management of the poisoned animal Flashcards
bleeding could mean
sweet clover tox
extremity injury could mean
ergot
resp disease could mean
3 methyl indol tox
blindness differentials
-lead, Thiamin, sulphates, vitamin A,
Bracken
zonal skin disease think
-liver toxins
sudden death differentials
– blue green algae
- salt poisoning
approach to treating poisoned animal
- Stabilize
- Prevent further
exposure - Decontamination
- Supportive care
- (antidote) is available
herd outbreak investigation
-history: food, water, enviro, medications
-physical exam
-post mortam exam
-differentials: tissue, food and water collections
-triage: euthanasia, treatment or unaffected
-prevent further exposure: move animals, switch feed/water
-decontaminate
triage
- Complex decision making
- Severity of illness
- Value of animals
- Cost of treatment
- Welfare considerations
- Public safety – food animals
- Euthanize – How? -disposal
- Treat
- Unaffected
- (may need further testing)
Decontaminate – may need serious PPE
- Wash
- Purgatives:
- Stomach lavage-Rumenotomy
- Mineral oil
- Activated charcoal
- Change gut pH
- All unlikely to work
supportive care
Simple food
* Fresh water
* NSAIDs
* Rest
- Potentially:
- Oral fluids
- Iv fluids
- (Antidotes):
- Rare
- Quanitiy
botulism
-Clostridium botulinum: anaerobic, gram-positive, spore forming rod
* Extremely resistant spores
* Multiple exotoxins
* Type C and D usually involved with animal poisoning, B humans and horses
-ingested in preformed toxin in feed, water or cattion
-livestock: improperly ensiled feed/ poultry litter or dead animals in feed/ water. manure on pastures
dogs: ingestion in garbage, dead animals, water
* Other forms: wound botulism, toxicoinfectious botulism
ways for introduction of C. botulinium into the farm
-sialage/ wraps
-litter
-water
-food
-pasture
-forage
B O T U L I S M – T O X I C I T Y &
M E C H A N I S M
- Species sensitivity: all are susceptible
- Horses»_space;» ruminants, pigs, cats, dogs
- Very small amounts of carrion-contamination can kill horses
-large deaths of water fowl - Target: lower motor neurons
- Mechanism: prevents release of acetylcholine from presynaptic nerve terminal
- Flaccid paralysis
B O T U L I S M –
C L I N I C A L F E A T U R Es
- Ascending lower motor neuron paralysis**
- Onset: 12 hours to multiple days post-exposure
- Earliest signs: hindlimb weakness
- Decreased LMN reflexes and muscle tone
- Neuro exam: decreased reflexes and muscle tone
- Tongue, eyelids, tail
- Later: cranial nerve deficits
- Conscious
- Progresses to quadriplegia
- Death due to respiratory failure, aspiration
- No PM lesions
Botulism clinical in foals
- Shaker foal syndrome:
- 2 weeks to 8 months
- Source: soil
- Tremors that progress to recumbency
- Dysphagia
- Constipation
- Reduced tonge tone
-mydrasis
B O T U L I S M -
M A N A G E M E N T
Symptomatic and supportive care – intensive care cases
* Mechanical ventilation
* Enteral/parenteral feeding
* Repositioning
- Antitoxin:
- Botulism neurotoxin antibodies
- Purpose: reduce circulating toxin prior to binding to neurons
- Side effects possible, antitoxin DOES NOT REVERSE exsiting clinical signs
- Prognosis: guarded to poor
- Rapid development of symptoms: poor. recumbant horse=grave
botulism diagnosis
Diagnosis
* History of ingestion of spoiled food or carrion
* Progressive LMN signs
* Toxin identification or bacterial identification
* ELISA, PCR, mouse inoculation test, mass spectrometry
* Serum, stomach contents, feces, suspect food/carrion
* Serum: can be challenging due to low amount of toxin present
* Previously: mouse bioassay
- Differential diagnoses: coonhound paralysis (polyradiculoneuritis), tick paralysis, myasthenia
gravis, rabies - Horses: EPM, EMND, EHV1, EEE/WEE
-CSF normal
botulism prevention
- Round bales are risky
- Interior of bale may be rotten
- Exterior: visual inspection, feel for warmth
- Avoid feeding wet hay
- Avoid feeding spoiled silage and haylage
- Horses: vaccination
tetanus
-caused by clostridium tetani: gram positive, spore-forming anaerobe
* Ubiquitous
* Commensal of GIT
* Spores are very resistant
- Exposure scenario: spores enter a wound
- Creates anaerobic environment
- Recent field surgery, shering, retianed placenta, docking, castration
tetnus species sensitivity and toxin types
- Species sensitivity: horses, small ruminants > cats, dogs, cattle»_space;> birds
- C. tetani produces two exotoxins:
- Tetanospasmin: prevents release of GABA and glycine → uncontrolled muscular contractions
- Tetanolysin: local tissue necrosis, lysis of red blood cells
tetnus clinical features
- Onset: latent period
- Days to weeks after wound infection
- Generalized musculoskeletal stiffness: sawhorse stance**
- Extensors > flexors
- Progresses to muscle tremors (“tetany”)
- Prolapsed third eyelid**, abnormal blinking
- “Sardonic grin” in dogs, lock jaw
- Flared nostrils, fixed gaze, erect ears and tail
- Opisthotonus
- Death due to respiratory failure
tetnus clinical cardiac and resp
- Reflex spasms – responsive to external stimuli
- Cardiac and respiratory disturbances
- Tachycardia, bradycardia
- Hypertension, hypotension
- Sweating
- Congested MM
- Consciousness is unaffected**
tetanus management
- Penicillin, antitoxin, toxoid
- Wound management, supportive care
- Prognosis: guarded to poor in symptomatic animals
- Recovery can take several weeks to months
- Fatality rate in horses: 50-80%
- Prevention: vaccination
- Core vaccine (horses)
- Risk based (cattle)
tetanus diagnosis
- Clinical diagnosis: history and clinical signs
- Spastic paralysis
- No specific PM lesions
- Confirmation: typically based on history and clinical presentation
- Difficult to detect tetanolysin in plasma
- PCR for C. tetani
- Differential diagnoses: strychnine, tremorgenic mycotoxins
- Meningitis, polioencephalomalacia
anthrax cause/ species
Bacillus anthracis
* Anthrax toxin complex – 3 proteins
* Spores are extremely environmentally resistant
* Soil
* Outbreaks associated with liberation of spores**
in the environment
* Flooding, excavation, contaminated feed
* All species susceptible
* Outbreaks most common in cattle and sheep
anthrax clinical cattle sheep
- Onset: Peracute/acute
- Sudden death: animals found dead
- Septicemia: febrile, tremors, respiratory
difficulty, collapse, death - Edema
- Terminal hemorrhage from orifices** – nostrils,
mouth, anus, vulva - Bleeding due to breakdown of lymphatic
tissues and blood vessels - Incomplete rigor mortis
anthrax clinical pigs/ horses and PM lesions all species
- Pigs: subacute to chronic → swelling, fever, enlarged lymph nodes
- Horses: acute → fever, depression, subcutaneous swelling, colic, signs of sepsis
- Postmortem lesions
- Dark, unclotted blood
- Enlarged spleen
- Swollen, congested, hemorrhagic lymph nodes
anthrax management
- Often cannot intervene fast enough to save a symptomatic animal
- Antibiotics: penicillin
- Quarantine: separate sick animals, remove from contaminated area
- Field test kits available
- Reportable disease**
anthrax diagnosis
- If anthrax is suspected, DO NOT NECROPSY
- Inform lab of risk group 3 materials
- Samples: blood, edema fluid
- Microscopy, culture, PCR
- PPE
- DDx: water hemlock, urea, cyanide, nitrate, bracken fern, dicoumarol
- Non-toxic: blackleg, redwater, grass tetany, lightning strike
- Prevention: vaccination
cyanobacteria/ blue green algae
- Not true bacteria, but not true algae either
- Photosynthetic prokaryotic organisms
- “Harmful Algal Blooms” (HAB)
- Major public health and environmental health problem
worldwide - Numerous species of BGA, multiple toxins
- Not all BGA species are toxic
- How do animals become exposed?
- Consumption of contaminated water**
- Common in dogs and livestock**
factors leading to blue green algea HAB
Warm, sunny weather (15-30 °C) – multiple consecutive days
* Time of year: mid-summer to autumn
* Shallow water bodies
* Nutrient input / eutrophication
* Nitrogen, phosphorous
* Agricultural run-off, manure, etc
microcystines
- Microcystis aeruginosa, many others
- Clumped colonies
- Global distribution
- Prototypical toxin: microcystin-LR
- “Fast death factor”
- Many toxin congeners
- Stable in the environment
- Extremely toxic
- Lethal dose: approx. 0.5 mg/kg
microcystins mechansism of action
- Inhibition of protein phosphatases → disruption of cytoskeleton, oxidative damage, inhibition
of glucose metabolism - Target organ: liver
- Selective uptake into hepatocytes via organic anion transport polypeptides
- Acute liver failure
microcystines clinical features
- Onset: within 20 minutes to several hours post-ingestion
- Acute liver failure
- Vomiting, diarrhea with blood
- Weakness, shock
- Pale and/or icteric MM
- Hepatic encephalopathy, seizures
- Death within several hours
- Hypovolemic shock secondary to intrahepatic hemorrhage or liver failure
- Clinical pathology: elevated liver enzymes, indicators of liver failure, coagulopathy
- Prognosis: poor to grave
anatoxin A
-Dolichospermum spp., many others
* Filamentous appearance
* Less stable in environment
* “Very Fast Death Factor”
* Extremely toxic
* Target organ: CNS
* Cholinergic toxidrome – post-synaptic nAChR agonist
and inhibitor of acetylcholinesterase
anatoxin clinical
- Peracute neuroexcitation symptoms**
- Rigidity and tremors that progress to seizures
- Collapse
- Abdominal breathing and dyspnea, cyanosis
- Urination
- Death within minutes to hours due to respiratory failure
- Often found dead near water
- No specific PM or histologic lesions
cyanobacterium toxins management
- No antidote available
- Window for decontamination is narrow – often missed
- Microcystin: aggressive symptomatic and supportive care
- IVFT, colloids, dextrose, vitamin K1 (coagulopathy), hepatoprotectants, plasma/blood transfusions
- Anatoxin-a: aggressive symptomatic and supportive care
- Seizure control
- Mechanical ventilation – can be several days to wee
secondary poisoning with rodenticides
Also known as relay toxicity
* Carcass of a poisoned animal poisons the animal that consumes it**
* Scavenging wildlife, dogs at the greatest risk
* Some rodenticides have a very high risk* of secondary poisoning:
* Strychnine
* Fluoroacetate
* Bromethalin
* Second generation ACR
strychnine toxicity
- Strychnos nux vomica – strychnine tree
- Recently banned in Canada, for control of ground squirrels
- Poisoning occurs by:
- Consumption of strychnine-laced bait
- Consumption of a strychnine poisoned animal
- Malicious poisoning
- All species susceptible → dogs most frequently poisoned
- Target: CNS
- Toxicity: extremely toxic
- Dogs, horses, cattle: 0.5 mg/kg
- Cats, pigs: 1.2 mg/k
strychnine mechanism of action
- Glycine antagonist* at post-synaptic receptors in the spinal cord and medulla
- Disinhibition of motor neurons
- All skeletal muscles affected
- Results in uncontrolled stimulation of motor neurons**
strychnine clinical features
- Onset: within minutes – peracute
- Behavioural: apprehension, anxiety, agitation
- Neuromuscular: generalized muscle spasms
- Severe extensor rigidity**
- Tonic-clonic seizures**
- Responsive to external stimuli**
- Cyanosis
- Dilated pupils
- Sudden death possible
- No specific PM or histologic lesion
strychnine management
No specific antidote: aggressive decontamination and supportive care
* Asymptomatic: activated charcoal, can consider gastric lavage under GA
* Seizure control: diazepam, general anesthesia
* Respiration: intubation and mechanical ventilation
* IV fluid diuresis
* Manage of consequences of seizures: hyperthermia (DIC), rhabdomyolysis, hypoxia, acidosi
strychnine diagnosis
- Key clinical exam findings:**
- Sudden onset of neurological signs
- Extensor rigidity
- Seizures that are responsive to external stimuli
- Lack of GI signs
- Presence of strychnine in stomach contents, vomitus, urine, liver, bait
- Prognosis: poor to grave
- If animal can survive 24-48 hours, the prognosis improve
bromethalin
-in home and garden stores, extremely to highly toxic
* Dogs minimum toxic dose: 2.5 mg/kg BW (LD50: ~5 mg/kg BW)
* Cats minimum toxic dose: 0.3 mg/kg BW - most sensitive species
B R O M E T H A L I N – M E C H A N I S M O F A C T I O N
- Two major mechanisms:
- Uncouples oxidative phosphorylation in mitochondria → ↓ ATP production → impaired
Na+K+ATPase → loss of oncotic control in the brain - Oxidative stress: cerebral lipid peroxidation
- Culminates in cerebral edema**
- Effect on the CNS: long nerve demyelination, accumulation of fluid within myelin sheath +
increases in CSF pressure - Characteristic histologic lesion: intramyelinic edema**
bromethalin clinical features high dose exposure
- High dose exposures in dogs: convulsant syndrome**
- Asymptomatic for a few hours (~2-12 hrs) → acute progression
- Muscle tremors
- Hyperesthesia
- Agitation/hyperexcitability
- Running fits
- Seizures responsive to external stimuli
- Obtundation
- Death due to respiratory paralysis
bromethalin clinical features low dose
- Lower dose exposures in dogs + any dose in cats:
paralytic syndrome** - Delayed onset (one to several days post-exposure),
progressive clinical course (2 days-2 weeks) - Hindlimb paresis, ataxia, decreased proprioception**
- Cats: abdominal distension**
- Progression to:
- Loss of deep pain sensation
- UMN bladder
- CNS depression
bromethalin clin path features
- Clinical pathology
- Few changes on bloodwork: mild hyperglycemia
- May be hypernatremic
- Increased CSF pressure
- Normal CSF cytology – no inflammation, normal specific gravity and protein
bromethalin management
B R O M E T H A L I N – M A N A G E M E N T
* No antidote
- Early gastrointestinal decontamination is key:
- Activated charcoal + emesis
- Hypernatremia**
- Symptomatic patient
- Management of cerebral edema
- Seizure control
- Supportive care
bromethalin diagnosis
- Antemortem: history of exposure and compatible clinical signs
- Consider in cases of progressive hindlimb paresis
- Confirmation: detection of desmethylbromethalin in fat, serum, brain, kidney, liver
- PM: characteristic histology
- Diffuse white matter spongiosis / intramyelinic edema
fluroactive
- Sodium monofluoroacetate: Found in many plants
- Use in Canada (Alberta): livestock anti-predator collars
- 5 mg tablets
- Collars: 10 mg/mL
- Exposure scenarios
- Stockpiled
- Malicious poisoning
- High risk of secondary poisoning + tertiary poisoning
fluroacetate mechanism + toxicity
- Inhibits key enzymes in the Krebs cycle
- Converted to fluorocitrate–> shuts down citric acid cycle
- Target organs: CNS, heart
- Toxicity: extreme
- Dogs are the most sensitive species
F L U O R O A C E T A T E – C L I N I C A L F E A T U R E S
- Onset: within 30 minutes to multiple hours after ingestion
- Sudden death without clinical signs possible
- GI: vomiting, salivation, urination, defecation
- CNS: hyperesthesia, frenzied, convulsions with extensor rigidity, running fits
- Cats: vocalization
- Cardiorespiratory: profound tachycardia, dyspnea, cyanosis, ventricular fibrillation possible
- Death from cardiorespiratory failure
PM: extensor rigidity, congestion and hemorrhage in several organs
* Pulmonary hemorrhage
flouroacetate clin path and management
- Clinical pathology
- Hyperglycemia, hyperammonemia
- Metabolic acidosis, hyperlactatemia
- Hypocalcemia
- Elevated citrate (not routinely tested
-no antidote
- Supportive care: seizure management, fluids, correction of electrolyte derangements
- Prognosis: poor to grave
flouroacetate tox management
-induce emesis if fully consious
-gastric lavage and activated charcoal
-fluid therapy
flouroacetate diagnosis
- Antemortem: history of exposure and compatible clinical signs
- Confirmation: detection of fluoroacetate in bait, stomach contents, vomitus, urine
- Nonspecific PM/histo lesions
- Congestion and hemorrhage
- Myocardial necrosis has been reported in sheep
- DDx: same for strychnine + bromethalin
anticoagulant rodentacides
- First generation: warfarin, diphacinone, chlorophacinone
- Multiple ingestions required
- Second generation: brodifacoum, bromadiolone, difethialone, difenacoum
- “Superwarfarins”
- Developed because of warfarin resistant rodents
- One ingestion can kill***
- Longer half-life
anticoagulant rodentacides mechanism NAVLE
- Defect in secondary hemostasis
- Inhibition of vitamin K epoxide reductase
- Prevents recycling of vitamin K → depletion and
inability to synthesis clotting factors 2, 7, 9, 10
(“1972”) - Relative vitamin K deficiency
- First to be depleted: factor 7 → PT prolonged first
anticoagulant rodentacides clinical features
- Onset: delayed by 3-5 days post-ingestion
- Anorexia
- Lethargic, exercise intolerance, weakness
- Pale MM
- Dyspnea, tachycardia
- Petechiae, ecchymoses, hematomas
- Bleeding into any body cavity possible – affects the
clinical presentation - Brain
- Anterior chamber
- Thorax
- Abdomen/GIT
- Joints
anticoagulant rodenticides management asymptomatic animal
- Asymptomatic
- Decontamination: induce emesis, A/C
- Bloodwork: PCV/TP, (a)PT/(a)PTT
- Antidote: Vitamin K1 (phytonadione)**
- Give with fatty meal
- Option 1: start Vit K1 treatment**
- Duration: 21-28 days for SGARs
- Check PT 48-72 hrs after last dose
- Asymptomatic animal
- Option 2: unsure if animal was exposed
- Baseline PT → re-check in 48-72 hours
- If normal after 72 hours: no treatment required
- Start Vit K1 if PT is prolonged
anticoagulant rodenticides management symptomatic animal
- Symptomatic animal
- Decontamination contraindicated
- Immediate goal: stabilize animal
- Hemorrhage ± anemia**: FP, FFP contains clotting
factors - Whole blood – cross match
- Autotransfusion
- Oxygen
Once stabilized → give antidote
* Treatment duration: 28 days for SGAR
* Imaging depending on location of bleeding
* Fluids, supplemental O2
* Bloodwork: PCV/TP, PT/PTT
* Close monitoring q 6-12 hr until normal
anticoagulant rodenticides-diagnosis
- Diagnosis usually made clinically
- History of exposure, compatible clinical signs, prolonged PT/PTT***
- PT: extrinsic + common pathways (includes factor 7)
- PTT: intrinsic + common pathways (includes factors 2, 10
Differential diagnosis
* Prolonged PT/PTT: severe liver failure, DIC, vitamin K deficiency
phosphide rodenticides toxicity and mechanism
- Toxicity: oral LD50: 20-40 mg/kg BW for most species
- Contact with stomach acid** → release of phosphine gas
- Differences
- ZP: pH <4
- AP, MP: neutral pH
- Phosphine gas:
- Extremely irritating
- Oxidative damage to multiple organ systems
- Liver, kidney, lungs, heart, brain
phosphide rodenticides- clinical features
- Onset: as soon as 15 minutes post-ingestion
- Severe GI distress: vomiting, diarrhea ± hematemesis, hematochezia
- Animals that cannot vomit are at higher risk**
- Horses: colic signs**
- Shock, pale MM → cardiovascular collapse, arrythmias
- Profuse sweating
- CNS: lethargy or hyperexcitation (tremors, seizures)
- Pulmonary edema – tachypnea, dyspnea, cyanosis
- Death within 3-48 hours
phosphide rodentocides clin path features
- Delayed onset kidney or liver failure is possible**
- Characteristic odour: rotten fish or garlic (acetylene)
- Human health risk
- Clinical pathology
- Dehydration
- Elevated liver enzymes
- Azotemia
- Metabolic acidosis
phosphide rodenticides management
- No specific antidote
- Decontamination: well-ventilated area**
- ZP: neutralize stomach pH**
- Carbonate antacids
- Dilute sodium bicarbonate
- Tremor and seizure control
- Monitoring: CBC/chem, blood gas, thoracic rads if PE
suspected, liver chemistry including PT/PTT
phosphide rodenticides diagnosis
- History of exposure and compatible clinical signs
- PM lesions
- Hemorrhagic GIT
- Pulmonary edema
- Hepatocellular necrosis and steatosis
- Confirmation: detection of phosphine gas in stomach contents, vomitus, liver, kidney
- Prognosis: symptomatic patients that survive 24 hours have a better prognosis
phosphide rodenticides- human health
Phosphine gas is toxic to humans**
* US EPA: highly toxic via inhalation
* Hazardous at 0.3 ppm; death at 7 ppm
* Tubing a horse, vomiting animal in clinic, etc
* Symptoms in humans
* Dizziness, lethargy
* Nausea, vomiting
* Cough, dyspnea
* Liver failure symptoms: jaundice, delirium
* Coma
cholecalciferol (vitamin D3) toxicity and mechanism
Toxicity: acute lethal oral dose >2 mg/kg (dogs)
* Clinical signs >0.1 mg/kg
* >0.5 mg/kg → metastatic calcification
- Disruption of calcium and phosphorous homeostasis
- Hypercalcemia → dystrophic mineralization and multi-organ damage**
- Relevant toxicokinetics:
- Lipophilic
- Long elimination half-life
- EHC
cholecalciferol (vitamin D3) functions
Calcitriol actions: acts in liver/ kidney
* Increased intestinal absorption
* Increased tubular reabsorption
* Increased bone resorption
Hypercalcemia, hyperphosphatemia
cholecalciferol clinical features
- Onset: 12+ hours post-ingestion
- Weakness, lethargy, anorexia
- Vomiting, diarrhea (± blood)
- PU/PD
- Clinical pathological changes: hyperphosphatemia, hypercalcemia, azotemia, iso/hyposthenuria
- 12, 24, 72 hours post-ingestion, respectively
- Ca*P > 60 mg/dL: metastatic calcification**
-kidney injury and renal failure
cholecalciferol management
- Decontamination if not contraindicated
Contraindicated: - Ca-containing fluids (LRS)
- Thiazide diuretics
- Dose-dependent treatment
- 0.1-0.5 mg/kg: SC fluids, outpatient monitoring (tCa/iCa, P, PCV/TP, BUN, creatinine,
electrolytes, UA) - > 0.5 mg/kg: IVFT, baseline bloodwork and monitoring q24 hrs, cholestyramine
- Clinically affected:
- Hypercalcemia: IVFT, prednisone, furosemide
- Hypercalcemic gastritis: GI protectants
- CV monitoring: ECG, blood pressure
cholecalciferol diagnosis
- History, bloodwork (R/O other causes of hypercalcemia)
: Serum 25-hydroxyvitamin D - DDx: hypercalcemia → neoplasia, hyperparathyroidism (primary or secondary), kidney disease
- Prognosis:
- Good with early decontamination and supportive therapy
- Guarded to poor with development of renal failure
- Considerations:
- Prolonged clinical signs
- Chronic consequences of tissue mineralizatio
cholecalciferol PM lesions
- PM lesions: soft tissue mineralization:
kidneys, GIT, aorta, striated muscle - Histologic lesions:
- Degeneration and necrosis of renal
tubules - Calcium accumulation
- Von kossa stain
