Rodenticide Toxicity In Animals by Dr.Amandeep
Transcript of Rodenticide Toxicity In Animals by Dr.Amandeep
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Rodenticide toxicity
Dr.AmandeepL2013V40M
Department Of Veterinary MedicineGADVASU
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ANTI COAGULANT RODENTICIDES
• 1st generation e.g warfarin,pindone
• Intermediate e.g chlorophalicone
• 2nd generation e.g brodifacoum
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MOA
• Direct capillary damage
Vit K is essential for hepatic synthesis of clotting factors
2,7,9 & 10
Disruption of normal coagulation
process of blood
Failure of blood clotting & inc
capillary permeability
Tissue hypoxia & massive internal
bleedingDeath
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Clinical signs
• Manifestation of hemorrhage including
anemia, epistaxis
• Ataxia,
• Colic
• Weakness
• Polpnea
• Depression & anorexia even before bleeding
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Lesions
• Hemorrhage in mm & body orifices
• s/c bleeding
• Blood fails to clot
• Hepatic necrosis
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Dx• On the basis of history
• Increased activated coagulation time of blood
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Rx
• Vit K1 (phytonadione)@0.25-5 mg/kg s/c
• Menaphthone @ 0.5- 2 mg/kg i/m
• Fresh frozen plasma @ 9ml/kg i/v
• Whole blood @ 20 ml/kg i/v
• Glucose and saline therapy
• Supplemental oxygen
• Oxalic acid derivatives
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ANTU
Increased permeability of lung capillaries
Massive pulmonary edema & pleural effusion
Animal drowns in its own fluid
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General considerations
• Abandoned rodenticide
• Ruminants are resistant
• Food increases chances of toxicity
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Clinical signs
• Vomition
• Labored breathing & cyanosis
• Incoordination & cyanosis
• Foam from nostrils & mouth
• Coma & terminal clonic convulsions
• Death within 2 hrs
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Treatment
• Emetics like apomorphine & gastric lavage if
respiratory distress is not evident
• Agents providing sulfahydryl groups eg thiosulphate
• Positive pressure O2 therapy
• Osmotic diuretic eg mannitol
• Atropine @ 0.02 – 0.25 mg/kg may relieve P. edema
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Cholecaciferol
Overdose of vit D3
Deposition of Ca in varoius
organs
Dysfunction of myocardial
conduction
Cellular degeneration in arterioles
Necrosis in renal tubules
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Clinical signs
• Develop within 18 – 36 hr of ingestion
• Depression & anorexia
• Polydipsia & polyuria
• Vomition with blood
• Hemorrhagic diarrhea
• GI smooth M excitability decrease results into constipation
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Treatment
• Gastric evacuation followed by administration of
activated charcoal@ 2-8 g/kg in water slurry
• Prednisolone @ 1-2 mg /kg
• Fluid therapy with NSS
• Furosemide@5mg/kg i/v followed by 3mg/kg tid
• Calcitonin @4-10 IU/kg s/c to reduce serum
calcium levels
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Strychnine
• Alkaloid from seeds of nux vomica
• Rapidly absorbed and metabolised to strychnine N oxide
• Used as malicious poison to kill stray dogs
• Competitive antagonist of inhibitory neurotransmitter
glycine
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Mechanism of action
Acts at glycine
receptors in spinal cord &
medulla
Lowers threshold
for stimulation
of spinal reflexes
Extensor rigidity &
titanic convulsions
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Clinical features
• Restlessness , muscle twitching & stiffness of neck
• Intermittent convulsions & relaxation
• Advance signs ar etonic seizures & opisthonous(saw
horse posture)
• Spasm of respiratory muscles or paralysis of respiratory
centre lead to death
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Lesions
• Cyanosis due to asphyxia
• Rapid onset of rigor mortis
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Diagnosis
• History and clinical signs
• Detection of strychnine(detected upto long
time after death)
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Treatment
• Phenobarbitone or chloral hydrate
• Gastric lavage with KmNO4 or tannins
• Acidification of urine & diuresis to promote excretion
• Muscle relaxants like glyceral guaiacolate@ 110mg/kg or methacarbamol
@ 150mg/kg followed by 90mg/kg
• Keep animal in warm and quiet environment
• Ketamine and morphine ar econtradicted
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Red squill
• One of the safest rodenticide with selective
action on rats and mice
• It induces vomition in dogs and cats
• Unpalatable for domestic animals
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Mechanism of action
• In small doses – induces convulsions
• In large doses – cardiac arrest
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Clinical features
• Vomition
• Ataxia & paralysis
• Alternate period of CNS stimulation & depression
• Bradycardia, aarhythmia & cardiac arrest
• Death occur wuthin 3 days
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Lesions
• Gastroenteritis with congestion , swelling & ulceration
of mucosa
• Congestion of abdominal & thoarcic organs
• Degenerative changes in kidney , lungs & myocardium
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Treatment
• Quinine sulphate or phenytoin @ 35mg/kg to suppress arrhythmia
• Atropine sulphate s/c at 8 hr interval to prevent cardiac arrest
• Other supportive measures
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Bromethalin
• Rapid oral absorption
• Metabolized by MFO to more toxic metabolite
desmethyl bromethalin
• Excreted through bile
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Mechanism of action
• Uncouples oxidative phosphorylation
• Loss of Na K ATPase & inhibition of Na pump
• Intracellular edema, swelling, & degeneration of cells
• Also induces cerebral lipid peroxidation
• Increased CSF pressure
• Dec impulse conduction, paralysis & death
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Clinical features
Acute toxicity
• Hyper excitability & seizures
• Muscle tremors & hind limb hyperreflexia
• Pyrexia & death within 10 hrs
Sub acute toxicity
• Tremors & ataxia
• Depression, vomition & lateral recumbency
• Effects reversible on termination of exposure
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Lesions
• Cerebral edema
• Spongy degeneration of optic nerve & posterior paralysis
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Treatment
• Symtomatic and supportive
• Mannitol @ 250mg/kg i/v 6 hrly to reduce cerebral edema
• Corticosteroids
• Ora fluiod therapy
• Diazepam or phenobarbitone to control seizures
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Fluoroacetates
• Most potent rodenticide
• Not specific for rodents
• Preparations are made black to distinguish from
other substances
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Mechanism of action
fluorocitrateInhibit active site of aconitase enzyme
Inhibiton of krebscycle
Most severely afeeted are brain
and myocardial cells
Blockage of cellular respiration
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Clinical features
• Dogs – exhibit signs of CNS excitation
• Horse, cattle, sheep, goat – cardiac abnormalities
• Cats – combination of both
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Lesions
• Severe enteritis
• Cyanosis
• Dark blood
• Organ congestion
• Hemmorhage in heart
• Pulmonary changes
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Diagnosis
• History symptoms and lesions
• Detection of excess citrate in kidney tissue
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Treatment
• Glycerol monoaceate @ 0.5mg/kg i/m in NSS
• Ethanol 50% or acetic acid 5% @8ml/kg orally
• Supportive treatment for convulsions & arrhythmia
• Emetics are contradicted
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Thallium sulphate
• Dec activity of –SH enzymes – succinic dehyrogenase &
MAO
• Toxicity is due to inhibition of S containing macromolecules
• It also competes with potassium for active transport
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Symptoms
• Gastroenteritis & abdominal pain
• Dyspnea & fever
• Conjuctivitis & gingivitis
• Tremors and seizures
• Hyper keratosis & dermatitis
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lesions
• Ulceration and hemmorhagic gastroenteritis
• Inflammation of resp mucosa
• Degenerative changes in heart , liver and kidney
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Treatment
• Emetics & gastric lavage with 1% sodium iodide solution
• 10 % iodide solution i/v
• Fluid therapy
• Sedatives
• Sod thosulphate/diphenyl thiocarbazone
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Zinc phosphide
• Non selective that is why hazardous
• More toxic after meals
• Due to increased acid production
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Mechanism of action
• Zinc phosphide + water & acid in stomach
• Production of phosphine gas
• Direct irritant to gut
• Inhibition of cyt c oxidase leads to tissue hypoxia
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Clinical features
• Dyspnea
• Abdominal pain
• Vomition of blood
• Ataxia
• Prostation
• Convulsions and coma
• Colic in horses
• Bloat in cattle
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Lesions
• Smell of phosphine from stomach contents
• Pulmonary congestion & edema
• Pleural effusions & sub pleural hemorrhage
• Congestion of liver and kidneys
• Gastroenteritis
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Diagnosis
• History and clinical signs
• Detection of Zn phosphide in stomach contents
• Analysis of phosphine in tissues
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Treatment
• Gastric lavage with 5% sod bicarb to neutralize stomach acidity
• Fluid therapy with cal gluconate or sod. Lactate to overcome acidosis
• 5% glucose i/v to prevent liver and kidney damage
• Demulsants & protectants to treat gastroenteritis
• Barbiturates to control convulsions
• Artificial respiration
• Activated charcoal
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Thanks