Herbicides Flashcards
Herbicides
-Ag and household use
-Selective: typically not poisonous
-Less selective: arsenicals, chlorates, dinitrophenols
Herbicide exposures
-Spray drifts, groundwater contamination, treated pastures; accidental ingestion of concentrates or sprays
*animal dose is low
Post harvest interval
Period in which animals should be kept of pasture to avoid exposure to herbicides
Glyphosate
Roundup
-non selective systemic broad herbicide (inhibits enzyme that is only present in some plants and microorganisms)
-not toxic (very high LD50s)
What is issue with roundup?
-carcinogenic?
-has irritating surfactant which can cause GI irritation
-issue is that it makes some plants more palatable so if you spray it on a toxic plant, animals may then go eat it
Chlorates
-includes Na, Ca, K, Mg
-access to concentrates or recently treated forage= tastes salty
Mechanism and toxicity
Very low lethal dose, need to consume a lot to be poisoned
-Targets RBCs and irritate GI tract
-Results in oxidative damage = hemolysis & methemoglobin formation= mucosal damage
Onset of chlorate toxicity
Acute
Chlorate toxicity clinical signs
-GI: anorexia, abdominal pain, diarrhea, salvation
-weakness, exercise intolerance
-hemolysis (pale, brown, cyanotic; dark discharge; pigmenturia)
-resp difficulty/distress
Clinical pathology signs of chlorates
-intravascular hemolysis: yellow serum, hyperbilirubinemia, heinz bodies
-chocolate brown blood and methemoglobinemia
-methemoglobinuria
Management for chlorates
- Antidote= methylene blue
- IVFT and forced diuresis
Diagnosis for chlorates
Brown MM and chocolate brown blood
Ddx for chlorates
Oxidative damage hemolytic anemia +MetHb
-chronic Cu toxicity, nitrate/nitrite, Brassica spp, onions/garlic, Zn, mothballs, skunk musk
Prognosis for chlorates
Typically poor because oxidative damage is continuous
Paraquat
Bipyridyl group of herbicides
-works on contact (strong oxidizing/desiccating agent
-formulation often contains an emeti and offensive odour to deter ingestion
Paraquat animal exposures
-excessive application to forages
-ingestion of concentrates
-malicious poisoning
Paraquat target
Lungs
-accumulation in type 1 and type2 pneumocytes and clara cells
Paraquat mechanism
Oxidative damage from free radicals= acute alveolitis
-lipid peroxidation
-damages to mucosal surfaces
Paraquat acute clinical signs
Acute- from caustic action
-GI (vomiting, abdominal pain, diarrhea, GI mucosal ulceration)
-skin contact (blisters
Paraquat signs after a few days
Development of acute, severe respiratory distress
-tachypnea, dyspnea, cyanosis, hypoxemia
-pulmonary edema
Renal damage
Liver damage
What would you see if animal survives paraquat toxicity?
Extensive pulmonary fibrosis
Paraquat toxicity radiographs
-does not show severity
-alveolar pattern
-Pneumomediastinum
Gross and Histo signs of paraquat toxicity
Gross:
pulmonary edema, congestion = wet heavy lungs, ulcers of GI mucosa
Histo:
-pulmonary fibrosis, congestion, edema
-proximal tubular necrosis
Paraquat management
-no decontamination
-no antidote
-supportive care- mechanical ventilation
Diagnosis of paraquat toxicity
- history
- tissue quantification:
-Antemortem: plasma, urine, vomitus, bait
-Postmortem: lung, liver, kidney, bait, stomach
DDx of paraquat
-zinc phosphide
-second generation anticoagulant rodenticides
-cardiotoxic plants
-caustic substances
Prognosis for paraquat tox
Poor to grave
