Potential toxins for "roaming around" pets (Proceedings)


Ingestion of paintballs has been associated with severe and potentially life-threatening acid/base and electrolyte abnormalities [most commonly hypernatremia] leading to ataxia, blindness, tremors, seizures and death.

Ingestion of paintballs has been associated with severe and potentially life-threatening acid/base and electrolyte abnormalities [most commonly hypernatremia] leading to ataxia, blindness, tremors, seizures and death. Depending on the brand, paintball ingredients can include a number of compounds that act as osmotic cathartics [polyethylene glycol, glycerol, sorbitol] which are thought to cause the water/electrolyte imbalances [moving fluid into the GIT lumen]. Emesis should be considered in the asymptomatic patient; and the use of activated charcoal and cathartics are considered contraindicated. Hydration status and subsequent acid/base and electrolyte status should be continuously monitored until the values are considered stabilized and any clinical signs resolved. Hypernatremic patients should be slowly rehydrated with 2.5% dextrose in 0.45% saline until sodium levels normalize.

Ice melts can pose moderate risks to pets, depending on the active ingredient. Most act as skin and gastric irritants, and vomiting and diarrhea are the most commonly observed clinical signs of illness. Ice melts that contain sodium chloride can lead to hypernatremia and an osmotic diuresis, which can lead to muscle tremors, acidosis and seizures. Hyperkalemia can occur following ingestion of ice melts containing potassium chloride. This can result in muscle weakness and cardiac abnormalities. Products containing magnesium chloride can cause muscle weakness, cardiac abnormalities and hypotension as a result of hypermagnesemia. Ice melts containing calcium carbonate and calcium magnesium acetate are primarily irritants, and cause few systemic effects. Pets are generally considered fairly resistant to the toxic effects of urea, and signs are generally restricted to its irritant nature.

Cyanobacterial blooms (blue-green algae) tend to occur in stagnant or slow moving, eutrophic water bodies, during periods of warm weather and calm conditions. These cyanobacteria are naturally present in the environment, but will rapidly grow and proliferate to produce blooms when environmental conditions are just right. Pets are exposed when they drink or swim in the contaminated water. Blooms can occur all year round. Blooms consisting of Microcystis or Nodularia spp. produce toxins that specifically target the liver. Usually within 1 to 4 hours of ingestion, dogs will display lethargy, weakness, depression, vomiting, diarrhea, pallor and shock. Death is a result of massive hepatic necrosis. Marked elevation in liver enzymes are consistently observed, and prolonged clotting times are seen terminally. Anabaena, Aphanizomenon, Oscillatoria, and Lyngbya are species that produce neurotoxins, primarily anatoxin-a and anatoxin-a(s). Anatoxin-a is a potent depolarizing neuromuscular blocking agent and anatoxin-a(s) inhibits acetylcholinesterase activity; this leads to overstimulation (signs of CNS excitation - tremors, seizures) and ultimate fatigue (signs of paralysis), along with SLUD signs. Pets poisoned with the neurotoxic cyanobacteria exhibit no characteristic blood or chemistry panel abnormalities or gross and histologic changes. Diagnosis is based on a combination of access to a suspect water source, signs of neurotoxicity or hepatotoxicity, characteristic (or lack of characteristic) clinical pathologic abnormalities and histologic changes, and detection of the cyanobacteria and/or toxin in the water and/or biological tissues (stomach contents, liver).

Myotonia in dogs has been associated with high exposures to phenoxy herbicides [e.g., 2,4-D, MCPP, MCPA]. Phenoxy herbicides are commonly used in agricultural settings and around the home, sometimes mixed with fertilizers, to be applied to crops and lawns. At low dose exposures, phenoxy herbicides can cause mild, transient and self-limiting anorexia, vomiting and diarrhea. However, with severe exposures, dogs affected with myotonia display reluctance to move, weakness, depression, ataxia and recumbency. The myotonia can be confirmed through electromyogram, where one can see an increase in insertional activity. Since the phenoxy herbicides are excreted in the urine, fluid diuresis is encouraged, along with appropriate supportive care. Patients generally recover over a 3 day period, depending on the severity of the exposure.

Ionophores, such as monensin, lasalocid, narasin and salinomycin, are well known feed additives in livestock rations, used as coccidiostats and to increase feed efficiency and rate of gain. Pets, particularly roaming in areas where livestock are housed, can be exposed to these products. Ionophore's toxic effect particularly targets skeletal muscle tissue in dogs [skeletal muscle degeneration and necrosis], and thereby causes an abrupt onset of depression, myalgia, stiffness and ascending muscle weakness [paresis, paralysis, labored breathing, recumbency]. Respiratory paralysis is thought to be the underlying cause of death. Clinical signs generally begin to occur within 12 hours of exposure. Monensin at levels > 5 mg/kg BW, lasalocid at dosages > 10 mg/kg BW and maduramicin at levels > 24 mg/kg in the diet have all been associated with clinical disease. Feed refusal is commonly observed as well. No specific changes have been observed on complete blood counts and serum chemistries, other than perhaps increases in creatine kinase activity. Myoglobinuria may be seen as the disease progresses. Diagnosis relies heavily on history of exposure, clinical presentation, and confirmation of the presence of the ionophore in the suspect feed, serum, feces, gi contents, bile and liver. There is no specific treatment for this clinical condition. Emesis and enhancing fecal excretion through the use of cathartics may be useful, along with providing selenium and vitamin E. In general, animals that survive the first few days will recover, but there may be permanent damage to the muscle with the replacement of fibrous connective tissue. Other diseases with similar presentations include botulism, tick paralysis, macadamia nut poisoning and delayed neuropathy associated with organophosphate exposure.

Despite its well known potential for causing serious, life threatening disease in people and pets, paraquat is not an uncommon poisoning in pets, particularly free roaming dogs. Paraquat is commercially used on many different crops throughout the US, and it is used as a desiccant. Despite the manufacturer of the most commonly used products adding an emetic and an odor agent to prevent serious exposure from occurring, poisonings continue to occur. Paraquat's main target organs are the gastrointestinal tract, lung and kidney. Immediately following exposures, abdominal tenderness, vomiting, anorexia, diarrhea and mucosal ulcers are commonly reported. This phase is typically followed by respiratory compromise [e.g., tachypnea, dyspnea, exercise intolerance, cyanosis, rales] due to severe edema, congestion, hemorrhage and necrosis of the bronchiolar and alveolar epithelium within the lung. If an affected animal happens to survive this phase, they can potentially go through a period of a few days where the clinical picture may appear to improve. However, if the dose is severe enough, fibrosis of the lung and necrosis of the renal tubule epithelium can ultimately lead to the demise of the patient. Successful treatment of this disease is rare, and even supportive measures like oxygen therapy may make the condition worse. Poisonings are generally confirmed post mortem by residue testing of urine, liver, kidney and lung tissue, along with characteristic histologic lesions of the lung and kidney. Malicious poisonings are common with this herbicide.

Poisonings of pets with organochlorine pesticides [e.g., aldrin, dieldrin, chlordane, endosulfan, endrin, heptachlor, methoxychlor] are not common, and as a group are often times confused with the acetylcholinesterase-inhibiting organophosphate and carbamate pesticides. Organochlorines do NOT inhibit ache activity, but do cause diffuse central nervous stimulation following exposures. The most commonly observed clinical signs following excessive exposure include excessive salivation, anxiousness and apprehension, hyperexcitability, muscle tremors, excessive response to external stimuli and continuous or intermittent seizure activity. Confirmation of poisonings relies heavily on finding residues of the pesticide in gastrointestinal contents, and treatment is aimed at providing seizure control, along with basic cardiovascular and respiratory support.


Donaldson CW. 2003. Paintball toxicosis in dogs. Vet Med 98(12):995-997.

Harrington M et al. 1997. Suspect herbicide toxicity in a dog. JAVMA 209(12):2085-2087.

Hautekeet LA. 2000. Ice melts are health hazards. Vet Med, February:110-112.

Hooser SB and Talcott PA. 2006. Cyanobacteria. In Small Animal Toxicology, Eds. ME Peterson and PA Talcott, Elsevier Inc., pp. 685-689.

Oehme FW and Mannala S. 2006. Paraquat. In Small Animal Toxicology, Eds. ME Peterson and PA Talcott, Elsevier Inc., pp. 964-977.

Raisbeck MF. 2006. Organochlorine pesticides. In Small Animal Toxicology, Eds. ME Peterson and PA Talcott, Elsevier Inc., pp. 934-940.

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