Common Feline Toxicities
by Chelsea Sonius
A variety of household chemicals, human medications, plants, and even
veterinary products marketed for dogs can be toxic to cats.
Further,cats are uniquely susceptible to a variety of toxins that other
species are not.
The aim of this paper is to promote awareness of common toxins
encountered by cats.
The first step in preventing intoxication is knowledge of the toxins
The author has chosen several toxins to elaborate on
throughout this paper.
This is by all means not an all‐inclusive list.
If you would like further information regarding common feline toxicities,
following this paper is a list of other commonly encountered feline poisons,
along with links to the Animal Poison Control website.
If you believe that your cat (or any other pet) has had exposure
to a toxin, contact the Animal Poison Control immediately at (888) 426-4435
and seek immediate veterinary care.
For all of the toxins described, time is the most crucial factor
in determining a successful outcome.
Acetaminophen is a commonly used human pain reliever and fever reducer.
It is the active ingredient of Tylenol and is also found in many other
over the counter products targeedt for headache relief, menstrual aches,
muscle aches, allergy relief, tooth pain, cold symptoms, sore throats,
and as a general fever reducer.
There are MANY brands that contain this product,
and all feline owners should be aware of what household medications
may contain this drug.
A list of brands that carry acetaminophen can be found at this
U.S. National Library of Medicine site.
Some of the more common American brands are provided below.
This list is by no means, all inclusive.
Many other drugs also contain acetaminophen.
For a list of medications containing this drug,
please follow the link above.
- Alka-Seltzer Plus Cold and Sinus
- Contac Sinus
- Midol PMS
- Robitussin Cold Cough and Flu
- Sudafed PE Cold and Cold
- Theraflu Sore Throat
The toxic dose of acetaminophen in cats has been reported to be 10 mg/kg
The typical amount of acetaminophen in a Tylenol tablet is 352 mg.
This means that even a very small, partial amount of Tylenol ingestion
(less than 1/10th of a tablet in some instances)
can cause toxicity in the feline species.
Acetaminophen should NEVER be administered to cats
and cats should never have access to drugs containing acetaminophen
or bottles previously containing acetaminophen.
Mechanism of Toxicity:
Following administration or ingestion,
acetaminophen is metabolized by the liver into a compound
called N-acetyl-p-benzoquinone imine (NAPQI),
a compound that can be toxic to cells in the body.
In humans with a normally functioning liver
this compound then becomes conjugated/attached to a molecule
called GSH to form a new compound called mercapturic acid.
This conjugation reaction neutralizes the toxic NAPQI.
In healthy humans, no more than 5% of acetaminophen
is converted to this toxic compound.
Cats, however, are very limited in their ability to produce GSH.
Therefore they have an extremely limited ability
to convert this compound into a neutral substance.
Consequently, cats are extremely susceptible
to the toxic effects of this drug as compared to humans.
and other species.
These toxic metabolites may cause illness
by any of the following routes:
Methemoglobinemia is a disorder in which the hemoglobin
of red blood cells is bound too tightly to the oxygen that it carries,
resulting in poor oxygenation of the tissues
and can cause serious subsequent tissue damage.
- Heinz body anemia:
Heinz body anemia is a condition in which damage occurs
to the red blood cell membrane such that it becomes more fragile
and susceptible to destruction.
This results in red blood cells that are easily destroyed.
Anemia also contributes to poor oxygen delivery.
Although less common in cats,
acetaminophen toxicity can also cause direct liver damage.
- Endothelial Damage:
There is also evidence that the endothelial cells
(cells that line blood vessels)
may be damaged with acetaminophen toxicity.
Clinical signs of acetaminophen intoxication are variable.
Clinical Signs commonly present after 1 to 2 hours of exposure,
but in some instances may not appear for a longer period of time.
Clinical signs in the cat are attributable
to the toxic effects described above.
One study attempted to document the prevalence of clinical signs
in cats presenting with acetaminophen toxicity.
- Depression/Lethargy — 76%
- Cyanotic, Pale, or Dark Mucous Membranes — 50%
- The color of the gums can be a very useful monitoring too
for owners, and owners should strive to familiarize themselves
with their pet's normal gum color.
In a healthy cat, the gums should be pink and moist.
In cats with acetaminophen toxicity, the gums
may have a brown hue (dark mucous membranes),
blue hue (cyanotic membranes),
become very light pink/white (pale mucous membranes),
or become very bright pink/red (hyperemic mucous membranes).
- Anorexia/Inappetence — 35%
- Vomiting — 35%
- Hypersalivation — 24%
- Diarrhea — 18%
- Elevated Heart Rate (Tachycardia) — 18%
- A typical heart rate for a cat can be very variable
ranging from 120 during periods of rest
to over 200 during periods of stress.
The best way to evaluate what is normal for your cat
is to take a pulse rate during periods of normal daily events.
This can be done by placing your fingers on the inner aspect
of their thigh and feeling for a pulse.
Knowing your cat's normal heart rate can be helpful to determine
when they are having tachycardia.
- Respiratory Distress — 12%
- Swelling (Edema)of the Face and Forelimbs — 29%
Diagnosis of acetaminophen toxicity is most commonly made
by historical evidence and clinical signs.
Common laboratory abnormalities seen in cats with acetaminophen toxicity
include Heinz body formation evident on a blood smear,
a decreased PCV (decreased red blood cell numbers), and
elevations in hepatic laboratory values.
Plasma, serum, and urine can be tested
for the presence of acetaminophen;
however, the tests results often take several days
and are not available at the time that treatment is needed.
Treatment components for acetaminophen toxicosis
include initial decontamination, antidotal therapy,
antioxidant replenishment, supportive therapy,
and potentially methemoglobinemia/anemia correction.
Decontaminations strategies aim to remove as much of the toxic agent
from the animal as possible.
If the cat is treated within six hours of ingestion of acetaminophen,
vomiting can be induced.
In cats, this is typically initiated with xylazine.
Additionally or alternatively, your veterinarian may also recommend
a gastric lavage under anesthesia.
Activated charcoal administration is also warranted to absorb
any toxins that may be present in the gastrointestinal tract.
Cathartics are also commonly used to increase the gastrointestinal
transit time and promote defecation of toxins.
- Antidotal and Antioxidant Therapy:
These treatment strategies aim to decrease production
of toxic metabolite and decrease oxidative damage
caused by these metabolites.
N-acetylcysteine should be administered to every patient
presenting with acetaminophen toxicity.
N-acetylcysteine has been shown to increase GSH levels of cats,
decreasing the amount of time that the methemoglobin molecule survives,
and can be useful in preventing anemia.
Additional therapies such as S-adenosylmethionine (SAMe),
Sodium sulfate, and antioxidant therapy may also be useful
in replenishing GSH levels and decreasing further NAPQI production.
- Supportive Therapy:
Supportive therapy is an integral part of treatment
for cats with any toxicity.
Oxygen therapy is very important for patients
suffering from methemoglobinemia.
Fluid therapy is utilized to maintain appropriate hydration
and correct any underlying electrolyte abnormalities
that may have been produced.
If severe anemia is present, a blood transfusion
may also be warranted.
- Methemoglobinemia Therapy:
Compounds are available that can convert methemoglobin
back to hemoglobin.
Methylene blue and ascorbic acid are two such compounds.
In some instances,
concurrent administration of N-acetylcysteine and methylene blue
may be contraindicated;
this will be at the discretion of the attending veterinarian.
Prognosis and Outcome:
The most important survival factor is the amount of time that passes
between initial toxicant exposure and treatment.
Cats that are treated sooner have a much better prognosis.
One study has shown that cats treated after more than 17 hours
typically do not survive (5).
As the old adage says, an ounce of prevention
is worth a pound of cure.
Owners should educate themselves about the ingredients
in all medications throughout the house.
Medications should be stored in a secure location
where pets have no access.
Further, old medication bottles should be disposed of immediately,
and pets should not have access to empty bottles.
Ethylene Glycol is a very dangerous toxin to cats.
It is most commonly found in antifreeze (coolant)
and windshield de-icing agents.
However, it can also be found in a variety of other substances,
such as photographic color film processing chemicals,
rust removers, brake fluid, motor oil, and in industrial solvents.
Mechanism of Toxicity:
Unmetabolized ethylene glycol is not toxic;
toxins are formed when ethylene glycol undergoes metabolism.
There are several steps in ethylene glycol metabolism.
Some of the most important metabolites that contribute
to ethylene toxicicity are glycoaldehyde, glycolic acid,
and oxalic acid.
Glycoaldehyde is the first metabolite formed.
It is formed by the action of the enzyme alcohol dehydrogenase.
This metabolic product causes neurologic changes
that owners often describe as "drunkenness".
This compound is formed immediately after ingestion of ethylene glycol.
- Glycolic Acid
Glycoaldehyde is further metabolized to glycolic acid
by the enzyme aldehyde dehydrogenase.
Glycolic acid is typically formed approximately 3-4 hours
after ingestion and causes metabolic acidosis.
This metabolic acidosis can cause severe changes in blood pH
and enzyme activity, resulting in damage to many organ systems.
- Oxalic Acid:
Oxalic acid is one of the many end-products
of ethylene glycol metabolism.
Its effects are often seen much later in the progression of disease,
commonly occurring 1-3 days after ingestion.
Oxalic acid is a compound that readily binds circulating calcium.
Calciumoxalate precipitates form in the body,
which can cause serious organ damage, most notably
damage to the kidney.
Owners should be aware that even a drop or two of ethylene glycol
lapped up or cleaned off a contaminated paw is enough
to cause severe illness in cats.
If ethylene glycol intoxication is suspected,
immediate veterinary care should be sought.
The clinical signs of ethylene glycol intoxication
are commonly described in stages.
- Phase I:
The initial clinical signs associated with ethylene glycol intoxication
that are seen are a commonly described as a "drunken" behavior.
Signs can start as soon as 30 minutes following ingestion
and often include mental depression, uncoordination, muscle weakness,
and gastrointestinal upset.
In cats, these signs often persist throughout the following phases.
- Pure ethylene glycol and glycoaldehyde
are the predominant metabolites causing clinical signs
at this stage;
other metabolites have not yet had time to build up in the body.
Because treatment strategies aim to stop the productiojn
of early ethylene glycol metabolites,
prognosis is best if treatment attempts
are initiated during this stage.
- Phase II:
The predominant metabolite of this phase is glycolic acid.
Clinical signs seen during this stage include nausea, vomiting,
inappetence, diarrhea, depression, and dehydration.
These clinical signs typically begin around 4-6 hours.
- Phase III
Oxalic acid is the predominant metabolite responsible
for the final clinical signs seen in ethylene glycol toxicity.
These signs typically begin at approximately 12-24 hours in the cat.
Oxalic acid binds to circulating calcium
and causes calcium oxalate crystal formation,
which causes severe damage to the tubules of the kidneys.
Clinical signs of this stage are very severe
and include continued depression, anorexia, and vomiting,
as well as extreme lethargy, coma, and decreased urine production.
Diagnosis is typically made by a combination of historical evidence,
clinical signs as described above, laboratory analysis,
and potentially diagnostic imaging.
During the different stages of ethylene glycol intoxication,
diagnostic testing will yield different results.
- During the early stages of ethylene glycol toxicity
bloodwork may reveal a decreased blood pH (acidosis),
a decreased bicarbonate (HCO3-), an increased anion gap,
and increased serum osmolality.
Elevations in phosphorus may also occur,
as many of the products that utilize ethylene glycol
also increase serum phosphorus concentration.
- During the later stages,
when kidney damage has occurred, elevations in BUN and Creatinine
(two kidney values) are typical.
Elevations in potassium may also be seen,
as well as decreases in calcium.
- A urinalysis is a critical diagnostic tool
in the evaluation of suspected ethylene glycol intoxication.
Urinalysis will often be minimally concentrated
and reveal calcium oxalate crystals in the urine.
As the degree of toxicity progresses,
other changes such as blood, protein, glucose, and inflammatory cells
may be seen in the urine, as well.
- Additional Diagnostic Tests:
- Ethylene Glycol Kit:
There is a specific kit that can be used to detect
the concentration of ethylene glycol in the blood.
This test may prove useful in some situations;
however, it does have some limitations.
The first being that it is most reliable if used
within the first 6 hours following ethylene glycol ingestion,
which may not always be possible.
Further, its minimal detection limit is 50 mg/dL,
and unfortunately, much smaller concentrations
can cause illness in cats.
- Flourescin Test:
Some antifreeze products contain a flourescin dye
that can be detected by a special light.
Inspection of the animal's skin, oral cavity, or excretory products
can be helpful in confirming
a suspected ethylene glycol intoxication.
Unfortunately, not all products contain this flourescin dye,
so this test also has limitations.
- Diagnostic Imaging:
Although not a typical test performed on patients
suspected of having ethylene glycol toxicity,
diagnostic imaging modalities such as ultrasound
can also be useful in providing further evidence
for ethylene glycol intoxication;
increased echogenicity (brightness) of the kidneys
may be seen on abdominal ultrasound.
Treatment aims are similar to those described above for acetaminophen
toxicity and include decontamination, antidotal therapy, and supportive care.
Decontamination procedures as described above may be performed,
and are the most useful if performed
within the first 4 hours of ingestion.
However, some studies have indicated
that decontamination procedures may not be very effective,
as ethylene glycol is very
rapidly absorbed from the gastrointestinal tract.
- Antidotal Therapy:
The aim of antidotal therapy is to inhibit
the enzyme alcohol dehydrogenase,
which converts ethylene glycol to glycoaldehyde.
This therapy has been shown to be most
effective in cats if given within 3 hours of ingestion.
Ethanol is one option that can be administered intravenously
by a veterinarian in an attempt to inhibit
ethylene glycol metabolism.
Ethanol binds more tightly to alcohol dehydrogenase
than ethylene glycol does.
Consequently, ethanol can decrease the amount
of ethylene glycol transformation/metabolism that occurs.
Although ethanol is often an inexpensive and effective
means of therapy for cats, ethanol also has
many negative consequences.
It may contribute to continued/worsened mental depression,
promote dehydration, and can also worsen metabolic acidosis.
- 4-Methylpyrazole (Fomepizole):
Fomepizole directly inhibits the enzyme alcohol dehydrogenase
and is useful in preventing further metabolism of ethylene glycol.
In the cat, very large doses of intravenous fomepizole
have been shown to be effective.
Fomepizole does not cause many of the side effects
that ethanol does, but may still
contribute to depression in cats.
- Supportive Care:
As with acetaminophen toxicity,
supportive care is an integral part
of the ethylene glycol toxicity treatment plan.
Intravenous fluid therapy is a core therapy
that will be initiated in all animals suspected
of ethylene glycol intoxication.
Fluid therapy aims to maintain/correct hydration status,
provides for diuresis, and is useful in promoting urine production
in animals suspected of kidney damage.
Depending on what phase of intoxication the cat is in,
other treatment strategies such as diuretics
to promote urine outflow and bicarbonate therapy
to correct metabolic acidosis may be employed.
Peritoneal dialysis and hemodialysis have proven
to be helpful/effective in patients with renal failure;
however, the availability of these modalities
is generally limited to large cities.
Prognosis and Outcome:
The amount of ingested ethylene glycol
and the time since exposure to ethylene glycol
will determine the clinical outcome.
Treatment outcomes are best for cats
that have therapy initiated within 3 hours of exposure.
The prognosis becomes much poorer with delays in treatment.
Prognosis is grave if kidney damage is evident.
All pet owners should take the handling of antifreeze very seriously.
Even a small drop on the garage floor can prove fatal to a cat.
Owners should read labels of the antifreeze, de‐icer
photography film chemicals, etc.
Bottles should be stored in a secure location
and should only be used in areas for which the pet has no access.
Empty bottles should be discarded
in an area for which the pet will have no access.
Vehicles should be checked immediately when leaks are suspected;
again, even a drop or two can prove fatal to a cat.
Liles are a very popular household and garden plant.
Unbeknownst to many pet owners,
lilies are extremely toxic to cats
and quickly induce acute renal failure.
Lily species that have been demonstrated
to induce kidney failure in cats include
the Lilium and Hemerocallis genera.
These plants are particularly common around Easter
and times of celebration.
They are also commonly planted in outdoor gardens.
Common names for plants included in these genera include:
- Asiatic Lily
- Calla Lily
- Day Lily
- Easter Lily
- Japanese Show Lily
- Leopard Lily
- Panther Lily
- Stargazer Lily
- Tiger Lily
- Trumpet Lily
- White Lily
All parts of the lily are toxic,
and ingestion of even a small portion of a leaf or stem can
induce illness, renal failure, and death in cats.
Mechanism of Toxicity:
The mechanism of toxicity has yet to be elucidated;
however, what is established is that these plants
ultimately lead to renal failure and death
in cats if left untreated.
Initially, it is thought that lilies
cause gastrointestinal upset in the first few hours after ingestion.
Over the next several hours this leads to polyuria
Without adequate fluid replenishment dehydration ensues,
which is thought to promote the development of acute renal failure.
Cats are uniquely susceptible
to the toxic effects of lily species,
and recent research suggests that cats
may have a unique metabolism that converts
:therwise nontoxic lily substrate to toxic lily substrate.
Clinical signs seen in cats with lily toxicity
are those of gastrointestinal upset and kidney disease.
Like ethylene glycol poisoning,
clinical signs are often seen in two stages.
- Initial Stage (0-3 hours at onset):
During the initial hours following ingestion,
gastrointestinal signs predominate:
Vomiting generally lasts for approximately 4-6 hours.
Vomiting may resolve within a few to several hours after intoxication.
This does NOT mean that a cat is recovering from lily intoxication.
Instead, it means that the window of opportunity for treatment
Vomiting may also reappear later on in the course of disease.
Salivation generally lasts for approximately 4-6 hours.
- Anorexia: Anorexia generally persists.
- Lethargy: Lethargy generally persists.
- Final Stages:
Polyuria is a medical term describing increased
amounts of urine production.
Polyuria can be seen approximately 12 to 24 hours
Loss of fluids through the urine eventually leads to dehydration,
as described below.
Following fluid loss from polyuria, cats become severely dehydrated.
This can be seen as early as 18 hours following ingestion.
If efforts are not made to prevent/correct this dehydration,
kidney failure will ensue.
It is thought that dehydration is a critical factor
required for the development of kidney failure
and anuria, as described below.
Anuria is a medical term that describes
the absence of urine production.
Anuria follows dehydration and can be seen as early as one day
following lily ingestion.
Once a cat has become anuric, the prognosis is very poor.
Treatment strategies should be undertaken early
in the course of intoxication to prevent anuria from occurring.
Again, diagnosis is typically made with a combination
of historical evidence, clinical signs,
and corroborating laboratory evidence.
Unfortunately, however, there are no specific laboratory tests
hat are able to discriminate lily-induced renal failure
from other forms of renal failure.
In the initial stages a CBC may reveal only a stress leukogram
(a pattern of white blood cell changes that occurs
in cats undergoing stressful events).
As nephrotoxicity continues, cats will show elevations
in BUN and Creatinine (kidney values).
In the late stages it has been demonstrated that Creatinine
is often disproportionately higher than BUN.
Other changes that may be seen on blood work
include hyperkalemia (elevations in K+)
and hyperphosphatemia, as is seen with other
causes of acute renal failure.
Changes in liver enzymes may also be seen.
Urinalysis will reveal damage to the kidney tubules,
as is seen with ethylene glycol toxicity
(no calcium oxalate crystals are seen).
Protein, glucose, damaged tubule cells, and
inflammatory cells are commonly seen
in the urine of patients suffering lily toxicosis.
The urine will be minimally concentrated
in the face of dehydration.
Unfortunately, no antidotal therapy is available
for the treatment of lily toxicity.
The mainstays of treatment are decontamination therapy
as described for acetaminophen toxicity
and aggressive fluid therapy for the purposes
of maintaining hydration status and diuresis.
It is imperative that these treatment strategies
be undertaken before the development of anuria and renal failure,
as the only effective etreatment strategy for renal failure
s peritoneal dialysis or hemodialysis.
Cats treated with decontamination and fluid therapy
in the initial stage of lily intoxication
(i.e. before polyuria develops) have been shown
to have an excellent prognosis.
However, cats that develop uncorrected dehydration,
anuria, and renal failure carry a very grave prognosis.
The only means for which a cat with renal failure can be treated
is with peritoneal dialysis or hemodialysis.
It is therefore, imperative that cats be treated
as soon as possible following known lily ingestion.
While both indoor and outdoor cats are commonly exposed
to a variety of toxic lily species,
strictly indoor cats more commonly present
for lily intoxication.
One explanation for this is that most owners
are not aware that lilies are toxic to cats,
and further, many owners are also not aware of all
of the species of plants that they bring into their home.
Additionally, it has been speculated that indoor only cats
commonly chew on houseplants from boredom.
Before bringing a plant into the home,
owners should check the
ASPCA plant website.
"A Guide to Plant Poisoning of Animals in North America"
written by Anthony Knight is another great reference for owners.
Lily species should be considered toxic
until proven otherwise by an exhaustive research effort.
Cats should never be trusted with access to lilies,
toxic lilies should not be brought into the home,
and toxic lily species should not be planted outside,
as roaming cats will have access.
Permethrin is a synthetic chemical that is as a topical insecticide.
It is commonly found in over the counter flea and tick control products
labeled for dogs, but is a neurotoxin in cats.
Because many owners are unaware of the toxic potential of these products,
they are often applied topically to cats
for purposes of insecticide control.
The cat then absorbs the chemical through its skin
and the toxic effects of this product become apparent
several hours later.
Products containing permethrins should never be used in cats.
Some common canine flea and tick control products
containing permethrin include the following:
- Adam's Environmental Flea and Tick Control Products
- Advantix Spot On Solution for Dogs
- Bio‐Spot Spot On Flea and Tick Control
- Hartz Control Pet Care System One Spot Flea/Tick Remedy for Dogs
- OmniTrol Spot On Flea and Tick Control for Dogs
- Seargant's Flea and Tick Shampoo for Dogs
- Sentry Pro Flea and Tick Control for Dogs
- Perky Pet Ant Guard
A brief internet search will reveal to you
the vast number of products containing permethrin,
and the list above is by all means, non‐inclusive.
Additionally, many environmental insect control products
Owners should evaluate the chemicals found
in all insect control products, insect repellants,
and human ectoparasite control products
(i.e. scabies and lice control products).
Additional information on flea control in cats
and products containing permethrin can be found on the
FabCats and ASPCA Animal Poison Control Website.
Mechanism of Toxicity:
Permethrin acts to alter transmission of neuronal impulses
and causes neuronal toxicity eventually leading to death in insects.
Most mammals are not susceptible to the toxic effects of permethrin,
however, cats are known to be exquisitely sensitive
to the toxic effects of permethrin and suffer neurologic symptoms
and toxicity following permethrin exposure.
Unlike the toxins discussed thus far,
permethrins cause toxicity by absorption through the skin.
Once absorbed into the skin it is metabolized by the liver.
As discussed earlier, cats are deficient
in their hepatic glucoronidation capabilities,
and it has been postulated that this is one mechanism
that makes cat susceptible to the toxic effects of permethrin.
The primary clinical signs seen in cats
with permethrin toxicity are neuromuscular in nature
and be apparent from the initial time of exposure
up to a few days following exposure.
A recent study documented the distribution
of clinical signs seen in cats presenting
for permethrin toxicity.
The following clinical signs, in order of most to least common,
may be observed:
- Muscle tremors
- Hypersensitivity to Stimuli
- Pupil Dilation
- Temporary Blindness
- Excessive Vocalization
- Increased Respiratory Rate
Diagnosis is made by history of exposure to permethrin
containing products and presenting clinical signs.
Unfortunately, there are no diagnostic tests that are useful
in identifying/diagnosing permethrin toxicity.
For this reason, it is imperative that owners
provide a thorough history of any recently utilized
canine flea/tick control, insect control products,
or insect repellants.
Decontamination and supportive therapy
are the only treatment strategies available
for cats suffering permethrin toxicity;
there is no antidotal therapy available.
Decontamination strategies are different
from those described above for ingested toxins.
Because the route of exposure to permethrin
is via dermal absorption,
decontamination efforts aim to remove
all permethrin containing products from the skin.
Although cats typically resent water and bathing,
bathing with warm water and dish soap
or a veterinary shampoo is crucial.
Less commonly, a cat may ingest permethrins.
In this scenario, decontamination efforts
as described above for acetaminophen, etc.
will be utilized.
- Supportive Therapy:
Supportive therapy for permethrin toxicity
aims to decrease further neurologic damage
and control neurologic signs.
Methocarbamol, a muscle relaxant, is commonly used
to control muscle fasciculations.
Other drugs such as diazepam, midazolam, phenobarbitol,
and propofol may also be used to control neuronal impulses
leading to seizure activity.
Prognosis is generally quite good
if appropriate decontamination and supportive care procedures
are initiated in a timely fashion.
Many studies have attempted to describe
the survival rates of cats suffering permethrin toxicity;
ranges from 63% to 95% have been reported.
Owners should be aware of the ingredients
found in all insect/pesticide control products
that they intend to use, including veterinary products.
Cats should NEVER receive any products containing permethrin.
They should not have intimate contact with dogs
that have recently had permethrin products applied,
nor should they be exposed to an environment
in which permethrin products have just utilized.
Before purchasing products,
owners should do a thorough investigation of all ingredients.
If in doubt of the ingredients contained in a product,
do not use the product.
A veterinarian should be consulted
with questions regarding flea, tick,
and other insect control products
for cats and dogs.
The above four toxins were chosen at the author's discretion,
and are by all means not an inclusive list of toxins to cats.
Below is a list of the most commonly encountered feline toxins.
The best way to prevent a toxin exposure
is to become educated on potential toxins!
If you suspect that your cat (or any other animal)
has ingested a potentially poisonous/toxic substance,
the Animal Poison Control should be contacted immediately.
Further information about the Animal Poison Control
can be found at the following links:
The telephone number for nimal Poison Control
is (888) 426-4435.
There is a $65 consultation fee for this service.
Commonly Encountered Human Drugs:
Insecticides, Herbicides, Rodenticides, and other Pesticides:
Amphetamines can be found in a variety of prescription
and over the counter human medications,
as well as illicit drugs.
It is often found in cold medications (pseudoephedrine),
medication targeting weight loss,
and is found in the commonly used illicit drugs
cocaine and methamphetamines.
Nervous system disturbances are common with exposure to amphetamines.
Marijuana causes central nervous system depression in cats,
as it does in humans.
Signs to be aware of include uncoordination, vomiting,
depression, and disorientation.
- Methylxanthines (caffeine-like substances):
Just as in dogs, the compound theobromine found in chocolate
can be toxic to cats.
Toxicity is reported much less than in dogs.
Other methylxanthines include caffeine, theophyilline,
Clinical signs may include vomiting, diarrhea, hyperactivity,
a racing heart or respiratory rate, muscle spasms, seizures,
and a variety of other signs.
- NSAIDs (Non-Steroidal Anti-Inflammatory Drugs):
Along with Acetaminophen and Aspirin (as described below)
all NSAIDs should be considered toxic to cats.
These drugs commonly induce depression, gastric ulceration,
and renal failure following ingestion.
Salicylates can be found in a variety of human substances,
including aspirin, antidiarrheals (such as Pepto-Bismol),
and even sunscreen.
Clinical signs are varied and range from mild gastric upset
to seizures and coma.
- Selective Serotonin Reuptake Inhibitors (SSRIs):
SSRIs are very commonly used in human medicine
for the treatment of depression, anxiety,
and other psychological disorders.
Some of these drugs have also been used in veterinary medicine.
Overdose of these drugs can ultimately lead
to cardiac arrhythmias and a variety of other clinical signs.
- Tricyclic Antidepressants (TCAs):
TCAs are another commonly encountered human drug
used for the treatment of psychological disorders.
A plethora of clinical signs may be seen
following intoxication with TCAs
ranging from gastrointestinal upset, neurologic disorders,
cardiac abnormalities, pulmonary abnormalities and death.
Additional Toxins of Importance:
Organophosphates and Carbamates are two classes of insecticides
that lead to toxicity in animals via both dermal and oral routes.
Signs commonly seen in animals that suffer toxicity
from organophosphates and carbamates include the "SLUDGE" signs,
which stands for Salivation, Lacrimation (tearing), Urination,
Defecation, Gastrointestinal upset, and Emesis (vomiting).
Seizures and muscle tremors are also commonly noted
as the toxicity progresses.
Other insecticides may also cause toxicity in pets.
A variety of herbicides are considered toxic to pets.
One such herbicide commonly reported is Paraquat.
Toxic signs may be seen following dermal, oral, and even ocular exposure.
Signs commonly encountered include skin lesions (blistering, etc.),
ocular redness and ulcers, and, if ingested,
initially causes gastrointestinal disturbances.
Paraquat ultimately causes severe pulmonary disease
if left untreated.
Other herbicides may also cause toxicity in pets.
A variety of rodenticides (rodent bait) are toxic to animals.
The most commonly used types of rodenticides
are those called Anticoagulant rodenticides
which kill rodents by interfering with proper blood clotting;
theoretically, a cat could not only be poisoned
by eating the rodent bait itself, but by eating the rodent
that ate the rodent bait, as well.
Other forms of rodenticides commonly encountered
include Bromethalin which is a neurotoxin
and Cholecalciferol, which essentially causes
a Vitamin D overdose.
Cholecalciferol can also be found in dietary supplements
and human medications.
Strychnine causes neuromuscular alterations.
Zinc Phosphide is an additional rodenticide
that can cause toxicity; clinical signs are variable.
All rodenticides are toxins by virtue of their purpose.
- Slug and Snail Control:
Metaldehyde is a commonly used compound
for slug and snail control.
In animals, it is a potent neurotoxin
that leads to signs such as uncoordination, muscle spasms,
seizures, and hypersensitivity to stimuli.
Other pesticides may also cause toxicity in pets.
- Bufo Toads:
Two species of Bufo toads live in the US.
Cats that come into contact with Bufo toads
can suffer neurological and cardiac toxicity.
- Carbon Monoxide:
Just as in humans, carbon monoxide exposure
from smoke inhalation, car exhaust, and gas fireplaces, etc.
Clinical signs may be very subtle.
Oxygen therapy at the veterinary hospital
is very important for treatment.
A variety of substances are considered corrosive;
any compounds that are acidic or alkaline
are considered corrosive.
These toxins cause local tissue damage and irritation.
Common presenting clinical signs include oral ulceration,
hypersalivation, vomiting blood, pain when swallowing, etc.
When a corrosive has been ingested,
induction of vomiting is contraindicated.
- Citrus Oils:
d-limonene and linalool are common citrus oils
that be found in a variety of household products,
including household and personal fragrances, cleansers,
insect repellants, and even pet dips.
These oils acts as irritants to the skin and gastric mucosa
and commonly cause skin lesions and gastrointestinal upset.
Exposure via the dermal or oral route can cause toxicity.
Lead is a commonly encountered household toxin
and can be found in items such as batteries, old paint,
fishing gear, toys, etc.
It primarily acts as a nervous system toxin and can
also cause gastrointestinal upset;
it also causes anemia.
Poisonous mushrooms such as those belonging to the genera
Amntia, Galerina, and Lepiota
can cause gastrointestinal upset and more seriously liver failure.
A variety of clinical signs ensue, including vomiting,
diarrhea, abdominal pain, and icterus
(a yellow tinge to the mucous membranes.
- Spider Bites:
Black widow spiders and brown recluse spiders
can both be very toxic to pets.
Black widow spider bites usually manifest
as a neuromuscular disorder and clinical signs seen
may include uncoordination, muscle tremors, and paralysis.
Extreme vocalizations are also commonly observed;
these bites commonly lead to death.
Brown recluse spider bites often manifest
as a local skin reaction that induces
severe blistering and ulceration.
These bites can ultimately lead to anemia,
clotting disorders, and death, as well.
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