Common Outdoor Hazards

Poison Prevention Month 2024

Sharon M. Gwaltney-Brant DVM, PhD, DABVT, DABT
Veterinary Information Network, Mahomet, IL

Blue-Green Algae

Blue-green algae (BGA) can cause nervous system or hepatic effects, and oftentimes exposed animals may die before veterinary care can be reached. There are also other algal toxins that can produce a variety of effects, from hemolysis to paralysis, but the most commonly encountered clinically in the US are the hepatotoxic and neurotoxic BGA toxins. Microcystin is the algal toxin most commonly associated with hepatotoxicity in the US. Microcystin is absorbed from the ileum and enters the liver, where it damages hepatocellular cytoskeletal structures, causing massive hepatic necrosis. Blood pools in the liver in place of the dead hepatocytes leading to hypovolemic shock and acute death, often within a few hours of exposure; animals that survive have signs of severe hepatic insufficiency. Anatoxin-a and anatoxin-a(s) are neurotoxic BGA toxins that can cause signs and death within minutes of exposure. Exposure to anatoxin-a results in rigidity, tremors, convulsions, paralysis, respiratory failure and death; affected animals frequently die within minutes and before veterinary intervention can be sought. Anatoxin-a(s) is a peripheral cholinesterase inhibitor that causes the classic SLUDDE (salivation, lacrimation, urination, diarrhea, diaphoresis, emesis) or DUMBELLS (diarrhea, urination, miosis, bradycardia, emesis, lethargy, lacrimation, salivation) muscarinic signs similar to those of organophosphate and carbamate insecticides. Death is due to bradycardia or respiratory compromise due to excessive bronchial secretions. Unlike microcystins, which result in grossly visible liver lesions, anatoxins do not cause any specific gross or histopathologic lesions. Treatment of BGA toxicosis includes providing symptomatic and supportive care. For animals with microcystin toxicosis, blood replacement therapy and hepatoprotectants are indicated. For animals showing the muscarinic signs of anatoxin-a(s) intoxication, atropine will help dry up the bronchial secretions and increase the heart rate. For anatoxin-a intoxication, seizure control and ventilatory support is necessary, although rarely do these patients survive long enough to receive veterinary care. Unfortunately, the prognosis for BGA toxicosis is generally poor.

Bufo (& Rhinella) Toads

The two most clinically important in the US are Rhinella (formerly Bufo) marinus (cane toad, marine toad) and Bufo alvarius (Colorado River toad, Sonoran Desert toad) due to the volume of toxins that they are able to produce, primarily due to their large size when compared to other toad species. The secreted toxins include bufogenins and bufotoxins, which act similarly to cardiac glycosides to inhibit myocardial sodium-potassium ATPase activity. Bufogenins also block nerve cell membrane sodium channels in a manner similar to local anesthetics. Secondary toxins such as serotonin, 5-hydroxytryptophan (5-HTP) and catecholamines are also present in toad secretions. Serotonin and 5-HTP can cause CNS depression, tremors, seizures, hyperesthesia, hyperthermia, vomiting and diarrhea. Catecholamines may cause tachycardia, hypertension, anxiety and dyspnea.

Exposure of pets to R. marinus or B. alvarius has the potential to cause significant systemic signs and/or death. Smaller toad species can cause mild signs when mouthed or swallowed by dogs or cats, but systemic toxicosis is unlikely unless the patient is very small, geriatric or in poor health. Following exposure to a o toad, almost immediate hypersalivation is seen, frequently with foaming and gagging. For smaller toads, these may be the only signs seen, but with B. alvarius or R. marinus (or rarely with larger specimens of other Bufo species) more advanced signs may occur within 15 minutes of exposure. Signs can include neurologic abnormalities (stupor, ataxia, nystagmus, seizures), profuse hypersalivation, hyperemia of mucous membranes, collapse, tachypnea and vomiting. A variety of cardiac arrhythmias may occur including bradycardia, tachycardia, ventricular fibrillation and AV block. Hyper- or hypokalemia may occur.

Management of patients that have mouthed, but not ingested, a Bufo toad include copious flushing of the oral cavities with water at home in patients that are showing signs no more severe than ptyalism and gagging. Patients with more advanced signs should be immediately brought to the veterinary facility, where oral lavage can be performed once it is determined that no life-threatening effects are present; animals with significant clinical signs should be stabilized prior to decontamination and endotracheal intubation during decontamination should be considered to reduce the risk of aspiration. Oral lavage will dilute the toxins and prevent their absorption from the oral cavity, and has been shown to reduce the severity of clinical effects when performed promptly after exposure. Ingestion of an entire toad may result in more severe clinical signs due to the potential for absorption of larger amounts of toxin present on the toad. Animals showing mild GI signs (hypersalivation, gagging) may be induced to vomit up the toad. In animals showing more severe signs, endoscopic removal, surgical removal or activated charcoal with a cathartic may be considered. Patients experiencing more advanced effects from exposure to toads should be managed symptomatically. Intravenous fluid support is recommended to help stabilize cardiovascular function. Serum potassium should be measured, and any excesses or deficiencies dealt with as needed. Seizures, tremors, agitation generally respond to diazepam; barbiturates may be indicated in refractory cases. Patients experiencing severe bradycardia may benefit from atropine, and propranolol may be used if severe tachycardia is present. Digoxin-specific Fab (Digibind®, DigiFab®) may be considered in case of severe hyperkalemia or cardiac arrhythmia unresponsive to standard anti-arrhythmic therapy. Most patients exposed to small toads make full recoveries, but exposures to B. marinus or B. alvarius generally require aggressive veterinary intervention to manage the potentially life-threatening signs. Similarly, aged, debilitated, or very small patients exposed to other toad species may have a more guarded prognosis if prompt veterinary care is not obtained


Fireflies in the genus Photinus have been associated with regurgitation in birds and rapid death when fed to reptiles and amphibians. The fireflies contain steroidal pyrones known as lucibufagins, which are thought to serve as a defense against predation by birds and spiders. Lucibufagins are structurally and mechanistically related to bufogenins found in toad toxins. As inhibitors of sodium-potassium ATPase activity, lucibufagins have adverse effects on myocardial function. A single firefly is sufficient to result in death in a 100 g bearded dragon. Although cases of Photinus toxicosis have not been reported in dogs or cats, based on experimental studies 1 firefly per kilogram would be sufficient to cause significant cardiovascular abnormalities and/or death in dogs or cats. Birds tend to regurgitate ingested Photinus, effectively self-decontaminating and minimizing risk of systemic effects. Reptiles, notably bearded dragons, ingesting Photinus experienced rapid onset of oral gaping, dyspnea, blackening of skin color, head shaking, regurgitation and death within 15-90 minutes of exposure. The rapidity of signs and death make veterinary intervention impossible in many cases. If treatment can be initiated, it would be similar to management of toad toxicosis: stabilization, manage cardiac abnormalities, and decontaminate when it is safe to do so. Because of the severity of onset and rapid progression of signs, the prognosis is generally poor.


Mushroom identification can be difficult, as many toxic mushrooms have the generic LBM (“little brown mushroom”) appearance. Attempts to identify mushroom using books or the Internet can prove frustrating to those not familiar with mushroom anatomy. Whenever possible, identification by someone experienced in mushrooms (e.g. an experienced mycologist) is recommended. When attempting to identify mushrooms, samples of the mushroom itself as well as information on where the mushroom was growing (e.g. lawn, garden, compost pile, woods, etc.) should be provided. The signs of mushroom toxicosis vary considerably with the species of mushroom ingested, and signs are rarely pathognomonic for mushroom poisoning. For this reason, unless there is a witnessed exposure to a known toxic mushroom, symptomatic patients should be worked up to rule out other potential causes. Toxic mushrooms are divided into 8 groups based on their toxins and the clinical effects that they produce.

Cyclic Peptide (Hepatoxic) Mushrooms: The cyclic peptide mushrooms include Amanita phalloides (death cap), Lepiota, Galerina, Conocybe,and Pholiotina spp. and are most commonly associated with deaths in pets, as a single mushroom cap may be lethal in an average-sized dog or cat. They can be found in most areas of the US and southern Canada. The toxic principle, amanitinm is heat stable, so cooking will not detoxify these mushrooms. The toxins in cyclopeptide mushrooms inhibit nuclear RNA polymerase which interferes with protein synthesis. Target organs are the GI tract, liver and kidney. After ingestion, no initial signs may be seen, or the animal may vomit up bits of mushroom in the first few hours and then appear to recover. Within 6-24 hours following ingestion vomiting, abdominal discomfort and diarrhea develop and evidence of hepatic injury (icterus, elevated liver enzymes, etc.) may be seen; in severe cases, fulminant liver necrosis results in shock, collapse and death within 24 hours. Some animals appear to recover from the initial stage only to present with liver failure within 72-96 hours. At this stage signs could include vomiting, diarrhea, icterus, hypoglycemia, coagulopathy, and hepatic encephalopathy (delirium, head pressing, seizures, etc.). Signs of renal failure may develop as well including vomiting, anorexia, polyuria, polydipsia, and increased renal values. Treatment includes decontamination immediately following exposure, managing clinical signs, and minimizing hepatic and renal damage. Animals ingesting known or suspected hepatotoxic mushroom within the previous 4 hours should be decontaminated by induction of emesis and administration of cholestyramine q 8 h. Intravenous fluid therapy (fluid diuresis) is thought to enhance elimination of amanitin, so a diuresis rate is recommended. Other treatment is supportive and symptomatic for hepatic failure and may include dietary alterations, lactulose, dextrose, vitamin K1, hepatioprotectants, and plasma transfusions. Hypoglycemia causes death in up to 50% of amanitin intoxicated dogs, so close monitoring of serum glucose and correction of hypoglycemia is essential.

Nephrotoxic Mushrooms: Members of the genus Cortinarius grow abundantly in North America. The toxic principle in these mushrooms is orellanine. In humans, renal injury from Cortinarius spp. has been reported in Europe, but only rarely in North America, and there are no reports of renal failure in animals from these mushrooms. In humans, GI signs are reported within a few days of exposure with renal injury developing within 4-15 days. Some humans have required hemodialysis until renal function returns.
Isoxazole Mushrooms: Isoxazole-containing mushrooms include members of the genera Amanita and Tricholoma. These mushrooms grow throughout North America. These mushrooms contain the isoxazole derivatives muscimol and ibotenic acid along with other minor compounds that may contribute to intoxication. Muscimol is a depressant due to effects on GABA receptors. Ibotenic acid has a stimulatory effect on the CNS through its action on glutamate receptors. Because of these conflicting mechanisms, the clinical syndrome tends to be a mixture of CNS depression, interspersed with episodes of agitation. A single mushroom may be sufficient to cause significant clinical signs in medium sized dogs. Signs usually begin within 15-30 minutes of ingestion and may persist up to 1-2 days. Cats develop initial sedation followed by a prolonged (up to 4 h) period of agitation with muscle fasciculations, followed by a deep sleep lasting up to 24 hours. Dogs develop disorientation, opisthotonus, paresis, seizures, paddling, chewing-gum spasm, miosis, and nystagmus. Signs may progress to respiratory depression, coma, and, uncommonly, death. Treatment for isoxazole mushroom exposure is symptomatic and supportive. Because of the rapidity with which signs develop, decontamination is frequently not feasible. Patients provided aggressive supportive care including ventilatory support for severe respiratory depression generally survive isoxazole mushroom intoxication.

Hallucinogenic Mushrooms: “Magic” or hallucinogenic mushrooms are of the genera Psilocybe, Panaeolus, Conocybe, Gymnophilus, and Stropharia which grow throughout North America, especially in the Pacific Northwest and Gulf Coast. Frequently used by people seeking a ‘natural high,’ these mushrooms are often placed in capsules for swallowing; they may also be used with foods such as incorporation into stews or milkshakes or covered in chocolate. Exposures in pets most frequently occur when they get into a human’s stash of mushrooms, but ‘natural’ exposure to wild-growing mushrooms also occurs. The main toxic principles are psilocybin and psilocin. In dogs, clinical signs generally occur within 20-60 minutes of ingestion and include ataxia, vocalization, aggression, nystagmus and hyperthermia; these signs are very similar to those of isoxazole mushrooms, but coma is not a feature. Seizures may occur rarely. Deaths are not expected from the direct effects of the mushroom, although death by misadventure during the period of CNS derangement is possible. Because life-threatening signs are not expected, treatment is generally aimed at providing supportive care until signs resolve. Signs can develop very rapidly, so decontamination is frequently not feasible. Animals showing severe CNS effects may benefit from administration of cyproheptadine, a serotonin blocker; rectal administration of the drug may be considered in animals too disoriented to safely receive the drug orally. Diazepam may also be used for severe CNS effects such as seizures. Because prolonged hyperthermia may lead to injury to vital organs, body temperature should be monitored and regulated as needed. Most signs resolve within 8-12 hours following ingestion.

Hydrazine Mushrooms: Hydrazine-containing mushrooms of the genera Gyromitra (false morels) and Helvella, as well as possibly some species of the genera Disciotis, Morchella, Peziza, Sarcosphaera, and Verpa contain gyromitrin, which is converted into the toxic metabolite monomethylhydrazine once ingested. Gyromitrin is heat labile and many humans consider cooked Gyromitra mushrooms to be a delicacy. Gyromitrin is a GI irritant and can cause vomiting, abdominal pain and diarrhea. Monomethylhydrazine is thought to cause convulsions due to depletion of pyridoxine (vitamin B6), which results in decreased CNS concentrations of GABA and increases in glutamate. Liver failure, renal failure and methemoglobin/hemolysis have been reported as well. In most cases, there is a 6-8 hour delay in onset of signs following ingestion. Initial signs are expected to be vomiting, diarrhea, abdominal pain and weakness. These signs may resolve or may progress to liver failure, pyrexia, methemoglobinemia or hemolysis. Treatment of hydrazine mushroom ingestion should include decontamination if the exposure was witnessed and <4 hours have passed since exposure. Activated charcoal should be considered, although efficacy is unknown. Pyridoxine may be used to manage convulsions/seizures but will not affect liver or red blood cell injury. Hepatoprotectants such as N-acetylcysteine and SAM-e should be considered. Symptomatic and supportive care for hematologic aberrations and liver injury should be provided.

Muscarinic Mushrooms: Members of the genera Clitocybe and Inocybe contain the toxic principle is muscarine, which stimulates peripheral muscarinic receptors, resulting in the typical muscarinic signs classically associated with organophosphorus insecticides. Because muscarine doesn’t degrade rapidly, the duration of action is prolonged. The signs include vomiting, salivation, lacrimation, urinary incontinence, diarrhea, miosis, excessive bronchial secretions, bradycardia and dyspnea. Muscarine does not inhibit acetylcholinesterase, nor does it affect muscarinic receptors in the CNS. Signs occur within 0.5-3 hours following exposure. Death is uncommon but may occur secondarily to respiratory compromise from bronchial secretions or cardiovascular collapse due to profound bradycardia. Treatment is aimed at managing life-threatening clinical signs such as excessive bronchial secretions and bradycardia. Stabilize as needed—oxygen is often beneficial. Atropine will aid in drying up the bronchial secretions and counteracting bradycardia (note that severely dyspneic animals may have normal or increased heart rate due to sympathetic stimulation). Atropine should only be used to obtain normal respiration and heart rate; following the old adage of administering atropine until mydriasis occurs or the mouth is dry can result in atropine toxicosis, which itself is potentially life-threatening. Decontamination can be done in animals showing no clinical signs, although animals with vomiting and/or diarrhea generally do an effective job of self-decontamination.

Gastrointestinal Irritant Mushrooms: Gastrointestinal irritant mushrooms (GIM) exist in a very wide variety of mushroom genera. Just as with plants, ingestion of ANY mushroom may cause mild, transient vomiting; however, there are many mushrooms that can cause more intense GI distress. A variety of compounds contribute to the GI signs seen upon ingestion of these mushrooms, with a variety of mechanisms of action. Many are direct GI irritants, some cause hypersensitivity reactions, while others may interfere with metabolic enzymes in the GI mucosa. Ingestion of GIM results in onset of GI upset with 30 minutes to 6 hours of ingestion, and signs generally resolve within 24-48 hours, sooner if symptomatic treatment is given. Vomiting, drooling, diarrhea and abdominal discomfort are the primary signs; fatalities are rare and are usually related to exacerbation of pre-existing disease due to protracted vomiting, diarrhea and/or electrolyte abnormalities. Treatment is aimed at resolution of GI signs and managing any hydration or electrolyte imbalances. Antiemetics, parenteral fluid therapy, and general supportive care can reduce the time to recovery. Prognosis is generally good, and fatalities are rare. Because vomiting is a common clinical sign in pets, other potential causes for severe GI upset will need to be ruled out.

Coprine Mushrooms: Coprine mushrooms, are only a problem if alcohol is ingested after consuming the mushroom so these are more of an issue for those humans. In pets, no signs beyond gastrointestinal upset would be expected.

Mystery Mushrooms: But what to do in the most common scenario, i.e. the patient who just ingested an unknown type of mushroom? In asymptomatic animals, induction of emesis is recommended, followed by administration of activated charcoal. Ideally, patients should be monitored at a veterinary facility for at least 4 hours for the development of clinical signs, and baseline liver and renal values should be obtained. Remember that signs developing within 4 hours usually indicate a neurotoxic or GIM rather than the more lethal hepatotoxic mushrooms. While the patient is being monitored attempts at mushroom identification should be made. Ideally use the actual mushroom ingested if it can be obtained through prompt induction of emesis. Or, clients can bring in mushrooms from the same area (with the caveat that multiple species can arise in the same area). Collected mushroom should be stored in paper bags, not in plastic or glass, to prevent them from “melting”. Consulting with a mycologist (university, museum, etc.), mushroom book or mushroom website may help.


Many lawn care products (fertilizers, herbicides, insecticides, etc.) come in granular form. It is important to know that the granule itself is NOT the active product, but is instead some type of organic or inorganic substrate (often bits of clay or corn cob) onto which the active ingredient has been sprayed. The granules simply make a good vehicle to allow even distribution of the active ingredient over the ground. When the granules are watered in following application (or after a rain), the active ingredient is then washed into the ground where it does its thing (kills weeds, provides nutrients to plants, etc.). The granules are left behind on the surface of the soil and will eventually be assimilated into the soil components. Pet owners are often concerned that they can still see granules on the surface and worry that the granules may be harmful if the pet should ingest them. Once watered, the granules have very little if any of the active ingredients left so should not pose a hazard to the pet. Some yard products are combination products, so it is best to have pet owners read the ingredient list on the label to verify that you are only dealing with a fertilizer rather than a combination product. Remember that certain names, such as ‘Round-Up’ or ‘Miracle Gro’ are used generically by some people when they are talking about yard products, so be sure to verify that the product is indeed ‘Round-Up’ rather than some other herbicide—when in doubt, verify via EPA registration number (you can Google the EPA Reg. No. to get the exact name and ingredients). For virtually all home yard care products, if the products are applied per label directions and pets are kept off of the yard for the stated amount of time, there is no risk of serious problems for the pet walking, rolling or playing on the yard. So, if a patient presents with vomiting and diarrhea, it is extremely unlikely he got that by walking across a lawn where a fertilizer was watered in the day before even if he licked the ground or ate some grass (both of which are likely signs of, rather than causes of, nausea).

Fertilizers: There are 2 types of fertilizers: inorganic and organic. Inorganic fertilizers are salts of nitrogen (N), phosphorus (P), and potassium (K), and are often designated as NPK fertilizers. The relative amounts of each component are listed on the container, so 13-13-13 means there’s 13% each of N, P, and K. As salts, they are irritating if ingested in excess, so when pets are exposed to large amounts (e.g. chewing into a bag, drinking fertilizer-spiked water from the watering can) we can see vomiting. With very large ingestions, diarrhea may also be seen. The main hazard for fertilizer ingestions is for protracted vomiting leading to electrolyte and hydration issues; for patients with previously existing health issues such as renal disease, exacerbation of their pre-existing problem may occur. Treatment is symptomatic and supportive: antiemetics, gastroprotectants and fluid therapy as needed. The prognosis is excellent, and many patients require little treatment beyond withholding food and water to allow their stomach to settle down.

Organic fertilizers include fish emulsions, various manures/guanos, bone/blood/feather meals and sewage sludge derived fertilizers (which will be discussed separately). Because of their organic nature, many of these products are attractive to pets, especially dogs, which may seek them out and ingest considerable amounts. Besides the obvious issues with GI distress due to the dietary indiscretion, some of these fertilizers can be prone to mold growth if exposed to moisture within the packaging (e.g. leaky garden shed, high humidity). Molds growing in these products may produce tremorgenic mycotoxins, resulting in toxicosis if pets should gain access to the products. Additionally, the use of these organic fertilizers with more toxic compounds, such as the use of blood meal and disulfoton around rose bushes, may increase the likelihood of the pet being exposed to the more toxic compound as it is co-ingested with the organic fertilizer. For ingestion moldy organic fertilizer, organic fertilizer mixed with other compounds or ingestion of large amounts of very rich fertilizers (e.g. blood meal), induction of emesis might be indicated. GI signs can be treated as for inorganic fertilizers as needed. The prognosis for ingestion of organic fertilizers is generally quite good.

When sewage-sludge based fertilizers are ingested, in addition to the expected GI upset (vomiting and diarrhea), we can sometimes see what appears to be muscle stiffness, soreness and weakness that occurs about 24 hours after exposure and lasts about 72 hours. These patients really seem miserable but fortunately do respond to pain and/or antiinflammatory medications. Sewage sludge-derived fertilizers also tend to have somewhat high levels of iron, but overt iron toxicosis doesn’t seem to be an issue in overdose situations; we think the iron isn’t terribly bioavailable. In general, we don’t get too worried about the iron unless there’s evidence of breakdown of the GI barrier (i.e. bloody diarrhea), which might allow increased iron absorption.

Herbicides & Fungicides: These products are designed to prevent or kill weeds and molds, and many of the modern products have mechanisms that are targeted against biochemical pathways not found in animals. For instance, glyphosate (active ingredient in Round-Up), disables the shikimate pathway in plants; this pathway is used to synthesize aromatic amino acids. Since mammals get their aromatic amino acids via their diet, they have no shikimate pathway, so glyphosate has no activity in our bodies and has extremely low toxicity. However, the ‘inert ingredients’ in many of the glyphosate formulations are products such as surfactants, which can be mildly irritating to eyes, skin and/or GI tract. So pets licking the wet glyphosate product can develop vomiting, oral irritation, drooling and gagging; ingestion of larger amounts may result in diarrhea. Signs are expected to be mild and often self-limiting, although animals with persistent vomiting may require antiemetics.

Paraquat is one herbicide that can cause serious problems in pets; fortunately, it is not approved for residential use, and its use in agriculture is limited. However, occasional episodes of malicious poisoning of dogs with paraquat have occurred in the US in the past decade. The production of oxygen-derived free radicals from paraquat results in oxidative damage to tissues; because paraquat concentrates in the lung with its high oxygen tension, pulmonary injury is pronounced in patients that survive the acute systemic poisoning. Paraquat causes severe GI upset and corrosive injury to mucosal surfaces. Acute systemic toxicosis from paraquat results in electrolyte abnormalities, renal injury, hepatic necrosis and adrenal necrosis. Patients may succumb within 1-4 days from multiorgan failure. Patients surviving beyond this time are at risk for the development of pulmonary edema and fibrosis; death due to progressive pulmonary fibrosis may occur in days or weeks. Treatment of paraquat poisoned patients is symptomatic and supportive; supplemental oxygen in dyspneic patients will only accelerate the degree of lung injury so is generally not recommended. Once paraquat has been absorbed, the prognosis is grave, so prompt decontamination is essential.

Lime: Garden lime is calcium carbonate and it is of low toxicity, although it can cause respiratory irritation if inhaled. Many people confuse garden lime with quicklime (calcium oxide), which is corrosive when it comes into contact with water (such as on mucous membrane surfaces). What is sold in garden and department stores is garden lime; quicklime would be purchased from a specialty supply store.

Mulches: Mulches come in a variety of types ranging from cocoa bean shells to pine/cypress bark to recycled automotive tires. With the exception of cocoa bean shell mulch, most mulches pose little toxicological hazard to pets, although they may pose foreign body hazards if large amounts are ingested. Cocoa bean shell mulches can have varying amounts of methylxanthines in them; some have had the methylxanthines extracted for other purposes and contain very little methylxanthine content, while others can contain up to 255 mg of theobromine per ounce of mulch. Toxic dose of methylxanthines for dogs are 20 mg/kg for mild signs (vomiting, hyperactivity), 40-50 mg for cardiotoxic signs, and >60 mg/kg for seizures. Dogs ingesting large amounts of cocoa bean shell mulch should be decontaminated and monitored for signs of methylxanthine toxicosis. Treatment of symptomatic animals should include IV fluids, antiarrhythmics, diazepam, and thermoregulation as needed.


Ethylene glycol is present in high concentrations in automotive antifreezes, many brake fluids, winterizing fluids and aircraft deicers. Inks, ink pad, polishes, finger moistening compounds (e.g. Tacky Finger®), and other stationery supplies may contain ethylene glycol. Some ink pens contain relatively high levels of ethylene glycol, but the total volume of ink is only a few milliliters, so ink pens would only pose an ethylene glycol risk to very small animals such as birds, pocket pets, or dogs/cats less than 2-3 pounds. Some ornamental “snow globes” were found to contain significant amounts of ethylene glycol that resulted in pet poisonings when the globes cracked and contents leaked out. Unfortunately, reliable toxic doses of ethylene glycol have not been established for most animals, including dogs and cats. Parent ethylene glycol acts as a potent alcohol and toxic metabolites contribute to metabolic acidosis and damage kidney tubules, resulting in renal failure. Because of the different mechanisms involved in ethylene glycol toxicosis, clinical signs frequently change throughout the course of the toxicosis. Classically, 3 different stages of toxicosis are described, although considerable overlap between these stages may be seen and some animals will not experience each stage; death can occur at any stage. The stages are 1) neurologic—the initial inebriation due to the effects of alcohol on the CNS, 2) cardiopulmonary—due to severe acidosis and electrolyte disturbances, and 3) renal—due to renal tubular injury from calcium oxalate crystals.

Stage 1—Neurologic: initial inebriation due to alcohol effects on CNS. Generally begins within 30 minutes of exposure and lasts up to 12 hours. In mild to moderate cases, this stage may pass quickly and may not be noted by the pet owner or veterinary staff. Animals are initially ataxic, disoriented, “drunk,” stuporous, hypothermic (especially cats), polyuric and polydipsic (PD/PU more pronounced in dogs). Coma and death may occur during this stage, or the animal may appear to partially or fully recover over 3-6 hours. By 6-12 hours, the neurologic status of the animal may again deteriorate due to development of severe metabolic acidosis from ethylene glycol metabolites, resulting in marked CNS depression, stupor or coma. Seizures are possible.

Stage 2—Cardiopulmonary: severe acidosis and electrolyte disturbances due to alcohol and toxic metabolites. Generally occurs from 12 to 24 hours following exposure. Signs may be more recognizable in dogs than cats. Tachypnea, tachycardia, depression, +/- seizures, and pulmonary edema may occur. At this time, a high anion gap and severe metabolic acidosis are generally present.

Stage 3—Oliguric renal failure: due to acidosis, direct effect of metabolites on kidney and precipitation of crystals in tubules. May seen as early as 12 hours, especially in cats, but generally occurs within 24-72 hours following exposure. Clinical effects include azotemia, depression, anorexia, vomiting, abdominal pain, oral ulcers, halitosis, and oliguria progressing to anuria. Low urine specific gravity and glucosuria are common. Calcium oxalate crystals occur in the urine in ~40% of cases (absence of crystalluria does NOT rule out the possibility of EG toxicosis). Seizures are possible.

Clinical pathologic abnormalities include increased osmolal gap and anion gap, hyperglycemia, hyperkalemia, decreased blood pH, and hypocalcemia. BUN and creatinine become elevated but usually not before 12 hours post exposure; therefore BUN and creatinine are of minimal benefit in diagnosing early exposures. Diagnosis is based on history, clinical signs, and confirmatory laboratory testing. Currently (2017), the Catachem VetSpec test kit appears to be the most reliable in-clinic test available; it gives the same false positives as did the “old” PRN test (i.e. propylene glycol, etc.), but it does not give false positives with other alcohols, as some of the other test kits do (e.g. KACEY, REACT). This test has separate controls for both dogs and cats. Some forms of activated charcoal and most diazepam injectable products contain propylene glycol that may interfere with the interpretation of the test, so ideally blood for testing should be taken prior to administration of propylene glycol-containing activated charcoal (check the label) or diazepam. Other products that may cause false positives for the test are formaldehyde, metaldehyde, glycerin/glycerol, or diethylene glycol. It is generally recommended that the test be run an hour or more following ingestion, as this is when blood levels should be sufficient to get reliable test results; testing prior to an hour following ingestion may lead to false negative results. Alternatively ethylene glycol levels can be determined by a human hospital laboratory on a STAT basis. Blood ethylene glycol levels ≥ 50 mg/dL (or 5 μg/mL, be sure to check the units reported greater in dogs and ≥ 20 mg/dL (2 μg/mL) in cats would be considered significant. Measuring anion gap (>25 mEq/L) or serum osmolality (> 20 mOsm/kg) may assist in diagnosing ethylene glycol toxicosis, although by themselves these tests are fairly non-specific. Observation, via Wood’s lamp, of fluorescence in urine, stomach contents or on paws/muzzle may suggest exposure (fluorescein dye is added to automotive antifreeze to help in detecting radiator leaks).

Treatment of ethylene glycol toxicosis must be timely and aggressive as delay in therapy can result in irreversible renal damage or death of the animal. For recent (< 45 minutes) exposures and asymptomatic animals, induce vomiting or perform gastric lavage; because food in the stomach may slow absorption, emesis or lavage may be of benefit up to 1 hour in animals that have recently eaten. The use of activated charcoal is controversial, as aliphatic alcohols are not thought to be well adsorbed by charcoal, but many clinicians routinely use activated charcoal in ethylene glycol exposures. Based on exposure history and/or diagnostic test results, the use of either fomepizole or ethanol infusion (see below) may be indicated. If awaiting test results to determine whether ethylene glycol exposure has occurred, it is safest to initiate treatment, which can then be discontinued if testing shows no significant ethylene glycol exposure. Symptomatic animals should be stabilized as needed. Seizures can be controlled with diazepam or barbiturates, but care must be taken to minimize any further CNS depression. Intravenous fluids are the cornerstone of treatment, especially in symptomatic animals. High infusion rates of crystalloids are necessary to correct dehydration and hypoperfusion; fluid ins and outs should be monitored to avoid fluid overload and possibly pulmonary edema. Treatment of acidosis and renal failure may be required. Oliguric or anuric animals may require peritoneal dialysis. Intravenous ethanol and fomepizole (4-MP, 4-methylpyrazole, Antizol-Vet™) are used to delay the breakdown of ethylene glycol to its more toxic metabolites, allowing the parent compound to be excreted in the urine unchanged. Best results with either of these treatments require initiation of treatment as soon as possible following ingestion, preferably within the first 6-8 hours. Ethanol has the advantages of being inexpensive and readily available, but it has some serious drawbacks, including worsening of metabolic acidosis and CNS depression, making evaluation of degree of ethylene glycol toxicosis difficult. Additionally, ethanol treatments are time-intensive and require constant patient monitoring because of the severe side effects. Ethanol can be used in both cats and dogs. The preferred treatment regime would be to administer 8.6 ml/kg (600 mg/kg) of a 7% (70 mg/ml) ethanol solution and then maintain at 1.43 ml/kg/hr (100 mg/kg/hour), up to 200 mg/kg/hr as a constant rate infusion. The animal must be constantly monitored and the dosage adjusted to prevent severe respiratory depression and acidosis. Alternatively, a 20% ethanol solution can be used in dogs at 5.5 ml/kg every 4 hours for 5 treatments then every 6 hours for 4 treatments. Cats are given 5.0 ml/kg every 6 hours for 5 treatments, then every 8 hours for 4 treatments. Fomepizole will not cause hyperosmolality, metabolic acidosis or CNS depression. In contrast to ethanol, which is administered every 4 hours or as a constant-rate infusion, fomepizole is administered every 12 hours for 36 hours. The initial dose for dogs is 20 mg/kg (slow IV over 15-30 minutes), then 15mg/kg (slow IV) at 12 and 24 hours, and then 5mg/kg is given at 36 hours. Although not approved for use in cats, a treatment protocol has been developed that was effective at preventing lethality if administered within the first 3 hours following ingestion (Connally et al., 2010). The dose of fomepizole used in cats was 125 mg/kg IV followed by 31.25 mg/kg IV at 12, 24 and 36 h after the initial dose. The main drawback with fomepizole is availability (some compounding pharmacies do provide it) and the cost of the medication. Treatment should be continued until animals are clinically normal with at least 24 hours with normal renal function and acid base parameters. Alternatively, a negative ethylene glycol test indicates that ethanol/fomepizole treatment may be discontinued (although treatment may need to be continued for any residual renal impairment). The prognosis for recovery depends on degree of exposure, length of time between exposure and treatment, and aggressiveness of treatment. Surviving animals may fully recover or may have residual renal insufficiency requiring lifetime maintenance. The presence of oliguria/anuria indicates a grave prognosis.


Many of the insecticides used in the yard these days are the same or similar compounds to flea control products used on pets, such as imidacloprid, fipronil and pyrethroids. Most are present in yard products at levels well below those used in, say, spot-on flea control products, so problems are not expected from routine use of these products. Pets ingesting large amounts of granules can develop GI upset from the granules themselves, though these signs are usually either self-limiting or resolve with symptomatic care (e.g. antiemetics). Some pyrethroid products, such as bifenthrin granules, can cause problems if ingested in large amounts relative to their body size (i.e. dog gets into the bag of compound or ingests a pile of granules). In these cases, we can occasionally see tremors similar to those seen with permethrin toxicosis in cats. These tremors generally respond well to administration of methocarbamol. Diatomaceous earth is another compound that is frequently used as an insecticide. The insecticidal activity of diatomaceous earth is said to be due to desiccation of the insects. Like garden lime, it can be irritating if inhaled or if it gets into the eyes, but it has a fairly low level of toxicity in mammals.

Mosquito Dunks: Mosquito dunks contain compounds designed to kill mosquito larvae in the water. Most mosquito dunks are composed of a mixture of organic and inorganic materials as a base (e.g., clay, seed husks/hulls etc.) along with subspecies of Bacillus thuringiensis. This bacterium can be thought of as “anthrax for mosquitoes” and it is not-infectious and non-toxic to species other than dipteran insects. As the mosquito dunk dissolves, it releases the bacteria into the water to provide a constant population of bacteria to infect mosquito larvae. Ingestion of mosquito dunks by pets is not expected to cause more than mild GI upset, although large pieces may cause a foreign body hazard. Some mosquito dunks contain larvicidal compounds such as methoprene, which is a commonly used insect growth regulator in pet flea control products. These products have very low toxicity to non-insects and are not expected to cause serious problems if accidentally ingested by pets.

Disulfoton: Disulfoton is a “hot” (i.e. highly toxic) organophosphate insecticide used in systemic rose products. Dogs are often exposed to these products after the owner mixes them into the soil along with bone or blood meal to fertilize roses; dogs can ingest enough via the soil to cause severe clinical signs. Not only can these animals present with the typical SLUDDE signs, but they can also have hemorrhagic diarrhea plus liver and pancreatic enzyme elevations; pancreatitis is not uncommon. Successful management of these cases requires rapid and aggressive therapy, including seizure/tremor control (diazepam, methocarbamol or barbiturates), atropine as needed for bradycardia and bronchial secretions, pralidoxime (2-PAM) for nicotinic signs, IV fluids, and other supportive care. If large amounts of dirt or bone meal are ingested, and if the animal does not yet have diarrhea, an enema may help to increase excretion of the product. Because disulfoton ‘ages’ on the acetylcholinesterase molecule, the effects of disulfoton can persist for several days up to a week or more. The prognosis is good to guarded depending on amount ingested and response to treatment.

Methomyl: Methomyl is a “hot” carbamate insecticide that is primarily found in fly baits. These fly baits contain large amounts of sugar that make them very palatable to dogs and other animals. In addition, methomyl often is mixed with other highly appealing foods, such as hot dogs. Clinical signs can be seen within 30 minutes of ingestion. Vomiting, seizures, dyspnea, and death are the most common. Death can occur quickly, but if veterinary intervention is obtained in time, the signs generally respond well to atropine (for bronchial secretions and bradycardia) and diazepam (for seizures). Because carbamates are rapidly broken down in the body and do not ‘age’ on the acetylcholinesterase enzyme, signs are generally of short duration. Patients that do not die of the acute toxidrome may appear clinically normal within 4-6 hours.

Snail Baits: Snail baits come in two types—metaldehyde and iron-based. Both types of products are formulated with ingredients such as molasses or bran to attract snails and slugs; these products frequently attract pets, especially dogs. Metaldehyde is highly toxic to mammals. A 10 pound dog ingesting a teaspoon of 2% metaldehyde bait is at risk for significant toxicosis. The mechanism of action of metaldehyde is not fully understood, but may involve depletion of neurotransmitters such as GABA and serotonin in the CNS. Signs can occur within several minutes to a few hours following ingestion. Initial signs are anxiety, tachycardia, nystagmus (more pronounced in cats), mydriasis, hypersalivation, ataxia, and panting. Vomiting, diarrhea, tremors, hyperesthesia, CNS stimulation, muscle rigidity, tremors, seizures, metabolic acidosis and hyperthermia may also occur. Liver failure may develop within 2-3 days of exposure. Death is due to respiratory failure, hyperthermia or multiorgan failure. Treatment of metaldehyde exposures includes decontamination in asymptomatic animals, and symptomatic management of clinical signs. Methocarbamol is preferred for managing tremors. Electrolyte and acid/base should be monitored and abnormalities corrected as needed. Hyperthermia frequently resolves once tremors and seizures are under control, but external cooling measures may be required. Liver and renal values should be monitored throughout the acute toxidrome and up to 72 hours following exposure. Prognosis depends on the amount ingested, promptness of treatment and response to therapy. Iron-based snail baits have been marketed as less toxic alternatives to metaldehyde for control of snails and slugs. While not completely non-toxic, these products do have a much wider margin of safety to mammals than metaldehyde. There are two formulations currently marketed—a 1% iron phosphate product and a 6% sodium ferric EDTA product. Both are said to kill snails and slugs through interaction of the iron with hemocyanin, the copper-based respiratory protein in the blood of molluscs that transports oxygen. Iron interferes with oxygen carrying capacity of the blood, resulting in death of the slug or snail. Since hemocyanin is unique to some arthropods and molluscs, these iron-based products have low toxicity to most non-target species. Most pets ingesting these baits will have no more than mild GI upset, although iron toxicosis is a concern if very large quantities (>20 mg/kg of iron) are ingested.


Pressure Treated Lumber: Pressure treated lumber in the US used to be made with CCA (copper-chromium-arsenic) and there are many decks, fences and outdoor structures that still contain CCA-treated wood. Because of concerns over the potential exposure of children to arsenic that might leach from the wood, use of CCA-treated wood was restricted from use in residential settings in the US in 2004. Pressure treated wood now being sold for residential use in the US has been treated with non-arsenic containing compounds. Older CCA wood is not an arsenic issue should pets chew on the intact wood—in this case the arsenic is still bound up in the CCA matrix, making it unavailable for significant acute exposure. However, ashes of burnt CCA wood do pose a hazard for arsenic toxicosis as pyrolysis will release arsenic from the matrix, making it available for ingestion and absorption. Arsenic causes vascular leakage resulting in massive subserosal hemorrhages in the GI tract; in severe cases, rapid onset of hypovolemic shock and death can occur following ingestion. Initial signs might include vomiting (+/- blood), weakness, pallor, and collapse. Animals surviving more than a few hours generally show GI signs, and renal failure may develop within 2-5 days. Treatment is symptomatic and supportive. Chelation with BAL or dimercaprol can be attempted, but animals showing more than mild to moderate GI upset have very guarded prognosis.

Grill Products: Charcoal briquets are not toxic, but can pose foreign body hazards if ingested. Charcoal lighter fluid can cause defatting of skin and mucous membranes, leading to chemical burns on the skin of dogs and cats. Ingestion of lighter fluid may result in vomiting due to the irritant nature of the fluid; systemic signs are not expected unless aspiration of the fluid occurs. Matches contain chlorates that can cause hemolysis, although even a small dog would have to eat the tips of many matches to develop signs. Ashes from charcoal fires may contain traces of lighter fluid or other components that may trigger vomiting. Ashes that have been sitting out in the environment can grow bacteria and/or molds that can cause GI upset and/or tremorgenic mycotoxicosis.


Swimming pool chemicals encompass a wide variety of potential toxicants including chlorine tablets, sodium hypochlorite, calcium hypochlorite, chlorinated isocyanurates, lithium hypochlorite, sodium bicarbonate, hydrogen peroxide, and muriatic acid. These products are used to adjust the pH, sanitize and clean the pool. It is important to determine exactly which product was involved. Most of these are strong acids or bases and are highly corrosive. Emesis and lavage are contraindicated in acid and alkali ingestions because of the potential for re-exposure to damaged tissues of the esophagus, possible rupture of an already damaged stomach and the possibility of aspiration. Alkalis can be diluted with milk or water if milk is not available. Diluents can also be used for acids, but not at the increased risk of vomiting. Activated charcoal is not beneficial in exposure to either acids or alkalis. Mucosal injury should be managed with pain medication, antibiotics and dietary alterations as needed.


Water intoxication is not an uncommon occurrence during the summer. Most often, the history is of a ‘water fool’ of a dog who spends hours happily lapping up water as it is paddling away in the pool or pond. Eventually, the kidneys can’t excrete enough water to match what is being ingested, resulting in hemodilution, hyponatremia and hypo-osmolality; ultimately cerebral edema ensues. Dogs frequently present comatose, hypothermic, and bradycardic; initial signs of ataxia, disorientation and polyuria might be reported. Treatment is symptomatic and supportive: control of tremors/seizures, encourage urine output (normal saline +/- diuretic, catheterize bladder prn), thermoregulation, etc.


Finally, a story about the dog who spent the whole day at the beach, running and swimming (and ingesting) the salt water. Sometimes owners forget that, with all that salt water around, the dog needs fresh water to drink. Or the dog was too excited to drink. Or he ingested so much salt water that he vomited up the fresh water. So they packed up the family and Fido and head home, only to have the dog seizure before they reach home. In this case, the excessive sodium has resulted in hypernatremia, causing elevations in cerebrospinal fluid sodium levels. Water is pulled from the brain, stressing neurons and stretching meningeal vessels, resulting in severe CNS signs. Generally, affected animals will show depression, disorientation, muscle fasciculations (often begin in the face), tremors and seizures. Blood work will reveal hypernatremia and increased osmolality. In these acute cases (< 24 hours duration), the serum sodium level can be lowered quickly through the use of dilute fluids (1/2 normal saline or dextrose in water) or, because the distal colon is highly efficient at absorbing water, through the use of warm water enemas. After about 24 hours, the synthesis of idiogenic milliosmoles in the brain increase the risk of cerebral edema developing with rapid hemodilution, so if it has been > 18-24 hours since exposure to the water, lowering the sodium needs to be done very slowly (no more than 0.5-1 mEq/L/hr).