Week 7 Flashcards
Amides
- Alachlor, Bensulide, Propachlor, Propanil
Benzoic acids
Chloramben
Carbamates
Chloropropham
Dinitroanilines
Benefin
Diphenyl esters-
Nitrofen
Nitriles
Dichlobenil
Organoarsenicals
MSMA (methyl arsonic acid)
Phthalamic acids
Naptalam
Thiocarbamates-
EPTC & Triallate
Triazines-
Atrazine & Simazine
Phenoxy derivative of Fatty acids (2,4‐D
Sources: accidental ingestions of concentrates or sprays (cattle), grazing freshly sprayed pastures (cattle), Access to freshly sprayed lawns (pets)
• Generally sprayed forages @ recommended concentrations do NOT cause poisoning
Properties:
• Alter the metabolism of plants which increases their toxicity by increasing accumulation of nitrate or cyanide (making plants more toxic)
• Also improving palatability of some poisonous plants increasing poisoning
• Irritant to GI mucosa- acute exposure can lead to GI signs
• Not stable in the environment (this is true for the majority of chemicals used now, except Organochlorine)
• Not degraded by rumen microflora and do not alter rumen microflora (important)
Toxicity: depends on species and duration of exposure
• Cattle & Dogs = most susceptible (they eat everything)
• Dogs = most sensitive [Acute oral LD 50 ~100 mg/kg = moderately toxic]
TK:
• Readily absorbed from the GI tract or by inhalation [Poorly absorbed from the skin
Dipyridyls (Paraquat & Diquat)-
- Dipyridyls (Paraquat & Diquat)- most toxic group
Uses: Broad‐spectrum dessicant contact herbicides
• Paraquat (Gramoxone) is RUP and Diquat is GUP (Diquat has less absorption, and toxicity is local in the GI tract)
• Two forms: Concentrated forms (5%‐20%) for agricultural use and dilute forms for lawns and gardens
• Sprayed as 0.5 lb/acre for agricultural use – 3.5 mg/kg
Source: Ingestion of Concentrates. Malicious (common in St. Kitts)
Properties: Unstable, rapidly inactivated by light and soil
• The salts are soluble in water, poorly soluble in alcohol, and insoluble in hydrocarbon solvents
• Solutions are stable in neutral or acid conditions but destroyed by alkali
• Paraquat binds strongly to soil (can give instead of activated charcoal)
• Caustic to mucous membranes (leads to ulcers on tongue, buccal mucosa, GI tract – worse than 2,4-D)
Toxicity: All animals are susceptible, but especially dogs
• The oral LD 50 ranges from 25‐75 mg/kg in cats, dogs, pigs, sheep and humans
• Toxicity of paraquat is enhanced by (deficient of antioxidants) vitamin E deficiency, depletion of tissue glutathione, and oxygen therapy
• Daily oral exposure to 170 ppm paraquat causes chronic toxicity and death in dogs
TK:
• Diquat is poorly absorbed from the GI tract
• Paraquat is absorbed from the GI tract (
Pentachlorophenol (PCP)
Use: Only used by certified applicators as a wood preservative (to protect limber from fungal rot and wood‐boring insects)
• No longer found in wood preserving solutions or insecticides and herbicides for home and garden use
Source:
• The vapors can penetrate the intact skin and dermal exposure is the most toxic route of exposure especially for newborn animals
• Inhalation of toxic amounts from treated walls in sheds and barns (even if it was applied months or years before) especially with poor ventilation
• Licking wood treated with pentachlorophenol
• Ingestion of contaminated feeds or water with spills of PCP
Properties:
• chlorinated hydrocarbon insecticide and fungicide
• Not very soluble in water but soluble in oils and organic solvents
• The salts are soluble in water
• Volatile and can give off toxic vapors in toxic concentration especially in high ambient temperature for many years
• Not persistent in water, sewage or soil because of bacterial decomposition
• Irritant to mucous membranes, respiratory tact and skin
• Older preparations contained dioxins which are carcinogenic and teratogenic
Toxicity
• The acute oral or dermal LD50 in domestic animals ranges from 100 to 200 mg/kg (moderately toxic)
• Chronic toxicity ranges from 40‐70 mg/kg
• Factors increasing toxicity (things that increase temperature)
o High ambient temperature, oily or organic solvent vehicles, previous exposure, poor condition, newborn, and hyperthyroidism
• Factors decreasing toxicity
o Cold temperature, antithyroid drugs and presence of body fat
TK:
• Readily absorbed form the GI tract, by inhalation, and form intact skin
• Distributed throughout the body with some accumulation in body fat
• The half‐life in various species is 1.5‐2 days
• Metabolized by conjugation to glucuronic acid Excreted as glucuronides or unchanged in urine
• Residues in tissues and fat are depleted from the body within 1 week of exposure
MOA: Uncouples oxidative phosphorylation and blocks or decreases ATP
• Increased oxygen demand in an effort to produce ATP Oxygen demand is more than oxygen supply
• Resulting in overheating, metabolic acidosis and dehydration
• Irritation of the eye, respiratory, GI mucosa and intact skin
• Decreased cellular energy may cause neurotoxic and other effects (weight loss, decreased milk production, reproductive problems)
• High exposures may lead to signs of CNS stimulation or seizures
Clinical Signs
• Acute toxicosis- Onset and duration may be so fast that no signs are seen – CNS Stimulation
o Hyperthermia, tachycardia, dyspnea, cyanosis, seizure, collapse and death
o Newborn pigs show hyperthermia, skin irritation, and rapid death
• Chronic toxicosis
o Weight loss, decreased milk production, anemia, fetal malformations and may be abortions
o Fever and respiratory distress may be absent
Lesions:
• Rapid rigor mortis
• Local irritation of the skin and mucous membranes
• Pulmonary congestion and edema
• Degenerative changes in liver, kidney, and brain
• Dark blood (oxygen deprivation)
• Hyperkeratosis of the skin and villous like hyperplasia of urinary bladder mucosa in chronic cases
PCP Chemical analysis in blood and urine in a live animal, and kidney and skin in a dead animal
PCP Diagnosis– History of exposure, rapid overheating and respiratory distress, lesions of rapid rigor mortis and dark blood, and chem analysis
PCP DDx:
• heat stroke
• other Toxicants causing respiratory insufficiency
o Nitrate (brown blood, no fever), CO (bright red blood, no fever), Pesticides (marked neuromuscular signs, autonomic signs)
• Peracute infectious diseases
Treatment:
• Removal of the animal from site of exposure
• Detoxification - Emetics or gastric lavage with 5% sodium bicarbonate, Activated charcoal or mineral oil, Soap and water bath (w/gloves)
• Supportive and symptomatic therapy - Oxygen therapy
o Lowering body temperature by applying cold water to the skin, or ethanol
o Intravenous fluids (no glucose) and electrolytes for dehydration and metabolic acidosis
o Prophylactic use of antibiotics and multiple vitamins may be used to prevent secondary bacterial infections
♣ (due to liver, kidney and intestinal damage)
PCP Prognosis: If the animal survives for 24 hours, chances for complete recovery are fair
Nonprotein Nitrogen (NPN)
Sources: Urea is the most commonly used (but also the most toxic)
• Excess urea in feed as a feed additive (to create bacterial protein)
• Inadequate concentrates
• Contamination of feed by urea fertilizer
• Ammonium salt and ammoniated feed products
Properties:
• Liberation of ammonia (= Lethal synthesis, very rapid reaction(only an acute disease) – can slow reaction with ice cold water)
• One part urea produces about three parts proteins (protein equivalent = 300%, very cost effective)
• Urea by urease (rumen microflora) changes to ammonia (NH3) and CO2
• Ammonia aminates ketoacids (from soluble carbohydrate) to form amino acids
• Amino acids form bacterial proteins
• Bacterial protein is converted to animal protein
• Alkaline pH enhances hydrolysis of urea by urease (why give acid to inhibit the reaction)
• Urea is weakly basic
Toxicity:
• Ruminants are most susceptible (especially cattle), but horses are also susceptible
• Urea is the most toxic of all NPN compounds
• Feeding Management
o Usual concentrations of urea is usually 3% of the grain ration and 1% of the total ration
o Animals preconditioned or adapted to NPN are more tolerant
o The toxic dose in cattle not preconditioned or adapted is about 0.45 g/kg while the lethal dose in adapted animals is 1-1.5 g/kg
• Age: animals
