231

-dermatitis of non-pigmented skin
-ID of photosensitive plants
-recovery after removal of suspected plants from diet

Front 232

How to identify photosensitizing plants

Back 232

-Inhibition of fungus (Candida albicans) grown under UV light

Front 233

Primary Photosensitivity
-treatment

Back 233

-avoid direct sunlight
-keep skin clean
-antibiotics for secondary infecitons
-recovery with supportive care

Front 234

Lilly
-plants

Back 234

-Lilium sp.
-Hemerocallis spp.

Front 235

Lilly
-main effect

Back 235

-nephrotoxicity

Front 236

Lilly
-animal affected

Back 236

-cat
-small-breed dogs

Front 237

Lilly
-toxic plant parts

Back 237

-leaves
-flowers

Front 238

Lilly poisoning
-clinical signs

Back 238

Initial
-vomiting, salivation, anorexia, depression

After 12-24 hrs
-PU/PD
-Vomiting
-Anuria
-Death (3-7 days)
-inc. BUN & creatinine

Front 239

Lilly
-treatment

Back 239

-induce vomiting
-antiemetic if cat is vomiting (metoclopramide)
-AC
-laxative
-IV fluid
-Peritoneal dialysis or hemodialysis

Front 240

Lilly
-prognosis

Back 240

-good with avoided anuria

Front 241

Macadamia nuts
-main effect

Back 241

-transient hind limb paresis in dogs

Front 242

Macadamia nuts
-clinical signs

Back 242

- < 12 hrs before hind limb weakness
-vomiting, ataxia, colic, pallor, recumbency
-recovery in 48 hrs

Front 243

Macadamia nut
-treatment

Back 243

-supportive
-induce vomiting

Front 244

Red maple
-main effect

Back 244

-hemolytic anemia in horses

Front 245

Red maple
-toxic parts of plant

Back 245

-wilted/dried leaves

Front 246

Red Maple
-mechanism

Back 246

-oxidant formas hydrogen peroxide in RBCs
-oxidative damage leads to Heinz body formation and methemogloinemia

-intravascular and extravascular hemolysis --> progressive anemia

-hemoglobin precipitation in renal tubules --> renal failure

Front 247

Red maple
-clinical signs

Back 247

-depression & anorexia
-tachypnea, tachycardia, icterus, hemoglobinuria, brown discoloration of mucous membranes
-peracute death
-abortion

Front 248

Red maple
-post mortem lesions (gross, histo)

Back 248

Gross
-splenomegaly
-icterus
-renal edema
-petechiae & echymosis

Histo
-tubular necrosis
-Hb casts
-erythrophagocytosis and hemosiderin accumulation in spleen

Front 249

Red Maple
-treatment

Back 249

-AC
-IV fluid
-blood transfusion & nasal oxygen insufflation
-ascorbic acid
-oxyglobin (blood substitute)

Front 250

Red maple
-prognosis

Back 250

-guarded to poor

Front 251

Red Maple
-management

Back 251

-don't have any Red Maple trees at or near equine housing
-avoid incorporation into hay
-remove red maple debris from wind storms

Front 252

Blue-Green Algae
-found where

Back 252

Water that is:
-fertilized
-warm
-stagnant

Front 253

Blue-Green Algae
-main effect

Back 253

-liver failure

Front 254

Blue Green Algae
-most common toxic algae species

Back 254

-Microcystis sp.

Front 255

Blue Green Algae
-hepatotoxic species
-neurotoxic species

Back 255

Hepatotoxic
-Microcystins
-Nudularin

Neurotoxic
-anatoxins

Front 256

Blue-Green Algae
-clinical signs

Back 256

-Gastroenteritis
-Liver failure (abdominal swelling, tenderness, jaundice)
-Anorexia
-Neurological dysfunction (tremor, seizure, respiratory paralysis)
-acute death w/ high dose

Front 257

Blue-Green Algae
-postmortem lesions

Back 257

-hepatosis (enlarged, congested liver with centrilobular necrosis & hemorrhage)

-no lesions with neurotoxins

Front 258

Blue-Green Algae
-diagnosis

Back 258

-ID algae in water samples
-Microcystin exposure confirmation by detection in water and liver (expensive)

Front 259

Blue-Green Algae
-treatment

Back 259

No specific
-emesis
-AC
-Bath (clean skin/hair)
-treat liver failure/neurological symptoms
-Atropine for some Anatoxin symptoms

Front 260

Blue-Green Algae
-management

Back 260

Public Health Problem!!!
-notify public health officials
-post warnings

Quarantine affected ponds for several weeks

Front 261

Blue-Green algae
-what are Microcystis dependent on for growth

Back 261

-Nitrogen