Toxicities Flashcards

1
Q

Lathyrus hirsutus(Caley Pea) Intoxication in a Herd of Horses

Holbrook et al, JVIM 2015

A

Results: Bermuda grass hay consumed by the horses contained large quantities of mature Lathyrus hirsutus. Acute clinical signs conform to earlier descriptions of Lathyrus hirsutus intoxication in cattle. Residual neurologic signs were characterized by incoordination in the rhythmicity of multiple gaits. Evidence of mild neurogenic muscle atrophy was recognized in 1 of 5 horses biopsied.

Conclusions and Clinical Importance: Caley Pea intoxication may occur within days of seed pod consumption. The neurologic signs are unique and suggest involvement of the upper motor neuron system and regions of the spinal cord influencing voluntary motor movement. Drought conditions during plant growth may increase the risk of toxicosis

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2
Q

Poisonweed

Staggerweed

A

delphinium

larkspur

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3
Q

delphinium:

toxin and mechanism

A

NEUROTOXIN

Diterpene alkaloid (methyllyca-conitine)

Mechanism: NMB –> resp paralysis

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4
Q

delphinium: toxic part

A

it flowers early, so poisonings occur in spring or fall

early growth or dried parts are worse - less bad after flowering happens

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5
Q

delphinium suceptibility

A

Cattle > horses > sheep

LD50 cattle is 0.5% BW = 17g/kgBW

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6
Q

delphinium CS

A

NEUROTOXIN

Sudden death
CNS signs, aspiration pneumonia, bloat, constipation, regurg, salivation

Death d/t resp paralysis/bloat  animals fall w/ head downhill
Fatalities within 3-4hrs

Lesions: nonspecific; bloat, congestion, pneumonia, GI inflamm

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7
Q

delphinium TX

A

Prognosis: guarded

(1) AC + SC
(2) Physostigmine (rarely have enough)
(3) Turn head uphill
(4) Relieve bloat
(5) Abx for asp pneumonia

Prevention: move to new pasture, spot spray, revegetate

*An affected animal may be mistaken for a grass tetany case; however, treatment with magnesium exacerbates the effect of larkspur’s toxins at the neuromuscular junction and should be avoided.

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8
Q

Lathyrus hirsutus

A

sweet pea vetchlings

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9
Q

Osteolathyrism

Neurolathyrism

A

Lathyrus hirsutus

sweet pea vetchlings

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10
Q

Lathyrus hirsutus / Osteolathyrism

A

neurotoxin of cattle in the SE US

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11
Q

Lathyrus hirsutus: toxin and mechanism

A

Aminopropionic acid derivative

Mechanism: interferes with glutamate receptors in the brain, causing influx of Ca2+ into cells = cell death

Heat-labile = cook it to destroy!

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12
Q

Lathyrus hirsutus: clinical signs

A

NEUROTOXIN

Neurolathyrism: neuronal degeneration; mm rigidity, paralysis, bradycardia; horse: abnormal gait, hopping gait, tying-up, head low, laryngeal hemiplegia

Osteolathyrism: cattle –> lameness after 3-5d; boney Δ
Horses –> skeletal deformities and aortic rupture (defective cartilage/connective tissue)

–>Holbrook case report

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13
Q

poison hemlock

A

Conium maculatum

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14
Q

Conium maculatum: toxin and mechanism

A
Piperidine alkaloids (like nicotine): conine
EXTREMELY TOXIC; LD50 < 10g/kg 

Mechanism: Direct cholinergic effects (antagonist and agonist) – large dose causes skeletal m stimulation followed by neuromuscular blockade and paralysis

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15
Q

Conium maculatum: toxic part

A

Young plants = LOW alkaloid concentrations

Roots, stem, leaves and fruit = toxic

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16
Q

Conium maculatum: clinical signs

A

Nicotinic: salivation, bloating, tachycardia progressing to incoordination and colic

2’ cardiac arrhythmias

Teratogen: 1st trimester = cleft palate, brain/face problems, arthrogryposis, hydrocephalus : Seen in cattle that consumed between 40-70 day gestation

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17
Q

Lathyrus hirsutus: TX

A

Prognosis: full recovery OR chronic

(1) Gastric lavage
(2) AC + SC
(3) Symptomatic + supportive therapy

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18
Q

Conium maculatum: TX

A

1) Emetics (don’t repeat if vomited)
(2) Gastric lavage
(3) AC + SC
(4) Resp support (IPPV or Dopram)
(5) Diazepam (seizures)

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19
Q

Water hemlock

A

(Cicuta maculatum or Cicuta douglasii)

Among most poisonous plants in US

also toxic to humans

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20
Q

Water hemlock: toxin and mechanism

A

Cicutoxin (unsaturated alcohol)  seizurigenic
EXTREMELY TOXIC
2oz kill sheep
8-10oz kill cow

Mechanism: Acts directly on CNS as a violent convulsant (GABA antagonist)

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21
Q

water hemlock: toxic part

A

stem and root

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22
Q

water hemlock: CS

A

Seizurigenic: rapid onset (15-60min) –> salivation, abdominal pain, tremors, seizures –> death due to respiratory failure

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23
Q

water hemlock: TX

A

Prognosis: good if survive 2hrs (excrete alcohol)
Control seizures
Alcohol molecule size too small for AC

Tx with barbituates to control seizures

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24
Q

jimson weed

A
Belladonna alkaloids:
Jimson weed (Datura stramonium)
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25
Belladonna alkaloids exposure:
seed contamination of grain, plant contamination of forage all plant parts are toxic
26
Belladonna alkaloids : toxin and mechanism
Belladonna alkaloids = antimuscarinic: Belladonna (Atropa) --> atropine Mechanism: competitive antagonism at muscarinic receptors preventing acetylcholine binding
27
Belladonna alkaloids: CS
mostly toxic to ruminants Antimuscarinic: tachycardia, tachypnea dry skin, ↓salivation, mydriasis (can be topical), blurred vision, hyperthermia, ↓feed, tremors, bloat, recumbancy
28
Belladonna alkaloids: TX
(1) Physostigmine (2) Emetic/AC CS resolve within 24hrs – death is rare
29
Yellow Star Thistle
(Centauria solstitialis) Russian Napweed
30
Yellow Star Thistle: toxin and mechanism
Unknown NOT HIGHLY TOXIC **only toxic to horses signs after grazing 30-90d (hundreds of ##) Contains a neurotoxin destroys dopaminergic nigrostriatal pathway – inhibiting effects on cerebral cortex pathways that control prehension and chewing (CN’s V, VII, IX)
31
Yellow Star Thistle: CS
Mixed CNS: hypertonic facial/lip mm, tongue lolling, head tossing, dysphagia, immerse head in water to drink  death 2’ starvation Lesions: pathognomonic bilaterally symmetric nigropallido-encephalomalacia – liquefactive necrosis in globus pallidus and substantia nigra “Sardonic grin” is class term used to describe facial lesions
32
Yellow Star Thistle: TX
Irreversible once symptomatic euthanize
33
Locoweeds
(Astragalus spp, Oxytropis sericea)
34
Most destructive to livestock of all poisonous plants
locoweed whole plant is toxic
35
Locoism: toxin and mechanism
Locoism:alkaloid swainsonine inhibits mannosidase  brain accumulation of oligosaccharides (generalized lysosomal storage disease of CNS)
36
Locoism: CS
Methemoglobinemia  fetlock knuckling (cracker heels), dyspnea, cyanosis, death (24hrs); abortion (fetal Hgb sensitive); brown blood Locoism:  CNS dep, dullness, emaciation, ataxia, then excitement; reduced fertility (cattle); abortion Teratogen: skeletal problems
37
Locoism: TX
Selenosis: no tx; allow to excrete; soft bedding; change diet Locoism: improve feed; horses = euthanize
38
Cardiac Glycoside Mechanism
Inhibit membrane sodium-Potassium-ATPase pumps – intracellular sodium increases and potassium decreases – changes in ions flux decreases electrical conductivity = arrhythmias Used therapeutically to increase myocardial contractility (by decrease intracellular sodium, increases intracellular calcium through Na:Ca Exchanger – more calcium available to actin-myosin apparatus
39
Nerium oleander
Oleander | Toxin = cardiac glycoside
40
Oleander suceptibility
ruminants on ionophores are MORE susceptible
41
CARDIAC GLYCOSIDE CS
Early (GI) = projectile vomiting, diarrhea; bloating, salivation Later (CV): hypotension, bradycardia,Vtach, SVT, conduction probs Even later: sudden death Death hrs or days after ingestion Lesion: cardiac mm necrosis
42
CARDIAC GLYCOSIDE TX
MEDICAL EMERGENCY (1) Emetics (2) AC + SC (3) AVOID K+ in tx (4) Manage cardiac effects for 1-3d (drugs designed for animals w/ pre-existing cardiomyopathy) = unless lethal arrhythmia, don’t be too aggressive w/ heart Treating arrhythmias: Bradycardia: atropine Heart block: phenytoin Tachyarrhythmia: propranolol Digitalis Abs (FAD antibody): Digibind (works well but $$$)
43
Milkweed
Asclepias spp Toxin = Cardenolides (Cardiac glycoside) AFFECTS SHEEP
44
Nerium Oleander Asclepias / Milkweed Taxus cuspidate / Japanese Yew Zigadenus / Black Snakeroot / Death Camas
Cardio toxins
45
Taxus cuspidate
Japanese yew Toxin = Taxine A and B cardio toxic
46
Zigadenus spp
Black snakeroot Death camas Toxin = steroidal alkaloids cardio toxic
47
Veratrum spp
teratogen in sheep toxin = cyclopamine, veratramine
48
Lantana, Crotalaria, and Ragwort and Groundsel are all
hepatotoxins
49
Crotalaria / Senecio: toxin and mechanism
Pyrrolizidine alkaloids --> pyrrole derivatives (must be bioactivated) --> irreversible liver damage (hepatocyte DNA alkylation, megalocytosis)
50
Crotalaria / Senecio: CS
Hepatic veno-occlusive dz --> icterus, ascites, edema--> fibrosis Liver necrosis and death: bipsy – triad of fibrosis, bile duct proliferation and megalocytosis
51
Ragwort mechanism
Pyrroles crosslink DNA – antimitotic effect and hepatocytes can’t divide = replaced by connective tissue = megalocytosis
52
Perilla frutescens
Perilla mint
53
Perilla mint: toxin and mechanism
Perilla ketone (similar to 4-ipomeanol from moldy sweet potatoes) --> reactive metabolite in Clara cells --> lung damage (especially alveolar Type I cells; proliferation of type II pneumocytes = interstial pneumonia)
54
perilla mint: CS
``` Acute bovine pulmonary emphysema & edema (ABPE) Respiratory distress (grunt on exhale), nasal discharge, cyanosis, hypersalivation ``` Lesions: pulmonary fibrosis, emphysema, edema, congestion
55
perilla mint: TX
No specific antidote Hard to reverse once CS Supportive: steroids, antihistamines, abx Prevention: eliminate Ddx for ABPE: moldy sweet potatoes, lush pasture (3-methylindole)
56
Pteridium aquilinum
bracken fern
57
bracken fern: toxin and mechanism
Ptaquiloside – primary carinogen Causes bone marrow supp  ↓neut/plt/anemia SE: thiaminase  thiamine deficiency (horses and pigs = NOT cattle)
58
bracken fern: CS
Bone marrow: hemorrhage on mucus membranes, hyphema, melena, anemia Thiamine deficiency: anorexia, wt loss, weakness, ataxia, crouching stance, arched neck in horses polioencephalomalacia (ruminants) Bladder neoplasia = Red water disease (cattle/sheep)
59
Veratrum tenuipetalum; V. californicum”
Hellebore Over 50 alkaloids – some are teratogenic Sheep: if consumed on 14th day of gestation = CYCLOPS LAMP (Boards ?) and monkey faced facial deformities After 30-35 days, shortened limbs
60
bracken fern exposure
Common in South East US Exposure: fresh plant or dried in hay (young fronds palatable) More likely in dry years
61
bracken fern tx
give thiamine
62
Organophosphates and carbamates
Both are acetylcholinesterase (AChE) inhibitors w similar chemical effects Carbamates are esters of carbamic acid OPs are esters of phosphoric acid
63
Organophosphates and carbamates: mechanism of action
Can enter body through oral, dermal or resp route Bind and inhibit the AChE (and other cholinesterases) within the nervous system, the neuromuscular junctions and blood, causing an accumulation of the acetyl choline neurotransmitter at postsynaptic receptors OP’s considered irreversible inhibitors of the enzymes, whereas carbamates are reversible inhibitors of AChE
64
Muscarinic signs of AChE inhibition
vomiting, dyspnoea, colic, salivation, lacrimation, urination, diarrhoea, miosis, tracheobronchial secretion, lung oedema, cyanosis
65
Nicotinic signs of AChE inhibition
twitching of muscles, tremors, followed by convulsions, and seizures which can finally progress to paresis and even paralysis
66
Organophosphates and carbamates: diagnosis
atropine test dose – preanaesthetic dose of 0.02 mg/kg IV à if HR decreases and mydriasis occurs, it is not an OP or carbamate poisoning antidote tx for OP: atropine sulphate and pyridine 2-aldoxime methochloride (2-PAM) - -atropine will control muscarinic R associated signs. 0.22 mg/kg (1/4 dose given IV, remainder IM or SC) - -2-PAM will control the nicotinic signs. 2-aldoxime methochloride reactivates the AChE enzyme and can control nicotinic and CNS associated signs. Has to be administered within 24 h of exposure. Dose in horses is 20 mg/kg slow IV, repeated q 4-6 h. Not recommended for carbamate toxicosis because this drug has less affinity for carbamates and the AChE inhibition is usu rapidly reversible
67
metalaldehyde toxicity
Cyclic tetramer of acetaldehyde Toxicity characterised by CNS signs, metabolic acidosis and resp alkalosis Exact mechanisms unknown, but decrease in the conc of the inhibitory NT GABA, noradrenaline and serotonin (5-hydroxytryptamine, 5-HT) as well as increased monoamine oxidase activity may be involved CS usu within 15 min to a few hours: agitation, ataxia, hypersalivation, hyperaesthesia, muscle spasms, profuse sweating, convulsions, tachycardia and hyperpnoea. Signs of severe and unrelenting colic also reported. Death, usu dt resp failure, can occur within a few hours of ingestion and oft preceded by violent convulsions