Toxicology
The study of poisons and their effects on normal physiological mechanisms.
Learning Outcomes
1. Explain the effects of adverse toxicology
1.1
Define poison, toxin, antidote
1.2
Discuss how animals obtain access to poisons
1.3
Review the common categories of poisons and major clinical signs
Range: rodenticides/pesticides, molluscicides, medicines, herbicides, household
chemicals, insect stings, plants, heavy metals
1.4
Explain the use and preparations required for standard emergency therapy
Range: removal from source, prevention of absorption, supportive therapy
1.5
Explain the products and equipment used in an emergency poisons kit
1.6
Explain the recommendations for inducing vomiting
Range: time of ingestion, type of poison, emetics available
1.7
Explain the information required from the owner at the time of contact
Range: poison source, degree of exposure, present clinical condition, rate of
deterioration
1.8
If applicable, be able to give advice to owner on convalescent patients
Definitions
Poison: substance causing injury, illness or death
Toxin: poisonous substance, usually a protein, produced by living cells and capable of causing tissue
damage. Usually induces an antibody/antitoxin formation.
Antidote: remedy to counteract the effects of poison
“The dose makes the poison”
To cause intoxication a substance must be absorbed and delivered to the site of action at a
concentration high enough to elicit a physiological response.
Toxins are susceptible to the same processes of absorption, distribution, metabolism and excretion
that drugs are.
Absorption: usually oral or dermal routes (occasionally respiratory)
 Prevention of absorption is clinically important in management of toxicities
either gastric decontamination (emesis, activated charcoal, gastric lavage, whole bowel
irrigation)
or dermal decontamination (washing skin)
Metabolism: it is preferable in terms of reducing toxicity to make toxins water soluble which aids
elimination. Note that metabolism of a toxin does not always alter its toxicity, it may be more less or
the same degree of toxicity.
Distribution: the toxin must reach the site of action to exert an effect. Distribution is affected by
organ perfusion, lipid solubility, protein binding, tissue affinity, special barriers e.g. blood/brain
barrier.
The volume of distribution is important: if large, plasma concentration is low and the toxin is
bound/concentrated in tissues, e.g. digitalis. If small, plasma concentrations are high and the toxin is
accessible for dialysis, e.g. ethanol
Excretion: consider urine, faeces, bile, air, milk saliva. Note public health significance of milk.
How do animals obtain access to poisons?
 Two most commonly involved species (French survey) are dogs (36%) and cattle (24%), both
animals that will eat almost anything.
In groups, discuss how you think animals obtain access to poisons, and list the ways below:
(any differences between small animals and farm animals?)
A survey of reported poisoning incidents showed the following distribution of types of poison in
animals:
Pesticides 45% (of which rodenticides 42%)
Pollutants 20%
Veterinary drugs 19%
Plants 14%
List some names of common poisons that fall into these categories:
Pesticides
Pollutants
Veterinary Drugs
Plants
Therapeutics
Treat the patient, not the poison. Discuss what this means
Six principles of treatment for poisoned animals







Telephone advice
Reduce absorption
Specific antidotes
Increase elimination
Supportive
Future exposure
TARA SAIES FuE
TA
RA
SA
IE
S
FuE
Telephone Advice:
On the telephone: be calm, clear and concise.
Small Animals:
Obtain a brief history
Clinical signs yet? If so, rate of deterioration
Probable toxin, route of exposure, amount, when?
Immediately to clinic, with package and any vomit
Decide if owner should induce emesis
(do not delay treatment, usually only if a long way from clinic, collect vomitus)
Large Animals:
In addition obtain the following information:
Number of animals
Recent management changes
Collect food and water samples
Farm visit
Role play: Discuss the role of the veterinary nurse in the first aid of poisoning patient. Then in
threes, one as a client, one as vet nurse on the phone, one observer. Choose a poison from the list
at the back of the notes(other than slug bait and rat bait), prepare what you will say for a few
minutes then do your role play, observer to feedback on what went well, points for improvement
etc.
Discuss your response to an owner ringing with concerns about a pet suffering from a possible
deliberate poisoning by the neighbour who has complained about the dog barking. Why is it
particularly important to take care with what you say and agree with the owner about in this case?
Reduce absorption:
Decontaminate:
Ocular = eye wash
Dermal = skin wash (protect yourself)
GI = emesis, charcoal, laxative
Decontamination of the Animal, How and Why
A schematic representation of the decontamination process.
ANIMAL POISONING
Conscious animal
POISON
KNOWN
DERMAL
UNKNOWN
ORAL
DERMAL
Wash off
< 4 HOURS
Home vs Vet Clinic
________________________
•
•
•
•
Hydrogen peroxide 3%
Sodium Carbonate
Dry mustard
Zinc sulphate
Wash off
ORAL
Same as with
Known poison
> 4 HOURS
Veterinary Clinic
DECONTAMINATE
• DOG – apomorphine
• CAT – xylazine
• ANTIDOTE use if one is
available for the poison
± GASTRIC LAVAGE
• Supportive therapy
_________________________
• NO emetic
• Activated charcoal
• Laxative
± GASTRIC LAVAGE
Principles of emesis
Remember contraindications: (corrosives, volatile hydrocarbons, unconscious, rabbit, rodent, horse,
ruminant, convulsive agents/convulsions, coma).
Explain why these situations contraindicate emesis.
Time: after 4 hours, emesis is of little value, Also depends whether poison is liquid/solid. Liquid
material passes through the stomach more rapidly.
Type of poison: if corrosive, dilute with milk
Effective emetics: apomophine, xylazine, soap flakes, ipecac syrup
Specific Antidotes:
Vit K1 (anticoags), atropine (OP’s), acetyl cysteine (paracetamol)
Improve Elimination:
Manipulate urinary pH
Peritoneal dialysis
Induce diuresis
Supportive:
Fluids
Seizure control
Maintain body temp
Control specific signs
Future Exposure:
Remember prevention, other at risk animals, public health.
Prepare a poster that you could put in the prep room to remind you what to do in poison cases.
Poisoning Crash box: see hand out from Sandra Forsyth.
Sources of Information about Poisons
1. National Information Centre for Poisons and hazardous Chemicals Dunedin.
Telephone: 0800 764 766 (urgent) or 03 479 7248
2. Product packaging
3. Toxicology textbooks
Common Poisons
Rodenticides COMMON
Usually anticoagulants.
Mechanism of action: interfere with blood clotting factors due to inhibition of vitamin K 1 :
therefore bleeding time is prolonged. Antidote – konakion (vit K1)
First generation = warfarin
Second generation = brodifacoum “Talon” 30 days + activity
Usually blue/green baits
Clinical signs: (2-5 days later)
Haemorrhage
Death
Anaemia
Epistaxis, melena
Bleeding into joints
Depression, lethargy, anorexia
Diagnosis: history, clinical signs (don’t rely on them)
 OSPT, APTT blood tests for clotting.
Note: citrate tubes, correct fill, control animal
Treatment: early: induce vomiting
Vit K1, injectable, then oral
Severe cases: transfuse with blood
Advice to owner: prevent future access.
Organophosphates and carbamates
Sources: insecticides, usually dips, pour-ons, flea collars, sprays, spot-on.
(methiocarb not metaldehyde)
Slug bait
Mechanism of action: inhibition of acetylcholinesterase in the nervous system.
Clinical signs: appear very quickly (over stimulation of parasympathetic nervous system)
 Salivation, lacrimation, urination, defecation
 Tremors, weakness paralysis
 CNS signs: ataxia, convulsions, hyperactive
 Delayed neuropathy
Diagnosis: history, test dose atropine
Treatment:
decontaminate skin
Atropine injection
2-PAM (not for carbamates)
Cholecalciferol (Vit D3)
Used for possum control. Has long half life.
Mechanism of action: causes hypercalcaemia which results in calcium deposit is throughout
body tissues, vasoconstriction, decrease in ADH, electrolyte disturbances and renal failure.
Clinical signs:
onset 12-24 hours
Lethargy, weakness, anorexia, vomiting, constipation
PU/PD, dehydration, azotemia
Cardiac abnormalities
Hypertension
Neurological signs (twitching, depression, seizures, stupor)
Diagnosis: raised blood calcium
Treatment: furosemide to enhance excretion, prednisolone. Continue for at least two
weeks, stop treatment and monitor calcium levels.
If known exposure within four hours, try emetics followed by activated charcoal. Repeat
activated charcoal for several treatments because of enterohepatic recycling. If exposure is
greater than four hours, with clinical signs, the animal will usually die within 2-5 days of
renal failure. Keep animal out of sunlight.
Phosphorus (white) rodenticide
Used for possums and rodents. Note red phosphorus is non-toxic. White phosphorus has a
garlic like smell and is fluorescent, often mixed with oil/grease.
Mechanism of action: unknown
Clinical Signs:
acute: GI, abdominal circulatory
Latent phase with apparent recovery (2 days+)
Reoccurrence: vomiting, jaundice, liver failure,
CNS dysfunction, Bleeding tendency
Ruminants may show delayed photosensitivity
Diagnosis: liver/kidney damage
Treatment: no antidote.
Use 1% copper sulphate as a lavage (no emesis as caustic).
Activated charcoal and saline cathartics. NO OILS
Supportive treatment for signs.
Very grave prognosis
Lead
Sources: old paint, batteries, lead shot, lubricants, pesticides.
Clinical signs:
CNS signs predominate, seizures, tremors, blindness, depression, anorexia,
dementia
Anorexia, colic, vomiting, constipation
Anaemia
Usually long after exposure
Diagnosis: blood test
Treatment:
decontaminate animal/environment
Chelate lead with calcium EDTA
D-penicillamine
Thiamine for cattle
If livestock are poisoned then MAF should be notified (public health)
Phenols
Sources: disinfectants, clay pigeons, tar, pitch.
Clinical signs:
pigs: sudden death, weakness depression, abdominal tenderness,
Jaundice, increased respiration rate, anaemia.
Cats; oral ulcers, seizures, coma, death
Do not use phenol disinfectants around cats
1080/fluoroacetate
Possum and rodent baits.
Mechanism of action: impairment of cellular respiration due to competition with citrate in
the Kreb’s cycle. Extremely toxic to all mammals.
Clinical signs:
rapid onset within 30 minutes to 2 hours of ingestion
CNS signs, especially excitation in dog and cat
Defecation, urination, vomiting
Convulsions
Ruminants: heart failure, tremble, stagger
Treatment: must be rapid
Decontaminate (activated charcoal and laxative)
Control convulsions
Sodium bicarb for acidosis, with fluids
Antidote is acetamide if given early
Advice client to give emetic immediately if known exposure
Prognosis grave unless immediate action taken.
Metaldehyde
Source: snail and slug bait
Clinical signs:
rapid onset following ingestion
Depression, vomiting
Increased respiratory and heart rate
Salivation
Watery diarrhoea
Muscle tremors, incoordination, seizures
Treatment:
no antidote, decontaminate and treat signs.
This is a very serious poisoning, rapid treatment is essential, even so many animals die.
Don’t forget to advise re future exposure for other pets.
Chocolate
Chocolate contains theobromine, a drug related to caffeine. This drug is what makes
chocolate toxic to dogs.
Clinical signs:
abdominal pain, vomiting
Restless, salivating, increased thirst
Difficulty standing/walking
Increased respiration rate, cyanosis
Blood in urine
Increased heart rate/rhythm problems
Convulsions, death
Signs usually occur within a few hours, but can be delayed for 24 hours. Dark chocolate is
more dangerous than milk chocolate. Cocoa powder is the worst of all. About 150g of dark
chocolate may be fatal to a 20kg dog.
Treatment: decontaminate, supportive. Prognosis depends on how early treatment was
started, many owners delay as they are unaware of the risks.
Ethylene Glycol (antifreeze)
Source: pools of antifreeze under cars during filling of the cooling systems, winter and
summer. Cats are more often affected more quickly than dogs.
Mechanism of action: metabolites cause damage to kidneys and changes in acid-base
metabolism.
Clinical signs:
early (few hours) incoordination
Delayed – vomiting, dehydration, renal failure, death
Treatment: if known ingestion, decontaminate and reduce absorption. If already absorbed,
prevent metabolism by treating with 20% ethanol IV, every 4-6 hours over two days. This
will cause severe depression. Newer drug available for this purpose with few side effects is
4-methylpazole (not used in cats though).
Poor prognosis because usually presented too late.
Paracetamol
Sources: human medicine, readily available, either given deliberately (but misguidedly) by
owner or animal eats medicine left out. More toxic to cats than dogs, half a paracetamol will
kill a cat.
Mechanism of action: cats cannot metabolise paracetamol properly and form toxic
metabolites. These cause red cells to be unable to carry oxygen and become more fragile
and easily destroyed, also liver damage occurs.
Clinical signs:
usually seen within 4-12 hours
Vomiting
Difficulty breathing
Swelling of face and paws
Dark discoloured gums
Salivating
Later signs: liver damage, jaundice, convulsions, death.
Treatment: if presented within two hours, induce vomiting.
If too late to prevent absorption, try to delay metabolism by administering acetyl cysteine
(mucomyst) which competes with paracetamol in the liver and slows down the metabolism
of paracetamol. Supportive treatment includes oxygen therapy, blood transfusion.
Poisonous plants in New Zealand
There are many potentially poisonous plants in New Zealand. These types of poisonings
usually affect large animals, often when the plant has been cut and incorporated in food
stuffs, e.g. pasture hay.
Ragwort
Tutu
Cestrum
Ngaio
Brassicas
Blue green algae
Rhodedendron
Oleander
Bracken
Yew
Tree nettle: anaphylaxis
Macrocarpa: abortion
Facial excema spores (see microbiology notes)
Aflatoxin
Cyanide accumulating plants, e.g. baled sorgum
Nitrate accumulating plants, e.g. beets, pigweed, docks. (these are reduced to
nitrites in the rumen, cause dyspnoea, methaemoglobineamia, death
Tutu
Found along stream banks and regenerating bush and road sides (access for droved animals
and extensive farming. Cattle and sheep are affected (Tutu, nd.)
Honey from bees feeding on large amounts of tutu is toxic for humans. (Tutu - Coriaria
arborea, nd.)
Tutin, the toxin and present in leaves sap and presumably the pollen. The red petals are not
toxic.
Signs of poisoning: vomiting dizziness excitability stupor leading to convulsions
Tx: supportive therapy and reduce absorption, no antidote and ruminants don’t vomit. Key
is avoidance and identifying the plant and access
Dx: history and clinical signs
Macrocarpa
Found in shelter belts and grazed by cattle horses sheep. Causes single or sporadic abortion
in late pregnancy and lack of milk production in many cases (Macrocarpa and pine, nd.)
Tx- None!-too late by the time abortion noted, but it may lead to complications such as
retained foetal membranes which will require uterine lavage and antibiotics
Signs: None evident except abortion, mostly the cow will be clinically fine once aborted. Dry
stock are not affected. Key is avoid feeding pregnant stock in areas with access.
Dx: history of access to macrocarpa which appears grazed and no other aetiology
discovered.
Ragwort
Found as paddock weeds. Can become serious in dry areas e.g. pahiatua and braided river
country in the south island. The toxin is a bitter alkaloid (nitrogen containing plant
compound-not a protein) which is ingested by cattle horses and sheep. Horses generally
avoid grazing it unless it is a dense component of the pasture or it is cut and wilted which
improves palatability (Ragwort poisoning, nd.). There are reports of it being absorbed by
skin in sufficient quantity to cause death in humans (a British woman weeded a dense
paddock of ragwort over 3 days with bare hands and died) but this is a rare occurrence.
Causes DNA damage and hepatic cell death. If the animal lives long enough cirrhosis of the
liver results. The toxin is extremely difficult for the body to remove and is cumulative. The
toxic dose varies with individuals sheep are less sensitive than cattle and horses as a species
so chronic poisoning is more likely to be seen in this species. Honey from bees feeding on
plants may contain very small amounts of toxin that are insufficient to cause human harm.
Signs: depression ataxia jaundice photosensitivity of exposed skin.
production wasting and ill thrift
Long term, poor
Dx: history clinical signs and liver biopsy/histology
Tx: supportive and remove from the source.
programmes
Key is avoid access by weed control
Reference list (for poisonous plants)
Macrocarpa and pine. (nd.) Retrieved 23rd April 2012 from
http://www.totallyvets.co.nz/macrocarpa.html
Ragwort poisoning. (nd.) Retrieved 23rd April 2012 from
http://www.equinehospital.co.nz/articles/Ragwort%20poisoning.pdf
Tutu. (nd.) Retrieved 23rd April 2012 from http://www.totallyvets.co.nz/tutu.html
Tutu - Coriaria arborea (nd.) Retrieved from http://www.karekare.co.nz/karekare/tutu.htm
Poisonous plants research and identification
Objectives
 Identify a few of the common poisonous plants that affect companion animals and stock.
 Research and report the cause and effect prevention and treatment of some common
poisonous plants.
Task
1. Research a common plant poison in NZ other than tutu, ragwort or macrocarpa. Write a
short summary (no more than half page) that covers access, toxin, signs, diagnosis, and
treatment. Record your reference in the format required by UCOL guidelines. Use in
text referencing at least once. Ask the librarians for help if required.
2. Post your research on the moodle forum with a photo of the plant or a picture obtained
from the net of that plant.
Note 6th ed APA does not require date of retrieval for online sources as a rule unless these
are likely to change such as wiki entries. Both Massey and Totally Vets regularly edit their
online material so the retrieval date was provided in the examples above.