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282 terms

Tox: All the Crap that ain't plants

STUDY
PLAY
Deet
non-toxic under normal use
excessive contact: peripheral/central nervous dysfunction
treat: symptomatically
Ant/Roach baits
usually not enough to cause poisoning.
More of a FB hazard
What do you do if your dog eats your girlfriend's Birth Control pills?
Feed your dog to your girlfriend.
Seriously...what happens?
May have excessive iron (concern level: >1mg/kg)
Estrogen (concern level: >20mg/kg)
May cause some bleeding tendencies. Don't do elective surgery.
How many typically pills would your dog need to eat to make this happen?
300. Yeah.
Consider the FB hazard and consider getting a more responsible girlfriend.
What about those little silica gel dessicant packet thingys?
Yeah, they're not poisonous.
May cause constipation or vomit.
FB hazard
So you went to a rave and got some of those glow bracelets. What will happen to your dog if he eats them?
He'll probably drool, become hyperactive, and do some head-shaking. Wow, the same things you were doing when you GOT them!
Tx: wipe off the fluid, use dark room to find
What about soaps (anionic/non-ionic)? Which soaps are these?
Bar soaps, hand dishwashing, household cleaners.
Are these soaps poisonous?
No. Remember when your mama washed your mouth out for saying ****?
May irritate the GI
Tx: symptomatically
What do I do if my dog drank out of the toilet???
Well, it depends if I went in there first. Assuming it was just water, the residue from the tablets/urinal cakes are only mild GI irritants
What if they eat the urinal cake?
Yummy...They will probably have severe vomiting and diarrhea
Mommy, I super-glued Fluffy's ears together!!!
Cyanoacrylate can be harmful to eyes.
Tx: don't pull skin apart
Flush eyes with water/saline for 15 minutes
Eyelids will separate in 1-4 days
Skin contact: mineral oil/vegetable oil
Mouth: let it wear away on its own
The next list of things are high risk chemicals.
So pay attention butt-hole
What is the hazard with polyurethane glue?
Can cause a blockage
How do you treat the ingestion of Gorilla glue?
usually need a gastrostomy.
emesis/AC is NO HELP
What if your dog likes to sneak a smoke occasionally? What are the signs?
Acute GI signs and transient severe neuro dysfunction
List off the toxic levels for tobacco...
Cigar 15-40mg
cigarette 15-30mg
butt: 5-7 mg
transdermal patch: 8-114mg

toxic effects occur at 1-2mg
LD50: 9.2mg/kg
Treatment for a smoking dog?
decon, fluids, take away his cell phone and car
What about those dermal patches? What kinds of patches are there?
Fentanyl: opiate (large amount)
Vitamin D (this is on the rise)
Nicotine

no treatment info.
How do cats get vitamin A toxicosis?
eating a diet high in raw liver (fish liver)
or Vit A supplements
a single dose can cause vomiting/diarrhea
What types of problems do you see with chronic toxicity?
cervical neck pain, neck/limb rigidity--exostosis, tense muscles
Tx: non-specific
What is the hazard of your dog eats a bottle containing citrus oil (D-limonene)?
eye/skin irritation, salivation, weakness, tremors, ATAXIA, POIKILOTHERMIA
Tx: wash, monitor, fluids, keep warm
Fido decides to eat a box of naphthalene moth balls (poor moths). What are the effects on the dog?
generates free radicals, changes Hgb to Mthgb, depletes glutathione
Can see secondary liver and kidney failure.
Heinz-body anemia
How would you treat for hyper-mothball-emia?
decontaminate
control vomiting
Methylene blue/N-acetylcysteine
What other kind of mothballs are there?
Paradicholrobenzene
What is paradichlorobenzene used for and what does it do to the dog?
used as a deodorizer in garbage cans/diaper pails/bathrooms.
It is a GI irritant: vomiting/diarrhea
Neuro effects: tremors seizures
How do you treat poisoning by pardichlorobenzene?
treat the neuro with Diazepam
IV fluids for the other crap
Paintballs...mmm, yummy. What do they do?
Act as osmotic cathartics
1-2hrs post ingestion:
GI, ataxia, tremors
Cardiac irregularities, blindness, seizures, hyperthermia
Acidosis, hypernatremia,
Damn...that's a lot of effects. How do you treat a dog that ate your brother's paintballs?
Emesis, IV fluids
correct the electrolyte imbalances.
Where is Xylitol found?
In sugar free gum.
What does xylitol cause?
stimulates bursts of insulin release and can cause hypoglycemia
Treat accordingly.
rarely it can cause liver failure
Caustic injury is caused by what type of solution?
Alkaline
Corrosive injury is caused by what type of solution?
Acidic
What if a dog ingests a battery?
Alkaline batteries are the biggest hazard due to possible leakage causing ulceration.
Lithium is becoming more common. If it is shorted out it may cause bad burns.
What about nickel/cadmium (ni/cad) batteries?
They cause kidney failure
What do you do?
Most batteries pass in 48-72 hours. Retained batteries cause perforation.

This is decision time. Surgery is non-life threatening, a retained battery is.
What is ethylene glycol?
a) Antifreeze
b) depressant
c) sweet tasting
d) BNB for pets
What does it cause?
acidosis then calcium oxalate in the kidneys and then renal failure 18-72h. BNB
What is the first sign?
the animal will be drunk (like you will be on friday night)
How do you diagnose it?
test serum for hypocalcemia & acidosis
Urine will show Ca oxalate crystals
BUN, creatinine
serum osmolality >20mOsm/kg
How do you treat this?
best option: 4-Methyl-1H-pyrazole (fomepizole) IV --works in dogs and high doses in cats
next option: 20% ethanol IV not a great choice b/c it can cause toxicity

Last option: Give the "finest quality Russian vodka IV", but booze can be toxic itself. WHAT???!!!
What are other antifreezes made of?
Methanol: windshield fluid
may cause CNS, GI issues
bad in humans, not so much in non-primates

De-icing agents: just cause skin irritation
Chocolate. Besides sticking to your ass, it has toxic effects. How do you determine which chocolate is of concern?
The more cocoa powder it has in it, the more toxic it is.
White chocolate: no worries
Milk chocolate: not much cocoa (candy bars)
Dark chocolate: bad
Baking chocolate: the worst
What does the effect depend on?
size of the dog, pre-existing heart conditions, epilepsy.
What are the toxins?
theobromine, theophyline: they are Methyl-xanthines (MX)
What are the signs?
6-12 hours, GI, ↑BP/HR, hyperexcitability, cardiac issues, seizures, DIC
death
Treatment for chocolate?
emesis/AC
CNS: diazepam
Cardiac: propanolol, lidocaine, atropine
What is Melaleuca oil?
Tea tree oil
used on animals for flea control
causes CNS effects in cats
no treatment
Petroleum
Toxicity: Sweet crude(TX) > sour crude (KS)
What will happen to cattle that ingest this?
laxative effect, aspiration
pneumonia, bloat, diarrhea
evidence of pain: grinding teeth
bone marrow suppression
Can have liver/kidney fail
How do you treat oil poisoning?
Mineral oil
Rumenotomy (add detergent)
What's the key to dealing with an oil exposure??
Don't settle with the crooked oil company for 6-12 mos to assess all the damage. Sue them bitches!!
What type of damage does a caustic agent do?
(drain cleaners/oven cleaners)
irritation but it is usually a bigger dose. Esophageal lesions with liquefactive necrosis
How do you treat caustics?
egg white, water/milk, sucralfate
DO NOT INDUCE VOMITING
Why are corrosives (acids) less hazardous?
They cause immediate pain and the animal learns quickly.
What do corrosives cause?
coagulative necrosis
the burnt tissue forms a protective layer.
How do you treat these?
milk/water/egg white
What are cationic detergents?
They are the ones used in automatic washing machines, fabric softeners, dryer strips.
What do they cause?
neuromuscular blocking (curare-like effect)
Oxidative toxicity to RBC's
How do you treat detergent toxins?
treat topicals like caustic/corrosive
ingestion: lavage, IV fluids, monitor cardiac/respiratory function
animal may die from resp effects.
Non-protein nitrogen: what is it?
Urea (most common)
Biuret
Ammonium sulfate
Mono ammonium phosphate (MAP)
Why is it used?
it boosts the protein of the feed
helps maintain neutral pH with high grain diets
improves microbial efficiency
improves digestion
How is it toxic?
excessive free gas (NH3) causes bloat
NH3 reacts with water to form ammonium hydroxide
forms a strongly basic solution
Increased pH promotes absorption of NH4 and causes CNS EFFECTS
How can you counter this effect?
NPN acclimation
feed carbs (microbes) consistently
clinical signs are?
bloat, excess salivation, uneasiness
then:
muscle tremors, tachypnea, tachycardia, freq. urination, stiffness, ataxia
Final stage:
collapse, convulsions death
What is the mechanism?
increased pH causes alkalosis which reduces oxidative phosphorylation and ATP production.
Lactate is produced and leaches into circulation causing acidosis.
How do you treat this?
Early and aggressive if possible
large volumes of cold water and vinegar into rumen
Antibiotics
10% formaldehyde
Rumenotomy
Diagnosis
Ammonia smell
history
high rumen pH
postmortem diagnostics
rumen content in sealed container and frozen immediately.
Feed assays
look for bloat-line
pulmonary edema and froth/fluid in trachea
What are some risk factors for NPN toxicosis?
high levels/abrupt intake of NPN
inadequate mixing
open fertilizer containers
high levels of soluble protein
NPN feeding recommendations (know this)
The rule of 3:
acclimate over 3 days
feed no more than 3% NPN
NPN should not be more than 1/3 of total nitrogen
AMMONIATED FEED: what is this condition called?
Bonkers
What causes it?
treating hay with anhydrous ammonia to increase digestibility, palatability and protein
This usually happens with better quality hay and causes the formation of what?
toxic pyrazines and imidazoles
What do pyrazines and imidazoles cause?
abnormal nerve function and convulsions
What happens to the animal?
Like an ex of mine, the animal goes bonkers. But this only happens in the animals for brief periods.
Define "bonkers".
they begin trembling, twitching, become ataxic, have apparent blindness, tachypnea, frothing, urination, defecation. Yep, just like ol' 'crazy Nancy' did.
Can this effect calves through milk?
yes
What is the recovery time?
1-3 Days after removal
Now how do you think you would treat this?
yeah, remove the toxic feed
prevent injuries
prevent nursing
(and in crazy-Nancy's case, change your number and move out of state)
NITRATE and NITRITE
NO3 and NO2
Plants absorb nitrate and nitrite. Which is the most important?
Nitrate
Uptake is controlled by 2 systems, what are they?
LATS: low affinity transport system
HATS: high affinity transport system (this one is ATP dependent)
What happens to nitrate in a plant?
it is reduced to ammonium by nitrate reductase.
When is NR production decreased?
when there is reduced protein production.
What are the risk factors for nitrate accumulation in plants?
during drought, Hot/cold weather
during growing season
in fertilized fields
herbicides
Basically:
anything that stops plant growth will increase nitrate concentration. Also plants that are bred to be crops take up and store LOTS of nitrates.
Where else can you find nitrates?
septic tanks
fertilizers
some soils
What happens in the ruminant with nitrates?
it is converted to nitrites (rapid, high capacity)
Nitrite is reduced to ammonia and belched out (not efficient or polite)
What are the toxic effects of nitrate?
GI irritation at high concentration
oxidation of Hgb to Mgb
What does Mgb (methemoglobin) do?
reduces oxygen carrying capacity of blood
How much Mgb is bad?
30-40% causes signs
70% + causes severe signs and death
Who is most sensitive?
neonates and fetuses (can see abortions)
Typically what would you see clinically?
Acute syndrome:
signs of hypoxia
(weakness, intolerance, tachypnea, collapse, convulsions, death)
What about the subacute and chronic syndromes?
Abortions 3-7 days post-exposure
weak calves
↓ milk production
↓ feed conversion
↑ infections
How do you treat the acute syndrome?
Methylene blue
How do you treat the subacute syndrome?
injectable/oral Vit A, D, E
iodized salt or organic iodine
high quality feed and many carbs
What do you see postmortem?
brown discoloration of blood and tissues
signs of GI inflammation
late term abortions/placental necrosis
What are good samples to submit?
serum
eyeball or aqueous humor (that's funny water)
What are the hazardous concentrations?
>3000-5000 may affect pregnancy/lactation
>10000 acute poisoning
(>1000 in water)
Management
test feed (yeah, right)
mix high/low nitrate feeds
abundant carbs
adaptation
propionibacteria inoculations into rumen 3wks prior to exposure
SULFUR-ASSOCIATED POLIOENCEPHALOMALACIA
Sulfur and sulfate
Where do you find sulfur around here?
in the ground water
feed supplements
manure wastes
algal blooms (fish die-offs)
fertilizers
How do sulfur/sulfate cause toxicity?
they are converted to sulfide
sulfide may or may not:
block neuronal energy metabolism
interfere with cerebral blood flow
generate reactive oxygen species
What's this animal look like now?
weight loss, rotten egg smell, diarrhea, rumen stasis, head pressing, convulsions, death
How about the clinical pathology?
metabolic acidosis
hypokalemia
hypochloremia
Treatment
if there is cerebral necrosis you're S.O.L.
postmortem findings
gray/black sulfide deposits in GIT
swelling, flattening of cerebral gyri
focal malacia or cavitation in midbrain and thalamus (may fluoresce)
may see herniation into foramen magnum
diagnosis
HS in rumen >2000 ppm
dietary sulfur/sulfate >.4%
GOSSYPOL: what is it?
a byproduct of cottonseed meal.
it is a yellow, toxic terpenoid aldehyde
What does it affect?
Heart, reproductive system, liver, membrane function
What are the 3 toxic effects?
Reactive oxygen species formed
suppression of cellular redox cycle
DNA scission
Where are the most potent effects?
in the heart
What are the risks?
Having protein in the rumen is protective. (gossypol bound to protein is less toxic)
so....ruminants on poor diet or very young
Clinically
acute: heart failure on exertion
Chronic: unthriftiness, ascites, death following exertion/stress
Chronic is similar to fescue toxicity
Postmortem lesion?
none in rapid cases
signs of heart failure
nutmeg liver (centrilobular necrosis)
Treatment?
duh, remove feed
SELENIUM POISONING
Selenosis
due to ingestion of poisonous plants or excessive supplementation
What is the most bioavailable type?
Selenate (SeO4 -2)
What type is used for supplements?
Selenite (SeO3 -2)
Plants
some are obligate accumulators: need Se for growth
some are facultative accumulators
What plants are responsible for most poisonings?
grasses and grains
Mechanism of poisoning
Se-methionine mimics Sulfur-methionine
What are the problems seen with Se poisoning?
keratin issues (hair, hooves, skin): those things that require sulfur
Acute syndrome
acute is usually iatrogenic
(polo cases in Florida)
weakness, ataxia, death in 48h
may have acute heart failure
Subchronic syndrome
hindlimb ataxia
paralysis
hoof separation
animals still alert
(happens in hogs)
Chronic syndrome
(alkali disease)
bilateral symmetrical alopecia
lameness
hoof separation
immunosuppression
DJD
anemia
Diagnosis
Se levels in diet/blood/liver/kidney
Treatment for Se poisoning
supportive, vit E?, poor prognosis
Chronic: arsenic, NSAIDS
What other mineral may exacerbate Se toxicity?
Copper (Cu)
IONOPHORES: what are they for?
originally as coccidiostats
Now also used for growth promotion
What adverse effects does monensin have?
it is corrosive and may cause allergic rxns
What is the mechanism of effect?
assists exchange of Na & H, et al
shifts microbial fermentation to propionic acid
causes net intracellular Ca buildup
inhibits mitochondrial function (↓ ATP) apoptosis
What is the lethal amount in cattle?
>10x the max label dose
What about horses?
they are more sensitive but as long as you stay in the labeled dose for cattle, horses shouldn't be affected.
What is a big risk factor?
compromised liver metabolism due to P450 enzyme
What does this cause ultimately?
Heart failure and death.
death my look like pneumonia
What is the clin path details?
↑creatinine phosphokinase (CPK) and alkaline phosphatase
↑LDH, AST, BUN, bilirubin, hematocrit
Postmortem findings
myocardial hemorrhages, paleness, fluid accumulation, lung congestion
Histo: myocardial/muscle degeneration/necrosis
necrosis in liver/renal tissue
FLUORIDE: what does it do?
about 50% sequesters in bone/teeth
What does chronic exposure do?
causes exostosis and spurring around joints.
Prominent effects in long bones, ribs, mandibles
What does it do to teeth?
causes excessive weakening, discoloration, hypoplasia
How do you diagnose this?
feed, mineral, water analysis
biopsy of coccygeal vertebrae or ribs
urine fluoride: within 1-3 wks
Kidney/liver: post mortem
Treatment
no specific Tx
Al or Ca-carbonate will reduce absorption
Anticholinesterase types
Organophosphates
Carbamates
Organophosphates
Sulfur group: -thion
Oxygen group: -oxon
How do OP's work?
OP-enzyme bond is very stable and may become permanent
Causes damage to neurons
phosphate:oxygen bond
(chem warfare: sarin, Vx)
Carbamates
carbon:oxygen bond
Carbamate:enzyme bond is unstable
POTENT & LETHAL
Carbamate example
aldicarb (illegal) called Tres pasitos
mechanism identical to OP's
aldicarb is extremely effective
Mechanism of acute poisoning
parasympathomimetic effects
neuromuscular
cumulative
Syndrome
delayed neuropathy (Dursban)
inhibition of neuropathy target esterases
persistent paresis/paralysis 10-14 days
not the same for every OP
Clinically for OP's
rapid (minutes)
salivation, vomiting, diarrhea, dyspnea, lung edema
paresis/paralysis/tremors
long duration in ruminants (slow abs)
diagnosis of OP poisoning
live: ChE inhibition in serum
dead: ChE inhibition in brain (active for several days)
chemical detection in liver/kidney/brain/fat
no pathognomonic lesions
Treatment for OP's
remove the source
bathe with soap (no H20)
AC
Atropine for cholinergic effects (doesn't work in cattle: nicotinic)
2-PAM for release from ChE
supportive
Pyrethrins/Pyrethroids
come from mums
excitatory neurotoxic effects
insects>mammals; toxic in aquatics
Pyrethrins
pyrethrin
cinerin
jasmolin
Pyrethroids (synthetic)
bifenthrin
permethrin
cypermethrin
these are more lipophilic, flip-flop kinetics. skin/fat are reservoirs
synergists: Piperonyl butoxide (p450) no incr toxicity in mammals
Mechanism
slows opening of voltage ion channels
uncontrolled nerve impulses
local irritiation
Clinically
Salivation due to lack of swallowing
Hyperaesthesia
twitching, paw shaking
tremors
fearful, restless, rolling, scratching
mainly peripheral nerve effects
Treatment
no antidote
Decon
Diazepam or Methocarbamol
May need Pentobarb/propofol/gas anesthesia
recovery may take 24-48h
Anticoagulants
1st gen: less potent, shorter acting
warfarin, coumafuryl
2nd gen: more potent, longer
bromadialone, brodifacoum, diphacinone, chloropacinone
mechanism of anticoagulants
interfere with Vit K recycling
interrupts coagulation pathways
kinetics
1st gen: 1/2 lives hours
2nd gen: 1/2 lives days
effects 12-30 days
drugs that suppress liver metab increase duration (cimetidine, sulfonamides, fluconazole, phenylbutazone)
Clinically
signs delayed 12-24h
initially non-specific
Bleeding tendency
anemia
melena/bloody vomit
bleeding into joints (lameness)
clin path
regen/non-regen n/c, n/c anemia
leukocytosis
abnormal OSPT, TT, ACT
Treatment
Decon
Vit K1 (must be K1)
transfusions
good prognosis if early tx/low dose
Now the uncommon pesticides
yeah, uncommon
Cholecalciferol
Vit D3
Rodenticides/human vitamins
Mechanism
acute lethal dose: 13mg/kg
chronic lethal dose: .55ug/kg
active metabolites in liver
incr Ca/PO4 abs in GIT
incr Ca re-abs in renal tubules
incr bone resorp
hypercalcemia/hyperphosphatemia
Clinically
lag time 36-48h
signs from hypercalcemia
weakness, ataxia, depression (nervous sys)
PU/PD, dehydration
Bradycardia/arrythmias
Tissue mineralization (specific to this)
Diagnosis
Clin path: PTH, hypercalcemia/-uria
Post mortem: tissue mineralization
Treatment
Decon: emesis/AC
restrict Ca & Phos
Pred, furosemide, IV
Pamidronate disodium
Metoclopramide
prog: good if no hypercalcemia
Strychnine
from Indian tree
very Potent
used in baits for mammals/pigeons
Mechanism
blocks effect of glycine on GABA
(suppresses reflex suppressors)
suppresses Cl conductance: uncontrolled depoloarization
Exaggerated reflexes
Clinical
Rapid onset: 10min-2hrs
seconds after injection
early signs: apprehension, anxiety,salivation
later: muscle spasms, rigidity, convulsions
Diagnosis
history
confirmed by testing stomach contents (serum, urine, liver, kidney)
Treatment
Decon: emesis, lavage, AC, cathartics
Control spasms: diazepam, P-barb, methocarbamol (can be life-saving)
supportive
Zinc Phosphide
Rodenticide moles, gophers, rats
Mechanism
highly corrosive, hemorrhagic GE-itis
Reacts w/stomach acid to release phosphine gas
MUST WARN PEOPLE
(smells like garlic)
Clincal
rapid onset <1 hour
GIT upset & hemorrhage
tremors/fasciculations, respiratory distress, shock
death in hours
lack of garlic odor doesn't mean safe
Confirming Diagnosis
collect phosphine gas with stomach contents (freeze; airtight)
Zn elevated in stomach/kidney
Treatment
Decon: Antacids to reduce gas, lavage
control muscle contractions
Metals...
yeah. Metals
Most important toxic effect of metals
Oxidative damage
(zinc)
Other effects
altered electrophysiology & osmotic states (Na)
competition (Mo/Cu)
errant binding on proteins (Pb/Ca)
Metals of veterinary concern
lead
copper
zinc
sodium
iron
arsenic (metalloid)
Lead effects
nervous system is primary target
GI irritant
Anemia
What is the public health concern?
increase Pb = decrease IQ
There is no safe exposure level in humans.
significant in animals
Sources
Lead carbonate in paint
Lead-acid batteries
Industrial/mining pollution
Lead shot/fishing weights, toys
kinetic factors
more surface area=more absorption
Acidic environment=more absorption
more time=more absorption
half lives from least to most
blood: days
liver/kidney: weeks
Brain: months
Bone: 1000 days
mechanism
Lead deposits where calcium should be
neurotx disruption, brain swelling
reduced/abnormal RBC production
GI irritation: esp in monogastrics
fertility issues
Diagnosis
Whole blood (not serum) because lead is associated with RBC's
Liver/kidney in dead animals
ALAD suppression (aminolevulinic acid dehydratase) used in wildlife
Lead line at growth plates on radiographs
Treatment
remove source
diuretics/corticosteroids for edema
Thiamine (for clinical signs)
Sulfate salts (to reduce absorption)
Chelation
Ca-EDTA (used in cattle due to cost)
Dimercaperol (BAL): crosses BBB
Succimer (DMSA): high cost; d.o.c. in small animals
Penicillamine: birds/cats
Management
poisoned pet means probable affected human
remove lead! duh
Copper is biggest concern in what animals?
Sheep and goats
pigs are very resistant
classic sign of copper toxicity
gun-metal black kidneys
Sources of copper
feed (Mo deficiency)
Orchard sprays
Algaecides
Footbaths
Industrial
mechanism
Cu accumulates in sheep liver over time
High Cu and stress cause Cu release from blood
Oxydative damage to RBC's: hemolysis
Clinical
chronic exposure or acute stress
signs: Anemia, icterus (dramatic)
Liver/renal failure/GI Irritation
Clin path for Copper toxicosis
methemoglobinemia
Anemia
Hemoglobinuria
decreased Glutatione
signs of liver failure: ALT/AST CRT,BUN
Post mortem
icterus, gun-metal black kidneys
Treatment
poor success in acute poisoning
Remove the source (no ****)
Chelation with penicillamine
Give molybdenum
Management?
don't feed cow feed to sheep
Cu:Mo ration at 6:1-10:1
Molybdenum poisoning
excessive Mo= Cu deficiency
lightening of coat
diarrhea
glucose intolerance/diabetes 2
American bison have this
Zinc effects
hemolytic anemia in dogs
other species: pancreatitis
Hemolysis and non-specific signs
Confirming dx
incr liver enzymes
incr zinc in serum, liver/kidney, pancreas
collect serum in royal blue tops
Treatment for zinc
Antacids (immediately)
Chelation: Ca-EDTA, Succimer
supportive
Sodium effects
brain edema
eosinophilic meningoencephalitis
How does sodium toxicity occur?
too much salt, not enough water
in desert/brackish water
most common in pigs
signs slower in cattle
Signs of sodium toxicosis
neuro: circling, ataxia, blindness, dog-sitting position, seizures, opisthotonis etc..
Confirming
brain sodium > 2000 ppm
Treatment
slow rehydration (by enema, perhaps)
furosemide
poor prognosis w/neuro signs
IRON poisoning sources
usually miscalculated injections in pigs
human supplements enough to poison dogs
Fertilizer:
ferrous fumarate (33%)
ferrous sulfate (20%)
ferrous gluconate (12%)
Iron mechanism
corrosive to GI mucosa
Bound in blood to transferrin, unbound leads to oxidative damage
uncoupling of ox-phos (no ATP)
DIC
Clincally
1-6 hours: vomit, diarrhea
6-24 hours: heart & liver failure
2 weeks +: GI scarring/strictures
On injection the GI effects are bypassed: anaphylactic shock
Post mortem
gastric ulceration
yellow-brown discoloration
swollen liver, discolored
Icterus
dark kidneys w/ periportal necrosis
Confirming
history
radiographs may show
Serum iron and TIBC
Treatment for iron
emesis/lavage
laxatives
GI protectants don't help much
fluids
transfustion
CHELATION: Deferoxamine (iron specific)
ARSENIC (and old lace?)
Inorganic: GI issues, irritant
Organic: crosses lipid membranes & easily absorbed/distributed
Many tissues
Inorganic arsenic sources
herbicides, insecticides, treated wood, paint
Paris green/Scheele's green
Organic treatment
Chelation (early): DMSA (succimer)
BAL (dimercaprol) most effective but difficult to obtain
supportive
fluids
bicarb
blood
antibiotics
Vit B
Organic aresenic
non-irritating
easily absorbed
neuro effects
Organic sources
feed additives
heartworm tx for dogs
Thiacetarsamide (Caparsolate)
Organic mechanism
Axonal demyelinating neuropathy
sciatic and optic
Capillary dilation in nervous tissue
interferes with thiamine (B1) role
clinical
onset: days to weeks
pigs: ataxia, goose stepping, paresis in hind limbs
blindness 1-2 days after paresis
pig at the bottom of the pile, prone to being chewed on
Post mortem
neuronal degeneration of sciatic/optic nerves
Treatment
remove source
recovery if effects <2 days
2-4 weeks withdrawal needed
All done with Metals
Yeah, done.
Toxicant
a poison
toxin
a poison derived from organisms: animals, plants, algae, fungi, bacteria
Toxicity
potency
Venom
poisonous secretion produced in special glands and delivered via specialized delivery system
Venin
a single component of a venom
Envenomation
act of venom delivery
Venomous reptiles
Pit vipers
Coral snakes
Gila monsters
Pit viper members:
Crotalus & Sisturus (rattlesnakes)
Agkistrodon (copperheads, cottonmouths, water moccasins)
Coral snake members
Elapids: Micrurus & Micruroides
Gila monster members
Heloderma
Amy Murphy
where is the pit on a pit viper
rostral to the eye
Venom delivery
venom travels from venom glands to accessory glands which activate the venom
What % of bites are dry?
25%
What % of bites are severe?
10-15%
Major venin classes
Hyaluronidase (spreading factor)
Myotoxins (muscle necrosis)
Hemorrhagic toxins (hypercoagulation, hypocoagulation, fibrinolysis)
Cardiotoxins (western/eastern diamondbacks)
Metalloproteinases (general tissue necrosis)
Neurotoxins (transmitter release stimulation/inhibition/blocking)
effects of envenomation
humans: much more necrosis
Dogs: more swelling
Systemic: mimics organophosphates (hypotension & neurotoxic effects)
Treatment
Crotalib Fab antivenom (CroFab)
IV fluids
antibiotics
NOT corticosteroids
Dose based on:
venom load (not patient weight)
delayed effects: anaphylaxis/allergy
Elapid snakes
coral snakes
not aggressive, bites are rare, dry bites common
Elapids also contain:
World's most venomous:
Australian fierce snake
Black mamba
Egyptian cobra
Is there an antivenom on the market for these?
Yes, but it is in Mexico. Not in the U.S.
Bite syndrome
Neurotoxin: blocks ACh receptors
muscle paralysis
may be delayed
resp. distress
Hemolysis up to 72 hours later
Treatment for Elapids
Antivenom (unavailable in U.S.)
Coralmyn in Mexico
Crepe compression bandage
not in pit vipers
Treat symptoms (hosp for 48 hrs)
Gila Monster (Heloderma suspectrum) venom
glands on lower jaw
venom stored intracellularly
slow envenomation (long contact time)
Hypotension, nausea, vomiting
teeth hang on victim
Treatment for Gila Monster
bite is painful: pain killers (lots)
check for retained teeth
treat hypotension
Control bleeding (really, do you need to be told this?)
Antibiotics
****ing Toads
Colorado River Toad: Bufo alvarius America
Can Toad: Bufo marinus (Australia)
Syndrome
Bufagenins/Bufotoxins (cardiac glycosides)
LSD-like hallucinations (dopamine, epi, serotonin)
Larger toads more toxic
These are SCHEDULE 1 drugs
Signs
hypersalivation, vomiting, pawing at mouth, inflamed mucous membranes
Cardiac arrythmias, ataxia, collapse, seizures
Treatment
antidote available for cardiac
Flush membranes, rub mucous off
AC may help
NOT Atropine (if tachycardic)
Digibind
Diazapam, phenobarb
IV, furosemide
Black Widow
Latrodectus
Bites
rare in animals
more common in idiots
Distribution
worldwide
dark, undisturbed, close to ground
Color
Black, brown, grey
Red/orange hourglass on ventral abdomen (they won't roll over for you)
Toxins
neurotoxins
sweating, cramping muscle contractions, restlessness, arrythmias, hypertension, pulmonary edema
Death
rare but usually from respiratory paralysis.
Cats are thankfully more susceptible
Treat?
Antivenin: very effective
Lyovac: slow IV injection
Symptomatic
NOT Calcium gluconate
Brown Recluse
Loxosceles reclusa
no web, roams at night
violin on dorsal thorax
Toxicity
initially not painful
necrotic lesion
hemolytic anemia with (-) DAT/Coombs test (not from venom)
Treatment
wound cleaning
Anti-inflammatory/analgesics
antibiotics
Fire Ants
Solenopsis
Syndrome
Papules develop into pustules in 24hrs (persist 2-3wks)
anaphylactic shock
treatment
symptomatic
antihistamines, steroids, epi
Bees and Wasps
contain vasoactive amines, peptides and phospholipase (coagulopathy)
Blister beetles
Epicauta
in alfalfa
produce cantharidin
Syndrome
digestive tract/urinary tract:
diarrhea/frequent urination
Colic
shock/rapid death
hypocalcemia/hypomagnesemia: diaphragmatic flutter & muscle fasciculations
unchanged in urine: vagina/vulva effect
Diagnostic tests
stomach & urine content
500ml
any concentration is relevant
wing shields float in water
Treatment
no antidote
enhance elimination (AC/mineral oil)
treat colic (analgesics/a2 agonists)
correct dehydration
correct mineral deficiencies (if heart flutters)
Fireflies
Photinus spp
poison
lucibufagins: related to cardiac glycosides
Acute cardiac toxicity and death
usually in bearded dragons
no treatment
Arizona bark scorpion
Centruroides sculpturatus
polypeptide neurotoxin
syndrome
pain, hyperaesthesia, agitation, tachycardia, hypertension
anaphylaxis possible but rare
Treatment
Antivenom: Alacramyn (mexico)
experimental in U.S.
control pain
maintain airway