INTRODUCTION

ACETAMINOPHEN

• Alka-Seltzer* Plus Cold & Sinus
• Contac Sinus*
• Dayquil*
• Excedrin*
• Midol PMS*
• Pamprin*
• Robitussin* Cold Cough and Flu
• Sudafed* PE Cold & Cold
• Theraflu* Sore Throat
• Vicodin*

The toxic dose of acetaminophen in cats has been reported to be 10 mg/kg (4.5 mg/lb).  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 1,2 . 

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 3 .  These toxic metabolites may cause illness by any of the following routes:

• Methemoglobinemia:  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 and the potential for subsequent tissue damage.

• Hepatotoxicity:  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 4 . 

• 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:  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 6 .  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 7 . 

Treatment:  Treatment components for acetaminophen toxicosis include initial decontamination, antidotal therapy, antioxidant replenishment, supportive therapy, and potentially methemoglobinemia/anemia correction.

• Decontamination:  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 4 . 

• 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 4 . 

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 survive5.

Prevention:  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

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:  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 9,10 . 

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.

Clinical Signs: 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 production 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: 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.

Bloodwork:

• 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 9,10 . 

Urinalysis:

• 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.

• Decontamination: Decontamination procedures as described above may be performed, and are the most useful if performed within the first 4 hours of ingestion 9 .  However, some studies have indicated that decontamination procedures may not be very effective, as ethylene glycol is very rapidly absorbed from the gastrointestinal tract 10 . 

• 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 11 . 

  • Ethanol: 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 12,13 . 

• 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 11 .  The prognosis becomes much poorer with delays in treatment.  Prognosis is grave if kidney damage is evident.

Prevention: 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.

LILY INGESTION

Toxicant Information: 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 14 . 

• 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 (increased urination).  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 otherwise nontoxic lily substrate to toxic lily substrate 14 . 

Clinical Signs: 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*: Vomiting generally lasts for approximately 4-6 hours. 
• Salivation: Salivation generally lasts for approximately 4-6 hours. 
• Anorexia: Anorexia generally persists
• Lethargy: Lethargy generally persists

*Note: 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 is closing.  Vomiting may also reappear later on in the course of disease. 

Final Stages

Polyuria:  Polyuria is a medical term describing increased amounts of urine production.  Polyuria can be seen approximately 12 to 24 hours following ingestion.  Loss of fluids through the urine eventually leads to dehydration, as described below.

Dehydration:  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:  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.

Diagnostics: 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.

• Bloodwork: 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 15 . 

• Urinalysis: 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 15 . 

Treatment: 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 15 . 

Prognosis: 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 14 .  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.

Prevention: 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 to see if this plant is toxic to cats (or any animal members of the household).  Information on toxic plants can be found at www.aspca.org/pet-care/poison-control/plants,  "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

Toxicant Information: 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 and 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 contain permethrin.  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 at www.fabcats.org/owners/fleas/info.html and on the 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 16 . 

Clinical Signs: 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 17 .  The following clinical signs, in order of most to least common, may be observed:

• Muscle tremors
• Hypersensitivity to Stimuli
• Seizures
• Fever
• Hypersalivation
• Incoordination
• Pupil Dilation
• Temporary Blindness
• Excessive Vocalization
• Anxiety
• Increased Respiratory Rate
• Vomiting
• Inappetence

Diagnosis: 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.

Treatment: Decontamination and supportive therapy are the only treatment strategies available for cats suffering permethrin toxicity; there is no antidotal therapy available.`

• Decontamination: 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 17 . 

Prognosis: 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 16-20 . 

Prevention: 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.

ADDITIONAL TOXINS

The above four toxins were chosen at the authors 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:

www.aspca.org/Pet-care/poison-control.aspx

www.aspca.org/pet-care/poison-control/what-to-do-if-your-pet-is-poisoned.aspx

The telephone number for the Animal Poison Control is (888) 426-4435.  There is a $65 consultation fee for this service.

Commonly Encountered Human Drugs:

• Amphetamines: 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 7 . 

• Marijuana: Marijuana causes central nervous system depression in cats, as it does in humans.  Signs to be aware of include uncoordination, vomiting, depression, and disorientation 7 . 

• 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, and aminophylline.  Clinical signs may include vomiting, diarrhea, hyperactivity, a racing heart or respiratory rate, muscle spasms, seizures, and a variety of other signs 7 . 

• 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 6 . 

• Salicylates: 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 7 . 

• 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 7 . 

• 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 7 . 

• Insecticides: 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 7 .  Other insecticides may also cause toxicity in pets..

• Herbicides: 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 7 .  Other herbicides may also cause toxicity in pets.

• Rodenticides: 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 7 .  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 7 .  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 7 . 

• Carbon Monoxide: Just as in humans, carbon monoxide exposure from smoke inhalation, car exhaust, and gas fireplaces, etc. is toxic.  Clinical signs may be very subtle.  Oxygen therapy at the veterinary hospital is very important for treatment 7 . 

• Corrosives: 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 7 . 

• 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 7 . 

• Lead: 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 7 . 

• Mushrooms: 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 7 ). 

• 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 7 . 

BIBLIOGRAPHY