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Rodenticides Flashcards

1
Q

Why are rodenticides dangerous?

A
  • Designed to attract and kill mammals
  • Widely sold - recommended safety often ignored
  • occasionally used for malicious poisoning
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2
Q

What are the different kinds of Rodenticides?

A
  • Anticoagulants
  • Bromethalin
  • cholecalciferol
  • strychnine
  • Zinc phosphate
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3
Q

What are the first generation anticoagulants?

A
  • Often contain 0.05%
  • Warfarin
    • ID at Wisconsin Animal Research Farm
    • From dicoumarol found in hemorrhagic disease of cattle
    • Grazing moldy sweet clover
  • Diphacinone - Tomcat, Ramik, Mousemaze
  • Chlorophacinone - Rozol
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4
Q

What are the second generation anticoagulants?

A
  • Efficacious against resistant rats
  • More potent (lethal in single feeding)
  • Longer acting
  • Possible relay toxicosis (mouse ⇢predator)
  • Typical concentration is 0.005%
  • Brodifacoum (most common, highly toxic)
    • Talon, Havoc, Bolt, Volid, D-con Mouse-Pruf II
    • Maki, Contrac, One-Bite, Hawk
  • Diphethialone
    • D-Cease, Hombre, Generation
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5
Q

What are the Toxicokinetics of anticoagulants?

A
  • Oral absorption levels peak in minutes to hours
  • Plasma half life:
    • Warfarin - 14 hours
      • effects last a few days
    • Diphacinone - 4.5 days
      • effects last 12-30 days
    • Brodifacoum - 6 days
      • effects last 12-30 days
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6
Q

What is the normal clotting mechanism?

A
  • Prothrombin II
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7
Q

What is the MOA of Anticoagulants?

A
  • Vitamin K1 is regenerated by Vit K1 epoxide reductase
    • Anticoagulants block this recycling
    • also interfere with utilization by blocking synthesis of Vit K dependent clotting factors
      • Facto VII (PT) affected early
      • Factor IX (PTT) later on
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8
Q

What are the different toxicity levels of anticoagulants?

A
  • Acute oral LD50 in dog (mg/kg)
    • Warfarin 20-300
    • Brodifacoum 0.22-4 (LD10 0.20)
    • Bromadiolone 11-15
    • Diphacinone 0.9-8
  • Therapy should be started if dosage estimate is ¼ of LD10
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9
Q

What factors increase a mammals risk of anticoagulant poisoning?

A
  • Geriatric or neonatal animals
  • Concurrent liver disease
  • Ruminants, horses - moldy sweet clover
  • Protein displacing drugs
    • Phenylbutazone
    • Also Corticosteroids, Aspirin
  • Impaired platelet function or low counts
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10
Q

What are the clinical effects of Anticoagulants?

A
  • Related to hemorrhage and blood loss
  • Often weak, anemic, dyspnea, epistaxis, melena, lameness, ataxia
  • Occasional CNS signs (subdural bleeding)
  • hemothorax (dyspnea, sudden death)
  • May be acute death with no early signs
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11
Q

What necropsy lesions are common with anticoagulant toxicosis?

A
  • Hemorrhage, hematomas, hemothorax
  • Hemarthrosis; subdural hematomas
  • Occur in a variety of tissues, organs, spaces
  • platelet function normal
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12
Q

describe the clinical picture of anticoagulant toxicosis?

A
  • Clinical signs delayed
  • Initial sins are non-specific
    • Lethargy, depression, pallor
  • Varied Sx of bleeding tendency
    • Anemia
    • Melena, bloody vomit/diarrhea, point/area bleeding on mucous membranes, epistaxis, hematomas etc.
    • Bleeding into joints/sc bleeding in feet can cause lameness
    • Persistent bleeding rom venipuncture sites
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13
Q

How is anticoagulant toxicosis diagnosed?

A
  • Presence of hemorrhagic syndrome
  • Clotting time prolonged
  • Prothrombin time (@2-3 days) post exposure
  • Activated partial thromboplastin time (@3-5 days)
  • PIVKA-Proteins Induced by Vit K Antagonists (aka Thrombotest)
    • detects precursor proteins of clotting factors
  • Detection of active ingredient in liver, blood, bait
  • Liver - sample of choice in deceased animals
  • Blood - sample of choice in live animals
  • Hay - for dicoumarol
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14
Q

What are the typical clinical pathology results of acute anticoagulant toxicosis?

A
  • PCV < 30
  • Whole blood clotting - delayed
  • Clot retraction - normal
  • ACT - 2-10x normal
  • PT - 2-6x normal
  • APTT - 2-4x normal
  • Platelets - normal
  • FDP’s - normal
  • Regen/non-regenerative normocytic, normochromic anemia
  • Often leukocytosis
  • +/- thrombocytopenia
  • Abnormal clotting profile
    • One-stage prothrombin time (OSPT) (most sensitive)
    • Activated partial thromboplastin time (APTT)
    • Thrombin time (TT)
    • Activated clotting time (ACT)
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15
Q

What are the differential diagnoses for anticoagulant toxicosis?

A
  • Dicoumarol - livestock via moldy hay
  • Idiopathic coagulopathy
  • Autoimmune thrombocytopenia
  • DIC
  • Hereditary (Von willebrand’s Disease)
  • Liver disease (⇣ clotting factor synthesis)
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16
Q

What is the treatment for anticoagulant toxicosis?

A
  • Supportive:
    • Relieve hemothorax, raise PCV, Rx shock
  • Vit K1 (K3 ineffective)
    • PO with fatty food preferred
      • 3-5 mg/kg/d for 10 days (Warfarin)
      • 3-5 mg/kg/d 2-4 weeks (Brodifacoum)
      • 5 mg/kg/d 3-4 weeks (diphacinone)
      • Horses 2mg/kg/d max
    • Time lag 3-6+ hours for effective coagulation
  • Blood or plasma transfusion - immediate clotting factors
  • Monitor clotting function for 1 week
  • Prognosis is good to excellent
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17
Q

Why is Vitamin K1 NOT given IV?

A
  • high incidence of anaphylaxis
  • When phytonadione is given with a high fat meal, rapid absorption and activation of Vit K1 is nearly equal to IV admin without the risks
  • Also risks of puncturing a vein with a coagulopathy
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18
Q

Why should vit K3 be avoided in horses?

A

nephrotoxic

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19
Q

What is Bromethalin?

A
  • Rodenticide
  • Blocks mitochondrial energy production
    • especially in the CNS
  • Major toxic effect is cerebral edema
  • LD50: 0.3 mg/kg cats ; 2.5 mg/kg dogs
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20
Q

What is the clinical picture of high dose bromethalin toxicosis?

A
  • >0.5 mg/kg
  • Above LD50
  • Signs develop 4-24 hourse after ingestion
  • Muscle tremors, hyperthermia, hyperesthesia, excitability, seizures
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21
Q

What is the clinical picture of low dose bromethalin toxicosis?

A
  • Below LD50
  • Signs develop within 2-7 days
  • Progressive CNS depression with ataxia, paresis, hind limb paralysis, coma
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22
Q

What are the toxicity levels of Bromethalin?

(0.01% bait)

A
  • Dogs:
    • LD50 - 3.65 mg/kg
    • Min toxic - 16.7 g/kg
  • Cats
    • LD50 - 0.54 mg/kg
    • Min toxic - 3.0 g/kg
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23
Q

What is the MOA of Bromethalin?

A
  • Metabolized to desmethylbromethalin
  • Parent and metabolite uncoupled oxidative phosphorylation especially in the CNS
  • Reduced ATP impairs sodium pump & leads to fluid accumulation in myelin sheaths and CNS
  • Edema of myelin tracts leads to paralysis
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24
Q

What histopathology is common with bromethalin toxicosis?

A
  • Edema and spongiform change of myelin
    • Brain and spinal cord
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25
What are the clinical signs of low dose bromethalin toxicosis?
* Onset @ 24-36 hrs * Tremors * Ataxia * Vomiting * Anisocoria * Progressive depression * Hind limb paralysis * Lateral recumbency * Coma
26
What are the clinical signs of high dose bromethalin toxicosis?
* Onset in 4-36 hrs * Muscle tremors * convulsions * hyperexcitability * running fits * hyperesthesia * focal or generalized motor seizures precipitate by light/noise
27
How is Bromethalin toxicosis diagnosed?
* History of exposure * **Characteristic microscopic lesions in brain and spinal cord** * **Chemical detection of bromethalin in tissues (Brain, fat, liver, kidney)** * Possible hyperglycemia * EEG: * Spike & wave activity, voltage depression, abnormal Hi voltage slow wave typical of cerebral edema
28
What is the treatment of Bromethalin toxicosis?
* Early - before seizures - emetics * limit absorption * Repeat activated charcoal, saline cathartic (q12hrs for 6x) at half the original dose * **Dexamethasone** prolongs survival time but does not reverse syndrome * **Mannitol/furosemide** for cerebral edema * **Diazepam, methocarbamol, or phenobarbital** as needed for seizures * **Supportive care -** up to 3 weeks for recovery (if ever) * ILE
29
What is the prognosis of bromethalin toxicosis?
* Very guarded in moderate to severe cases
30
What are the environmental and Food safety concerns of bromethalin?
* All animals species are targets * Low probability for relay toxicosis * Food safety impact is not known * Fat soluble so can pass through milk
31
What is Strychnine?
* Extract of Stychnos-nuz vomica * Indole Alkaloid * Rodenticide - gophers and ground squirrels * underground use only * 0.5% or less * Red/Green dye
32
What is the MOA of Strychnine?
* Rapidly absorbed * Antagonizes glycine (neurotransmitter in inhibitory neurons) * Renshaw Cells in spinal cord and medulla * Inhibitory effects of reflex arcs are lost * Uncontrolled excitation of spinal reflexes * Predominantly extensor muslces * Excreted via urine
33
What are the toxic levels of strychnine?
* Dogs: * LD50: 0.5-1.2 mg/kg BW * Cats: * LD50: 2 mg/kg BW
34
What is the clinical picture of strychnine toxicosis?
* Acute onset - 15min - 2 hours * Nervousness, restless, tremors early after exposure * Rarely vomit * Sensitive to external stimuli - especially loud noises, touch, light * Saw horse stance * Explosive onset of tetanic seizures - whole body rigidity * Death from anoxia
35
How is Strychnine toxicosis diagnosed?
* Does not reliably produce lesions * bruising, hemorrhage from trauma * Finding bait in stomach is common * dogs rarely vomit * Dye from baits is a clue * Detection of strychnine in stomach * Urine too * Liver last resort
36
What are possible differential to strychnine toxicosis?
* Tetanus, Metaldehyde, Penitrem A, Roquefortine, Avitrol, Theobromine, Nicotine, Caffeine, Amphetamines, Cocaine, OPs, carbamates, pyrethrin, mushrooms, Blue-green algae, chlorinated hydrocarbons, water deprivation, etc * DDX for seizures is tough * Strychnine intoxications are exceptionally sensitive to external stimuli * start a violent seizure with a loud clap
37
What is the treatment for strychnine toxicosis?
* Control seizures * Diazepam, phenobarbital, methocarbamol, gas * Supportive care - respiratory * Decontamination * lavage, charcoal * Fluids * Diuresis, acidic urine ⇢ion trapping
38
What is Vitamin D3?
* “cholecalciferol” * Vit D2 - “ergocalciferol” - plant derived form * Vit D2 = 40,000units Vit D/mg * Vit D3 - 40,000IU of Vit D * 1 USP or international unit = 25 ng D3/D2
39
Sources of cholecalciferol?
* Pellet or cereal based baits (0.075%) * Place packs (10-30g) * Careless placement often leads to toxicosis in non-target species * Calcipotrience (Donovex lotion for psoriasis) * Potent, high risk for dogs * Vit D3 supplements * Plants: * S. malacoxylon, C. diurnum, T. flavescens
40
How much more potent is D3 to D2?
10x more potent for calcium uptake
41
What are the kinetics of Cholecalcipherol?
* Dog daily req is 22 IU (0.55ug/kg/day) * Absorption- rapid and complete in SI * Circulates in plasma to liver and kidney * Liver: Metabolized to Calcifediol (25-hydroxy D3) * Cytochrome P450 dependent * Kidney: Converted to toxic metabolite calcitriol (1, 25 dihydroxy D3) * Rate-limiting step * D3 metabolites excreted in bile
42
What are the toxic levels of cholecalcipherol?
* Minimum lethal dose: 5 mg/kg * 1-3 mg/kg toxic = 2.6 g bait/kg BW * Calcipotriol toxic at 50 ug/kg
43
What animals are most sensitive to cholecalcipherol?
cats\>\>puppies\>adult dogs
44
What is the MOA of Cholecalcipherol toxicosis?
* 1, 25 dihydroxy D3 in kidney * Increase **serum** calcium in 3 ways * Increasing absorption (Ca & P) from gut * Increase bone resorption via PTH * Increase renal retention via distal tubule resorption * Persistent hypercalcemia and hyperphosphatemia * Early **renal tubular damage and necrosis** * **Abnormal soft tissue mineralization**
45
What is the pathohysiology of Cholecalciferol toxicosis?
* Hypercalcemia - Conduction disturbances * Shortened Q-T segment and increased P-R * Bradycardia * Vasoconstriction and hypertension * Reduces cAMP ⇢ low ADH * Decreased NaCl absorption ⇢ Diuresis * Renal tubular degeneration * Polyuria & hypsthenuria * Azotemia
46
What are the clinical pathology presentations of Cholecalciferol toxicosis?
* **Hypercalcemia** \>12mg/dL * **Hyperphosphatemia** \> 7 mg/dL * Increased **BUN** and **creatinine** * USG 1.002 - 1.006 ⇢ **hyposthenuria**
47
What is the clinical picture of cholecalciferol toxicosis?
* Delayed 12-36 hours post-ingestion * Progressive signs * Anorexia, vomiting (+/- blood), depression, muscle weakness * Cardiac and renal changes * Bradycardia, heart failure * Hypertension, PU/PD
48
What lesions are common to cholecalciferol toxicosis?
* Renal tubular necrosis * Soft tissue mineralization * Kidney, heart, lung, stomach, intestine * Aortic plaques * Thyroid changes - uncommon
49
How is cholecaciferol toxicosis diagnosed?
* Serum calcium \>12 mg/dL * Bradycardia * Azotemia * Elevated D3 metabolites: 25-dihydroxy D3 * not all diagnostic labs test for these * Serum iPTH depressed * Tissue mineralization * Elevated kidney Ca & P * Ca \>2,000 ppm (normal \<600ppm)
50
What are the possible differentials for cholecalciferol toxicosis?
* Hypercalcemia of Malignancy * Chronic Renal Failure * Primary hyperparathyroidism * Feline idiopathic hypercalcemia
51
What is the treatment for cholecalciferol toxicosis?
* Extended regimen - weeks, $$$ * Recent ingestion - Emetics, cathartics, activated charcoal ASAP (continued 1-2 days) * **Saline Diuresis** (0.9% at 2-3x maintenance) * **Furosemide** - 5mg/kg IV then 2.5 mg/kg PO * **Prednisone** - 2-3 mg/kg oral * Block osteoclasts, GI and renal uptake * **Calcitonin**- 4-6 IU/kg SQ @ 2-3 hours initially * **Pamidronate**- IV infusion 1.3-2 mg/kg over 2 hours * inhibits bone resorption * Calcium restriction, anti-emetics, GI protectants
52
What are the environmental and Food Safety concerns with cholecalciferol toxicosis?
* All species are susceptible * Secondary intoxication can happen * Excreted in milk
53
What is Zinc/Aluminum Phosphide?
* Rodenticide 2-5% in baits * Limited Use - underground * Grey-black powder (76% Zn) * Decomposes in moist, acidic environments (ie stomach) * Becomes phosphine gas * Pungent odor (acetylene/garlic/fish) * Also used as a grain fumigant
54
What are the kinetics of Zinc/Aluminum Phosphide
* Hydrolyzed in acidic stomach * full stomach ⇡ reaction * Zn3P2 ⇢ PH3 (phosphine gas) + Zn + 2 * Phosphine gas is the main toxicant * Zn moiety is a strong emetic * Protective in dogs * Rats can't vomit
55
What is the MOA of Phosphine gas?
* Blocks cytochrome oxidase - (cellular respiration) * Blocks membrane ion transport in myocardium
56
What are the toxic levels of Zn/Al Phosphide?
* More toxic when consumed with food * Gastric acid = hydrolysis * Dogs: * 300 mg/kg empty * 40 mg/kg consumed with food * Sheep- LD50 60mg/kg * Birds- LD50 7-10 mg/kg
57
What is the clinical picture of Zn/Al Phosphide toxicosis?
* Acute onset- 15mins - 6 hours * Notably variable clinical signs: * Vomiting +/- blood * Anorexia * Lethargy * Rapid respirations * Abdominal pain * Ataxia * Seizures * Hyperesthesia
58
How is Zn/Al Phosphide toxicosis diagnosed?
* Non-specific and variable clinical signs * History of exposure * Myocardial and renal tubular damage, pulmonary edema * Volatile - collect, seal, freeze samples * Phosphine gas in stomach can be a necropsy hazard (Large animals) * Detection of elevated Az and P in stomach content
59
What is the treatment for Zn/Al Toxicosis?
* Detoxification/symptomatic/Supportive Care * Activated charcoal and cathartics * Antacids - raise stomach pH over 5 * Combat acidosis, hypocalcemia * GI protectants * Guarded prognosis, hypocalcemia * GI protectants * Guarded prognosis
60
What are the environmental and food safety concerns with Zn/Al toxicosis?
* Necropsy hazard * All animals * susceptible * Mass deaths reported in birds * Potential for secondary toxicosis * Food safety impact unknown

Toxicology (25 decks)

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