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
2
Q
What are the different kinds of Rodenticides?
A
- Anticoagulants
- Bromethalin
- cholecalciferol
- strychnine
- Zinc phosphate
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
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
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
- Warfarin - 14 hours
6
Q
What is the normal clotting mechanism?
A
- Prothrombin II
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
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
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
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
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
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
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
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)
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)
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
- PO with fatty food preferred
- Blood or plasma transfusion - immediate clotting factors
- Monitor clotting function for 1 week
- Prognosis is good to excellent
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
18
Q
Why should vit K3 be avoided in horses?
A
nephrotoxic
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
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
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
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
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
24
Q
What histopathology is common with bromethalin toxicosis?
A
- Edema and spongiform change of myelin
- Brain and spinal cord
