Veterinarians are potentially exposed to myriad potent pharmaceuticals and other hazardous materials as part of their work environment, and particularly during patient decontamination procedures (most notably dermal decontamination). Therefore, knowledge of important toxicologic workplace hazards and basic personal protective equipment (PPE) is important. It is critical to recognize that PPE is the “last line of defense” and not a panacea for toxicologic hazards. The overarching principle is to avoid exposure if at all possible. Over-reliance on inadequately fitted or inappropriate types of PPE continues to be a substantial cause of human casualties because of the feeling of overconfidence these devices can provide. In particular, respirators should be selected, fitted, and tested by persons qualified to do this.
Most instances of algal poisoning of domestic animals and many affecting wildlife are caused by cyanobacteria that grow in freshwater systems worldwide. Clinical signs depend on the specific cyanotoxin(s) involved and multiple body systems can be affected. Tentative diagnoses are based on a history of exposure, clinical signs, and necropsy findings. However, analyses to identify specific cyanotoxins are important for diagnostic confirmation and are helpful for monitoring, surveillance, and to optimize treatment regimens. Early gastrointestinal tract decontamination is typically the key aspect when managing affected animals.
Allium spp toxicosis is characterized by development of hemolytic anemia after ingestion of large amounts of plant material. Toxicosis has been reported in livestock after feeding of onions, and dogs and cats have been affected after ingesting cooked, dehydrated, or granulated forms of onions or garlic. Several days after ingestion, clinical signs of acute hemolytic anemia develop, including weakness, pallor, icterus, and collapse. Treatment entails early decontamination and management of acute hemolytic anemia.
Herbicides are used routinely to control noxious plants and have also been used in warfare and conflict. Most of these chemicals, particularly the more recently developed synthetic organic herbicides, are quite selective for specific plants and have low toxicity for mammals; other, less-selective compounds (eg, sodium arsenite, arsenic trioxide, sodium chlorate, ammonium sulfamate, borax, and many others) were formerly used on a large scale and are more toxic to animals.
Smoke inhalation injury is the damage to the body associated with breathing in superheated air or steam, other harmful gases, vapors, and particulate matter resulting from thermal combustion. Smoke inhalation injury can be associated with thermal injury, chemical injury, systemic toxicity, or any combination of these. This chapter does not cover toxicity of theatrical "smoke" machines that do not depend on pyrolysis (ie, that work by nebulization, fogging, or misting).
Human drugs or nutritional supplements available without a prescription are known as over-the-counter (OTC) medications. Exposures to OTC drugs in pets can be accidental or intentional. A valid client-patient-veterinarian relationship must exist for veterinarians to recommend extra-label use of these drugs to their clients. Most are not approved for veterinary use by the FDA, and safety of most OTC drugs has not been determined in animals. Veterinarians should understand the potential risks of using OTC medications and communicate these risks to their clients.
Non protein nitrogen (NPN) poisoning (toxicosis) results from excessive consumption of sources of NPN or urea. It is acute and often rapidly fatal, with clinical signs including muscle tremors, abdominal pain, incoordination, respiratory distress, and recumbency, then death. Diagnosis can be made by analysis of postmortem samples for ammonia content and of suspected sources for non protein nitrogen content; ruminal pH > 7.5 is supportive of the diagnosis. Treatment includes removal of suspected source materials, ruminal infusion of acetic acid and cold water, as well as supportive therapy.
A variety of coal-tar derivatives induce acute to chronic disease in animals, with clinical signs that vary based on the constituents. Clinical effects are acute to chronic hepatic damage with signs of icterus, ascites, anemia, and death. Phenolic components may cause renal tubular damage. Coal tar–related poisoning has been reported in farm animals and pets.
Ethylene glycol toxicosis is often fatal and primarily affects dogs and cats, though all species are susceptible. Most commonly found in vehicle radiator antifreeze, it is also available in a variety of other automotive and household products. Systemic effects include metabolic acidosis, gastrointestinal irritation, early CNS depression, and cerebral edema, progressing to irreversible acute kidney failure. The toxic metabolite of ethylene glycol is oxalic acid, which binds to calcium, resulting in formation of calcium oxalate crystals in the proximal renal tubules. Treatment requires early intervention with fomepizole (4-methylpyrazole) or ethanol.
Nitrate poisoning (toxicosis) in animals (especially ruminants) results from excess consumption of nitrates from plants or water or via ingestion of nitrate-containing fertilizers. The nitrate ion (NO3–) is reduced to nitrite ion (NO2–), which is rapidly absorbed and leads to the formation of methemoglobin, which inhibits oxygen transport. This results in dyspnea, cyanotic mucous membranes, weakness; and, if severe, death due to anoxia. Ruminants are more susceptible because rumen flora can rapidly reduce nitrates to nitrites. Methylene blue, administered IV, will reverse the methemoglobinemia and may be effective as a treatment with supportive care. Ocular fluid specimens are most appropriate sample for postmortem, with laboratory testing of suspected sources of nitrate exposure.
Pentachlorophenol (PCP), commonly known as penta, has been used as a fungicide, molluscicide, and insecticide and as a wood preservative. Product names include Dowicide EC-7®, Penchlorol®, Pentacon®, Penwar®, Priltox®, Sinituho®, and Weedone®. PCP is defined by the US EPA as a heavy-duty wood preservative. It is used primarily to treat wooden utility structures including poles, crossarms, and log anchors. The migration of PCP beyond the immediate vicinity of treated utility poles has been documented nationally. PCP is commonly observed and measured in soil immediately adjacent to utility poles. PCP is a stable, persistent compound, has a restricted use, and is no longer available to the general public. It is banned in many countries and its use severely restricted in others, but it may be purchased and used by certified applicators. It is now only permitted for industrial purposes; agricultural and domestic uses are prohibited because it is classified as a highly hazardous pesticide.
Petroleum product toxicosis can be caused by ingestion of, inhalation of, and/or dermal contact with petroleum hydrocarbons in crude oil, gasoline, diesel, kerosene, naphtha, or other hydrocarbon mixtures. Clinical signs can include respiratory distress and aspiration pneumonia, generalized GI disturbance (eg, salivation, bloat, diarrhea and/or constipation, anorexia and weight loss), CNS depression and/or excitation, impaired reproduction, and death. Identifying and obtaining a sample of the petroleum product and samples (feces, stomach/rumen contents, lungs, fat [especially perirenal], liver, brain, and other tissues) from affected animals are important to match the hydrocarbon "fingerprint" in the source material to the biological tissue. Treatment is to stop the exposure and remove the animal from a contaminated environment, feed, or water. Prognosis depends on the animal and the type of hydrocarbon product, as well as the dose and duration of exposure.
Persistent organic pollutants are carbon-containing chemicals that are resistant to chemical and biological degradation. The persistent halogenated pollutants (PHPs) contain halogen atoms (chlorine, fluorine, or bromine). Important groups of PHPs include polybrominated diphenyl ethers (PBDEs), polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs), polychlorinated biphenyls (PCBs), the polyfluoroalkyl substances (PFAS), and some of the organophosphorus flame retardants (OPFRs).
Insecticides are any substance or a mixture of substances intended to prevent, destroy, repel, or mitigate insects. Similarly, acaricides are substances that can destroy mites. A chemical can exert both insecticidal and acaricidal effects. Based on their properties, these chemicals can be classified into four groups: 1) organophosphates, 2) carbamates, 3) organochlorines, and 4) pyrethrins and pyrethroids. Because of worldwide use, these chemicals pose health risks to nontarget species, including people, domestic and companion animals, wildlife, and aquatic species. In large animals, poisoning is often due to inadvertent or accidental use, whereas in small animals (particularly dogs) poisoning is often due to malicious intent.
Metaldehyde poisoning after ingestion of a molluscicide most frequently affects dogs and cats. Clinical signs include neurologic dysfunction, gastrointestinal distress, hyperthermia, and cyanosis. Sedation, administration of IV fluids, and gastric lavage often result in clinical improvement. Diagnosis may be confirmed via analysis of gastric contents.
The chemical element arsenic (symbol As, atomic number 33) is a nonmetal or metalloid in group V on the periodic chart. It is often referred to as arsenic metal, and for toxicological purposes it is classified as a metal. It exists in several forms and has a long history of various uses, including insecticides for animals, wood preservatives (used in some aspects of the lumber industry), herbicides (pre-emergent weed killers), and even some medicinal uses. It is responsible for many poisonings in humans and animals.
Acute and chronic copper poisoning may occur in most animal species, although susceptibility varies markedly between species. Chronic poisoning is more common and is characterized by low morbidity and high morbidity in species exhibiting the hemolytic crisis and severe liver damage. Diagnosis is confirmed by liver analysis for copper. Treatment is often unsuccessful.
The consequences of exposure to fluoride compounds of either environmental or medicinal or may be unclear. Benefits of fluoride supplementation in animals should be considered with potential adverse effects development of teeth and bones; and possible risk for osteosarcoma in some species. Diagnosis of fluoride poisoning (fluorosis) is made on the basis of history, clinical signs and testing of food, water, tissue and serum samples. Disease resulting from chronic exposure to high concentrations of fluoride compounds generally does not respond favorably to treatment.
Newborn pigs are iron deficient at birth and vulnerable to iron-deficiency anemia. Iron toxicosis in newborn pigs primarily occurs from administration of excess amounts of iron supplements by oral or parenteral routes. Vitamin E supplementation of the sow can help to prevent iron toxicosis in piglets.
Lead poisoning in mammalian and avian species is characterized by neurologic disturbances, gastrointestinal upset, hematologic abnormalities, immunosuppression, infertility, and renal disease. The nature of the clinical manifestations is influenced by the dose and duration of lead exposure. Chelation therapy, cathartics, thiamine administration, and sedation are common treatment methods. In food-producing species, treatment is discouraged because of food safety concerns, the prolonged treatment period, permanent degenerative damage, and a poor prognosis. Tissue analysis for lead supported by pathologic abnormalities is essential to confirm the diagnosis.
Poisoning associated with various forms of mercury has declined in recent years. Chronic exposure in fish and wildlife species associated with the bioaccumulation of mercury in the environment remains a problem. In domestic animal species, clinical signs of nervous, gastrointestinal, respiratory, and reproductive systems involvement are typical and influenced by the form, dose, and duration of exposure. Diagnosis may be confirmed on the basis of the clinical picture, histopathologic findings and results of analysis of tissue analysis for mercury concentration. Because tissue damage is permanent and food safety implications are important factors, treatment options may be limited and are often discouraged.
Molybdenum poisoning (toxicity) is most often the result of copper-molybdenum imbalance in feed. Ruminant species are most frequently affected, and clinical signs may include poor growth, infertility, diarrhea, lameness, ataxia, as well as osteoporosis. Copper supplementation to address the mineral imbalance is the most effective treatment.
Excessive salt (sodium chloride, NaCl) intake can lead to the condition known as salt poisoning, salt toxicity, hypernatremia, or water deprivation–sodium ion intoxication. The last term is the most descriptive, giving the result (sodium ion intoxication) as well as the most common predisposing factor (water deprivation.) Salt poisoning is unlikely to occur as long as sodium-regulating mechanisms are intact and fresh drinking water is available.
Selenium is an essential element that has a narrow margin of safety, with the difference between adequate and potentially toxic concentrations in the diet being approximately 10- to 20-fold. Feed supplements, resulting in final selenium content of 0.2–0.3 ppm, are added to diets to prevent deficiency and resultant diseases such as white muscle disease in cattle and sheep, exertional myopathy in horses, hepatosis dietetica in pigs, and exudative diathesis in chickens. The maximum tolerable concentrations for selenium in most livestock feed is considered to be 2–5 ppm, although some believe 4–5 ppm can inhibit growth.
In small animals, zinc toxicosis is usually a result of ingestion of objects that contain or are coated with zinc, most commonly US pennies. In large animals, the main causes are contaminated pastures and excess dietary supplementation. Clinical signs vary depending on species, source, and amount of zinc; however, GI signs are common initially, with intravascular hemolysis, organ damage, and DIC occurring in a second phase. Lameness may be seen in foals and swine. Diagnosis is based on history of exposure, abnormalities on laboratory testing (which may include measurement of serum zinc concentration), and identification of a suspicious object on abdominal radiographs in small animals. Treatment consists of removal of the source of zinc and supportive therapy; chelation therapy is controversial.
Bracken fern (Pteridium aquilinum) is found throughout the world and is among the five most numerous vascular plants in the world. Because the species includes numerous subspecies and varieties, plant size varies, with frond lengths ranging from 0.5 to 4.5 m.
Gossypol is produced naturally by the glands of the cotton plant. Although all animals are susceptible to gossypol toxicity, monogastrics, preruminants, immature ruminants, and poultry are affected most frequently. Affected animals may show cardiac failure and sudden death; hepatotoxicosis; liver necrosis secondary to congestive heart failure; hematologic effects, including anemia and increased RBC fragility; reproductive effects (including decreased libido and spermatogenesis in males; irregular cycling, disrupted pregnancy, and embryonic death in females; and green coloration of egg yolks and decreased hatchability in chickens); thumping in swine; and cardiotoxicosis in dogs. Treatment requires removal of the gossypol source, usually the feed, and supportive care.
Mushrooms are the fleshy fruiting bodies of fungi. They typically shoot up from growing vegetative (mycelium) portions, and they contain spores as reproductive units. Fungi lack chlorophyll; their nutritional requirements are met by using organic material from saprophytic, parasitic, or mycorrhizal life cycles.
Plants are an important part of the decor of homes; pets having access to these plants often chew on or ingest them, with toxicity a possible outcome (). Inquiries to poison control centers on plants ingested by children
Pyrrolizidine alkaloidosis is typically a chronic toxicosis that results in hepatic failure. It is caused by many toxic plants, most commonly of the genera Senecio, Crotalaria, Heliotropium, Amsinckia, Echium, Cynoglossum, and Trichodesma. These plants grow mainly in temperate climates; however, some (eg, Crotalaria spp) require tropical or subtropical climates. The plants most often implicated include ragwort (S jacobea), groundsel (S riddellii, S longilobus), rattleweed (Crotalaria retusa), and seeds of yellow tarweed (A intermedia).
Most animals are susceptible to Quercus poisoning, although cattle and sheep are most commonly affected. Most species of oak (Quercus spp) in Europe and North America are considered toxic. Clinical signs occur 3–7 days after consumption of large quantities of young oak leaves in the spring or ingestion of bark or green acorns in the fall. Fallen trees associated with a recent storm are often reported with outbreaks. Feed restriction before exposure plays a crucial role, enhancing susceptibility. Mortality as high as 70% may be seen. Malformed calves and abortions have been reported in cows that consume acorns during the second trimester of pregnancy. The toxic principle, which appears to be pyrogallol, gallotannins, polyhydroxyphenolic compounds, or their metabolites produced by microbial hydrolysis in the rumen; binds and precipitates proteins by astringent action, which results in GI, hepatic, and renal dysfunction.
This often fatal neurotoxic disease occurs in livestock of any age that graze pastures in which annual ryegrass (Lolium rigidum) is present and in the seedhead stage of growth. It is seen in western and southern Australia and in South Africa from November to March. Hay of Festuca rubra commutata (Chewing’s fescue) with Rathayibacter toxicus–infected seedhead galls has caused a similar disease in cattle and horses in Oregon. Outbreaks of ergot alkaloid toxicity in cattle on L rigidum have been reported in South Africa and should not be confused with annual ryegrass staggers.
Sorghum species are drought-tolerant plants with a high nutritional value related to protein, fiber, calcium, potassium, phosphorus, and antioxidant content. Unfortunately, the plants may produce neuropathic and teratogenic manifestations if consumed by animals. Sorghum poisoning has occurred primarily in the southwestern US and Australia. The syndrome is reported almost exclusively in horses, although a similar disease has been reported in sheep and cattle. Lathyrogenic nitriles such as beta-cyanoalanine, cyanogenic glycosides, and nitrates have been suggested as causative agents. The syndrome develops in horses after they have grazed hybrid Sudan pastures for weeks to months, and axonal degeneration and myelomalacia in the spinal cord and cerebellum develop. (Also All.see page Cyanide Poisoning.) Consumption of the seed will not produce the disease.
In the 1920s, cattle in North America developed a fatal hemorrhagic disease. Various causes, including pathogenic organisms and nutritional deficiencies, were investigated. Damp conditions caused stacks of hay to mold and spoil. Within several weeks, sheep and cattle eating the hay developed uncontrollable hemorrhages that were generally fatal in 30–50 days. Feeding trials and chemical analyses later definitively identified the cause as spoiled or moldy sweet clover (Melilotus officinalis and M alba) hay or silage.
Cantharidin is a potent vesicant and irritant produced by insects commonly known as blister beetles. Cantharidin can sometimes contaminate alfalfa. Cantharidin poisoning causes gastrointestinal and urinary tract irritation, and in severe cases can cause shock, circulatory collapse, and death. Cantharidin poisoning should be suspected in patients with compatible clinical signs, a history of alfalfa in the diet, and severe hypocalcemia and hypomagnesemia. Treatment includes correcting fluid and electrolyte imbalances, providing pain relief, and aiding elimination of cantharidin.
Venomous snakebites are emergency situations requiring prompt veterinary attention. Crotalid envenomation can cause neurotoxicity, tissue necrosis, hemolysis, and coagulopathy; North American elapid envenomation can cause neurotoxicity; and Australian elapid envenomation can cause neurotoxicity, myotoxicity, coagulopathy, and hemolysis. Treatment includes supportive care in addition to administration of antivenom, where available.
Toad poisoning (toxicosis) can occur when dogs or cats bite or ingest toads, although serious disease or death generally occurs only after exposure to large toads such as the Rhinella marina (marine toad) or Incillus alvarius (Colorado river toad). Clinical signs of toxicosis include hypersalivation, gagging or retching, vomiting, weakness, cyanosis, dyspnea, and seizures; hyperkalemia and cardiac arrhythmias can occur in severe cases. Treatment is generally supportive, although digoxin-specific F(ab) may be considered in cases of severe arrhythmias and/or hyperkalemia refractory to supportive care.
Spiders of medical importance in the US do not inflict particularly painful bites, so it is unusual for a spider bite to be suspected until clinical signs appear. It is also unlikely the spider will remain in close proximity to the victim during the time required for clinical signs to develop (30 minutes to 6 hours). Almost all spiders are venomous, but few possess the attributes necessary to cause clinical envenomation in mammals—mouth parts of sufficient size to allow penetration of the skin and toxin of sufficient quantity or potency to result in morbidity.
Through centuries past, a variety of methods, active ingredients, formulations, and control measures have been used for rodent pest control. These efforts become more apparent as urban areas expand and cohabitation with wildlife evolves. As humans increasingly encounter wildlife and rodent pests, attempts at rodent control also carry increasing risk of nontarget-species exposure.
Strychnine is a pesticide that typically causes toxicosis in companion and production animals by accidental ingestion or malicious poisoning. Onset of toxicosis is rapid and results in agitation, stiff gait, tremors, and seizures, leading to respiratory arrest and death. Diagnosis is commonly made by consistent clinical signs and analysis of the stomach contents. Treatment is aimed at controlling tremors and seizures and providing respiratory support.