Small Animal Toxicology- Recognizing Natural Toxins in Ontario

 Toxin ingestion is a common emergency in veterinary medicine, often requiring prompt recognition and intervention to prevent serious outcomes. Some of the most common toxic cases seen in veterinary clinics involving toxic substances such as medications, industrial chemicals, certain foods - grapes and chocolate. There is also instances of toxicoses caused by less widely discussed natural toxins present in the environment that can harm patients. As concerns about environment changes and urban expansion grow, alongside the rise in outdoor activities, animals are increasingly exposed to a variety of environmental toxins. 

According to Pet Poison Helpline, mushroom toxicosis represents 1.1 % of toxic cases, making it the fifteenth most common toxin reported in Ontario, while in 2024, plants and fungi toxicosis ranked sixth, according for 8.1% of all cases, based on data from the ASPCA Animal Poison Control Center. Harmful algal blooms are also significant source of natural environmental toxicity that impacts both humans and animals. According to data from the One health Harmful Algal Bloom (OHHABS) by the centers for Disease Control and Prevention (CDC)j in 2022, there where over 100,000 reported cases of animal illness in the USA linked to theses events. 

This article will explore the three significant natural toxins commonly found in Ontario: blue-green algae- Amanita mushroom, and cardiotoxic flowers. It is important for RVTs to be aware of how animals are exposed to them, their mechanism of action, and the appropriate treatment options and care plans for affected patients. As well as educate owners on preventative care. 

DIVERS OF ENVIRONMENTAL TOXIN EXPOSURE

The climate in Ontario is undergoing significant transformation, characterized by longer warm seasons, heavier rainfall, and milder winters. These changing conditions create an ideal environment for the growth and spread of certain natural toxins, such as those produced by plants fungi, and bacteria. 

Urban expansion is converting former green spaces like forests, wetlands, and meadows into residential and commercial developments. This disruption exposes animals to new risks, as pets increasingly encounter wildlife, soilborne toxins, and unfamiliar plant species in environments they where previously unlikely to access. 

the term "divers" is used in the section title to encompass the underlying environmental, behavioral, and seasonal factors that contribute to an animal's risk of exposure. There include climate change, landscape use, human-animal interactions, and pet management practices. 

BLUE-GREEN ALGAE- CYANOBACTERIA

Cyanobacteria, often referred to as "blue-green algae," are a unique group of plant- like bacteria that naturally thrive in lakes, ponds, rivers, streams and occasionally in marine environments. These bacteria can reproduce rapidly, leading to the formation of a  surface layer that appears as a "bloom". While blooms are most commonly seen in later summer or early fall, they can occur during other seasons as well. Cyanobacteria are capable of photosynthesis, allowing them to convert nutrients and sunlight into energy.  Supporting their growth and reproduction. The appearance of these blooms can vary significantly, often resembling green pea soup but they may also exhibit other colours, ranging, from deep green to red or pink. In some instances, there may be no visible changes in the water at all. Blue-green algae blooms are a global concern, as they have also been known for a century to cause the death of livestock, birds fish, wildlife and dogs. Among companion animals dogs are particularly vulnerable because they tend to swim in or drink contaminated water.  

Figure 1 l Blue-green algae blooms. Lake placid, ON.

MECHANISM of TOXICITY and CLINICAL SIGNS

Cyanobacteria is a phylum including many different genera and species. Over 2,000 species of cyanobacteria have been identified but only about forty are known to produce toxins harmful to vertebrates. Some species of cyanobacteria can produce multiple toxins, and cyanobacterial blooms may contain both toxic and non toxic strains. The ratio of toxic to non-toxic, distinguishing toxic species based solely on appearance is challenge in, as diagnostic analysis is often necessary. 

**Note: It is impossible to differentiate potentially harmful cyanobacterial blooms from harmless ones just by visually examining the water. Dogs are the most susceptible to cyanobacteria toxicosis, cats are rarely affected because of their much lower risk of exposure - indoor pets. Dogs have been reported to die after licking (including grooming) or eating algal material, or swimming in affected water. 

The most significant toxin-producing genera of blue-green algea found in fresh brackish water in Ontario include Microcystis, Doliochospermum (formerly known as Anabaena) and Anabaenopsis. Microcystis is recognized as one of the most common and harmful bloom-forming cyanobacteria in freshwater systems worldwide. the toxins produced by these cyanobacteria are referred to aa cyanotoxins. The clinical signs of cyanobacteria toxicosis can vary, depending on the specific toxins present in the water and the species of animals affected. The two most dangerous types of cyanotoxins are microcystin and anatoxin. 

Microcyst is a potent hepatotoxin that primarily affects the LIVER, potentially causing acute liver failure. Severe liver damage may lead to ACUTE INTRAHEPATIC HEMORRAGE, and as clinical signs progress, generalized hemorrhage can occur due to coagulopathy. Often death may follow within days, due to hypovolemic shock resulting from hepatic hemorrhage or liver failure. 

Anatoxin, primarily produced by the Doliochospermum genus, is a neurotoxin affecting the nervous system. It can cause acute paralysis and respiratory failure, presenting with nicotinic signs, including the classic SLUDGE symptoms: SALIVATION, LACRIMATION,URINATION,DEFECATION, GASTROINTESTINAL SIGNS, and EMESIS, along with other neurological symptoms such as TREMORS, PARALYSIS, SEIZURES, and CYANOSIS from bronchial secretions. 

Neurotoxin effects may appear as quickly as five to fifteen minutes to one hour due to reparatory paralysis. Gastrointestinal symptoms are often the first to appear and may include VOMITING, DIARRHEA, ABDOMINAL TENDERNESS, HEMATEMESIS, and EXCESSIVE SALIVATION. Skin reactions can also occur, leading to PRURITUS and URTUCARIA. Clinical signs may develop within minutes to a few hours after exposure, depending on the specific toxin involved. 

DIAGNOSIS

Diagnosis of Cyanobacterial toxicosis is primarily based on clinical signs and a history of exposure to potentially contaminated freshwater or brackish water. It's important to remember that cyanobacteria can also proliferate in containers such as: Open water tanks, troughs, or buckets. Detection of cyanotoxins can be performed using an Enzyme- Linked Immunosorbent Assay (ELISA), which helps confirm exposure and assesses toxin load in the patient. Diagnostic samples may include water or algal scum as well as materials collected from the animal such as hair coat, vomitus, gastric contents, feces urine, or liver tissue. 

TREATMENT

There is no specific antidote available for cyanotoxins; therefore, initial stabilization to manage life- threatening clinical signs is crucial. If exposure occurred recently, including emesis, administering activated charcoal, and/or performing gastric lavage may be helpful, depending on the patient's clinical signs and mental state. Emesis should NOT be performed in patients who are already vomiting or are NOT able to protect their airways- such as those who are neurologically compromised, as this may lead to aspiration. 

When the patient's condition allows, bathing with liquid dishwashing detergent and warm water can help remove any residual toxins from the fur. In the case of seizures, anticonvulsant such as diazepam can be administered and provided by the vet team. Hypovolemic shock is treated with IV FLUIDS- crystalloid and colloid therapy. One study found that 99% of microcystin toxin in vitro, and studies in rats have confirmed its effectiveness in reducing toxin absorption and protecting the liver, when given after exposure although keep in mind liver may have some scarring - meaning preventive care of liver is required for pet how : Preventing further or future episodes of liver inflammation by focusing on nutritional care which would prevent further scarring and can slow or partially reverse the inflammation. If precautions are not taken after the event, and with further scarring of the liver overtime the build up of scar tissue will physically block: Blood flow, Regeneration capacity, the liver becomes nodular and stiff and even surviving liver cells function less efficiently. 

Cholestyramine is available in powder form, and the current recommended dose from the ASPCA Animal Control Poison Control Center( APPC) are 0.3-0.5g/kg, dissolved in liquid and administered orally every 6-8 hours for 3-5 days. Its important to note that human formulations containing XYLITOL should never be administered to dogs check ingredients and ask before considering. 

Behind the Scenes RVT Intervention

During triage and history-taking, they require compliance and information from owner, owner should inform of any recent swimming or drinking from a lake, especially during the warmer months. In these cases RVTs are exposed to contact dermatitis when handling animals with cyanotoxins present on their hair coat, therefore the more honest owner is the more effectively medical staff can take on appropriate protective measures and address the problem at hand. 

For symptomatic patients, it is important to closely monitor neurological signs. This includes assessing the intensity of tremors , muscle rigidity, ataxia, and the frequency of the seizures, as the patient may progress to respiratory failure - again owners mentioning and keeping track of these signs prior to arrival at clinic can help better assess your pet and make the experience less stressful on everyone. 

Liver function should also be monitored carefully, how can that be done is by owner accepting blood work. Paying attention to Jaunice and signs of coagulopathy - petechiae, bruising, and bleeding. Monitoring urine output is essential, to assess renal function and guide fluid therapy. Urine output should be maintained at 1-2 ml/kg/hr, with frequent assessment of volume status, including respiratory rate and effort, edema, and chemosis. Body weight should also be monitored regularly. A balanced Iv fluid - crystalloid fluid should be administered and adjusted to meet the individual patient's needs.

while affected animals require aggressive treatment and monitoring, all asymptomatic patients should be observed closely for at least six hours post exposure to evaluate any possible exposure to neurotoxic cyanotoxins. Be aware that clinical signs MAY HAVE A DELAYED ONSET. How effectively the medical team can help a pet at first is 100% reliant on owner compliance, honesty, and patience. 

OWNER's ROLE:

Once discharged from clinic. Continue close observation and monitoring on urine output, water intake, weight, neurological signs, digestive abnormalities. Report any changes which is abnormal to prior to toxicity event without delay. 

TOXIC MUSHROOMS- AMATOXINS

Canada is home to numerous beautiful hiking trails and forested areas where mushrooms thrive, especially during the wet months of late summer and fall. While most mushrooms are harmless, a small number contain potent natural toxins known as amatoxins. Toxins are produced by certain species within the genera Amanita, some of which are commonly found in Ontario and pose serious risks to both humans and animals. Amanita mushrooms are responsible for the majority of fatal mushrooms are responsible for the majority of fatal mushroom poisonings worldwide and have been documented in cases throughout Ontario and other parts of Canada. Typically, these mushrooms grow in wooded or semi-wooded environments; however they can also be found in urban and suburban yards, parks and mulched garden beds. This proximity brings them close to curious pets, which can pose a danger

MECHANISM of TOXICITY and CLINICAL SIGNS

Figure 3 l Amanita bisporigera

Figure 4l Amanita phalloides

Some Amanita mushrooms contain amatoxins, which can lead to the irreversible inhibition of RNA polymerase II. This inhibition results in decreased protein synthesis and necrosis of high-metabolism cells, such as HEPATOCYTES, INTESTINAL CRYPT CELLS, and RENAL TUBULAR EPITHELIAL CELL. Amatoxins can cause serious and sometimes fatal effects in both animals and humans. However, not all species of amanita mushrooms contain this toxin, and other mushroom species outside of the Amanita genera also produce amatoxins. These toxins are not exotic or imported, they are part of natural ecosystems and be found in backyards, along dog-walking trails, and near campsites throughout Canada. 

Amanita phalloides

Commonly known as the DEATH CAP MUSHROOM, is one of the most poisonous fungi in the world and is responsible for the majority of fatal mushroom poisons globally. Although not native to Canada, it has started to establish itself, particularly in British Columbia. This spread has been facilitated by the importation of European trees such as hazelnut, hornbeam, oak, and Beech, which form mycorrhizal associations with the fungus. The first documented specimen in Canada was found in 1997 in the Fraser Valley. Tragically in 2016, a case emerged in Victoria, where a toddler died after ingesting a death cap mushroom was growing in a residential area, Recently local authorities in places like Oak Bay and Victoria have issued warnings urging residents to remove mushrooms from their properties to contact Poison Control.

TREATMENT

Treatment of amatoxin mushroom toxicity is primarily through supportive care, as no specific antidote exists, the best approach for owners to take is preventative care - be cautious and alert during trail walks especially during warmer months, when mushrooms are more likely to bloom avoid off-leash roaming in areas where mushrooms are common, DO NOT ASSUME A MUSHROOM IS SAFE because it looks edible. and if the event takes place take your pet immediately to emergency and cooperate with vet staff to stabilize your pet. Patients often require aggressive fluid therapy and intensive monitoring. If the patient presents early (within two or four hours of ingestion) the following approach is taken, GI decontamination followed by oral activated charcoal is 1-2 g/kg, orally, followed by two or three half-doses over the subsequent 24 hours, due to enterohepatic circulation of these toxins. Activated charcoal combined with a cathartic such as sorbitol is CONTRAINDICATED in dehydrated patients. Dextrose may be used to correct hypoglycemia, often as a constant-rate infusion, with close blood glucose monitoring to guide dosing. Vitamin K1 supplementation and blood products may be needed for patients exhibiting COAGULOPATHY 

BEHIND THE SCENES RVTs

During phone triage, RVTs aim to gather not only details about the pet's condition, but information about the location where the mushroom was found, This information can be crucial for later identification or environmental assessment. Owner Role: Provide all information requested by RVTs over the phone and  if possible bring in the mushroom itself, handled carefully and placed in a sealed bag. Or take clear photos from multiple angles, including the underside of the cap, and the base. These details can assist veterinary stapp or poison control specialists in making an identification.  RVTs may help prepare information for the veterinary poison control services and ensure that all relevant details including the species, size, time of ingestion, observed signs, mushroom appearance, and location, are clearly organized and efficiently communicated to the toxicology consultant if necessary. While some mushrooms such as puffballs, are non-toxic, than can closely resemble deadly species like Amanita, especially in their immature stage. During warmer months, when mushrooms are more likely to bloom and families are spending more time outdoors.  

NATURAL PLANT TOXINS

While cases of wild plant poisoning are often more commonly reported in large animals because of their grazing habits, certain outdoor plants found in Ontario can also pose a significant risk to companion animals, especially dogs. Accidental ingestion, particularly during unsupervised outdoor activities or backyard foraging, can lead to serious and even fatal toxic effects. Notably, MILKWEED, LILY of the VALLEY, and YEW are recognized for their potent cardiotoxins and are often found in wild, ornamental, and suburban environments.  

MILKWEED

A group of native wild plants commonly found throughout Ontario, particularly in meadows and along roadsides, and in open fields. These plants are well-known for their beautiful flowers and their ability to attract butterflies. 

Figure 5l Milkweed

LILY-OF-THE-VALLEY

Figure 6 l Lily-of-the-Valley

Features bell-shaped flowers and is admired for its appearance and fragrance; it is also frequently found in Ontario. Despite the name it is NOT a true lily species.

MECHANISM of TOXICITY and CLINICAL SIGNS

Plants containing CARDIAC GLYCOSIDES are among some of the most toxic plants and have a narrow margin of safety. These plants exert their toxic effects by disrupting normal cardiac conduction through distinct chemical mechanisms. Both Milkweed and Lily-of-the-valley contain cardiac glycosides which are naturally occurring chemicals that can be potentially life threatening to animals if ingested. the cardiac glycosides found in these plants act through a mechanism very similar to that of the cardiac drug DIGOXIN, which affects heart function by inhibiting the sodium potassium ATPase pump, and essential component if proper cardiac function. This inhibition results in an increase in intracellular sodium. The effect of this process is more forceful but slower cardiac contractions. The level of toxicity can vary depending on the specific plant, the part that is consumes, and the amount ingested. Generally, all parts of these plants are considered toxic. To be cautious, animals that ingest any part of the plant should receive prompt veterinary care. Other Clinical signs may include GI symptoms such as VOMITING, DIARRHEA, as well as GENERAL WEAKNESS. Cardiac symptoms might include BRADYCARDIA or TACHYCARDIA, ARRYTHMIAS, and HYPERKALEMIA. These clinical signs can begin to appear within two hours of exposure and may last for four to five days.  

Yew

Specifically Taxus canadensis, commonly known as Canadian yew, is a native coniferous shrub found in shady, moist woodlands across Ontario, particularly in the southern and central regions. This slow-growing evergreen features soft, flat, needle like leaves arranged in two rows along its stems and produces small red, berry like arils in the fall. Ingestion of yew can be extremely dangerous for dogs and cats, as taxines interfere with cardiac conduction by antagonizing calcium channels in cardiac myocytes.  This can lead to electrical conduction disturbances in the heart muscle, often resulting in ACUTE CARDIAC ARREST.  The amount of plant material required to achieve a lethal dose is quite small, with a minimum lethal dose (LD min) in dogs of about 2.3 grams of leaves per kilogram of body weight, or approximately 11.5 mg/kg of taxine alkaloids. For a small to medium sized dog, just chewing on a yew branch or consuming an ounce of leaves could be fatal. Yew plants are toxic throughout the entire year year, but their toxicity peaks late fall to winter due to the accumulation of taxine concentrations. Clinical signs of toxicity can vary depending on the amount ingested, and may include ATAXIA, BRADYCARDIA, DYSPNEA, MUSCLE TREMORS and SEIZURES which can lead to collapse and death. Death may occur one to three hours after ingestion. 

DIAGNOSIS    

Plant toxicosis in companion animals can be difficult, especially when ingestion is not directly observed. Similar to the intoxication caused by Amanita mushrooms, the diagnosis primarily depends on the history of exposure and the clinical signs observed. Finding plant material in VOMIT, FECES, or the ORAL CAVITY can aid in making a diagnosis, although this may not always be possible. Cardiac glycosides and taxines can sometimes be detected in gastric content for through specialised blood tests performed by the lab. Additionally, EKG abnormalities, such as bradycardia, heart blocks, and ventricular arrythmias, may be observed. 

TREATMENT

Gastrointestinal decontamination including emesis induction and activated charcoal, is recommended for ASYMPTOMIC PATIENTS shortly after ingestion. Antiarrhythmic agents such as Lidocaine may be administered for the treatment of ventricular arrhythmias. Bradycardia can be managed with anticholinergic drugs like Glycopyrrolate or Atropine. In cases involving CARDIAC GLYCOSIDE PLANTS, hyperkalemia may be addressed with fluid therapy alone or with Dextrose and insulin to help lower serum potassium levels. Digoxin specific antibody fragments (Fab) are effective antidotes for digoxin toxicity, including toxicity from plant-derived cardiac glycosides. Positive effects are often observed within one hour of administration. This antidote works by binding to digoxin and similar compounds, allowing the resulting complexes to be excreted in urine. However, digoxin-specific antibody is rarely stocked in general practise clinics because of its high cost and limited availability. An visit to the a EMEGENCY VETERINARY CLINIC for these cases is recommended, it is important to MONITOR SERUM POTASSIUM CONCENTRATIONS closely, especially during the first several hours after administration, as levels may drop rapidly following the infusion of digoxin Fab. 

With Yew plant toxicity, Atropine is considered to be most effective when administered early in the course of intoxication. Since Yew toxicosis is often diagnosed POSTMORTEM. 

Number one treatment for either case is PREVENTION. DO NOT allow dogs and cats to play with yew branches or leaves, avoid using decorations which contain poisonous plants such as wreaths. 

Behind the scenes RVTs

Similar to the approach taken for Amanita mushroom toxicity, RVTs play a crucial role in both immediate response and ongoing care of patients exposed to cardiotoxic plants. When taking a patient's history they require DESCRIPTION OF PLANT  or ACQUIRING A PICTURE  is even better, TIMING OF EXPOSURE,  and the LOCATION OF THE INCIDENT. Intensive monitoring is often necessary, especially for patients on CARDIAC MEDICATION or under going treatment for HYPERKALEMIA. Owner's Role: Bring in a sample or a photo of the suspected plant, provide information as accurately as possible and honestly, and patience, also continuing or learning from the experience can help prevent having to go through the same event causing stress and trauma to everyone.  

CONCLUSION

Environmental and naturally-occurring toxins can be especially challenging to manage, as their clinical signs often mimic those of other toxic exposures. Unlike pharmaceuticals, foods, or household chemicals where toxic doses are less studied, and their effects can vary widely. Their occurrences is also less predictable in outdoor environments, making exposure harder to control.