Toxicology of selected pesticides, drugs, and chemicals. Zinc

Zinc poisoning in small animals has been described in dogs, cats, birds, and ferrets, but the dog appears to be the species most often affected. Ingestion of zinc-containing metallic objects, including pennies, and zinc oxide ointments has been associated with the majority of the toxicoses. Clinical signs include anorexia, vomiting, diarrhea, hemolytic anemia, kidney dysfunction, and possible liver and pancreatic abnormalities. Treatments that have proven efficacious include fluid diuresis, blood transfusions as needed, general supportive care, and removal of the source of zinc. Further evaluation of the benefit of chelation therapy is urgently needed.     

Toxicology of selected pesticides, drugs, and chemicals. Smoke inhalation

Animals with smoke inhalation should be given a thorough diagnostic evaluation. Optimal care relies on the information derived, as well as judicious choice of therapeutic measures. Careful attention to such animals by the veterinarian and allied staff is important to minimize suffering and to enhance not only the likelihood of survival, but also the extent of recovery.     

Toxicology of selected pesticides, drugs, and chemicals. Boric acid

With the advent of boric acid insecticides, accidental ingestion of the compound can be encountered in animals. Toxic levels of boric acid most commonly cause vomiting, depression, and, occasionally, diarrhea. Boric acid is, however, cytotoxic to all cells. If a sufficiently high level is ingested, seizures, renal tubular nephrosis, and, rarely, hepatotoxicity may be noted. Gastrointestinal evaluation and supportive care are usually of primary therapeutic importance, although in severe cases, exchange transfusion and/or peritoneal dialysis may be required to decrease blood boron concentrations.     

Toxicology of selected pesticides, drugs, and chemicals. Illicit and abused drugs

Toxicoses involving exposures to illicit and abused substances are an occasional problem in veterinary patients. The difficulties of clinical diagnosis and the importance of obtaining a good history are emphasized. A discussion of some of the more common poisonings is presented, including available sources, clinical signs, toxicity, metabolism, mechanism of action, and the treatment for each agent.     

Toxicology of selected pesticides, drugs, and chemicals. Pyrethrin and pyrethroid insecticides

Pyrethroids have a wide spectrum of insecticidal potency, vertebrate toxicity, and environmental stability. The exceptionally high selectivity ratios of pyrethrins and pyrethroids have resulted in their use for insect control in numerous formulations. A primary effect of pyrethroids is to slow the closing of the sodium activation gate in nerve cells. All pyrethroids have essentially the same basic mechanism of action on voltage-dependent sodium channels but differ in the magnitude of effect. Based on clinical signs, electrophysiologic responses, and chemical structure, pyrethroids can be classified as Type I or Type II. Inhibition of the GABAA receptor appears to be an additional mechanism of Type II pyrethroids. Clinical signs in small animals during a pyrethroid toxicosis vary but are generally attributable to neural dysfunction. Treatment consists of decontamination procedures and application of appropriate symptomatic care, including control of seizures if necessary.     

Toxicology of selected pesticides, drugs, and chemicals. Petroleum distillates and turpentine

Companion animal exposures to volatile hydrocarbons and turpentine accounted for 2% of all calls received by the IAPIC in 1987. Volatile hydrocarbons are also used as vehicle solvents (e.g., pesticides), and both vehicle and active ingredients pose a significant hazard to companion animals. The most significant clinical effects of the hydrocarbons are related to aspiration pneumonia. The likelihood of aspiration is generally related to the compound's viscosity, with more volatile and most widely available compounds posing the greatest risk. Treatment generally is conservative. Gastrointestinal decontamination methods (e.g., emetics and activated charcoal administration) are used only in massive ingestions or when other toxicants are present in conjunction with the hydrocarbons. Oxygen therapy and cage rest are recommended for the dyspneic animal. Close monitoring of an exposed animal and symptomatic care as needed are also recommended for at least 12 hours after exposure.     

Toxicology of selected pesticides, drugs, and chemicals. Organophosphorus and carbamate insecticides

Organophosphorus and carbamate insecticides produce acute toxicosis via a common mechanism--the inhibition of acetylcholinesterase--and, therefore, these categories of insecticides are considered together. This article discusses the mechanisms, toxicity, clinical signs, lesions, and diagnosis of, as well as treatment for, toxicoses produced by these compounds.     

Toxicology of selected pesticides, drugs, and chemicals. D-limonene, linalool, and crude citrus oil extracts

Cats are susceptible to poisoning by insecticidal products containing D-limonene, linalool, and crude citrus oil extracts. Signs of toxicosis include hypersalivation, muscle tremors, ataxia, depression, and hypothermia.     

Toxicology of newer pesticides for use in dogs and cats.

The past 10 years have witnessed the development of several new insecticides that have been specifically designed to exploit physiologic differences between insects and mammals. This has resulted in products that seem to have a wide margin of safety when used in dogs and cats. Compared with the more acutely toxic organophosphorous, carbamate, and heavy metal insecticides as well as with the environmental problems of bioaccumulation associated with some of the organochlorine insecticides, these newer insecticides such as fipronil, imidacloprid, selamectin, lufenuron, and nitenpyram seem to alleviate these known problems while still providing satisfactory insecticidal activity.     

Toxicology of oncologic drugs

The drugs used in clinical oncology are inherently toxic because they are designed to kill host cells. For the most part, the toxic effects occur in tissues with high growth fractions--that is, bone marrow, gastrointestinal epithelium, and hair follicles. Nevertheless, certain drugs do cause harm to other organs. At therapeutic doses of anticancer drugs, the toxicoses are usually mild to moderate and can be managed without undue discomfort to the animal. Occasionally, however, life-threatening cytopenias occur. By contrast, with drug overdose, life-threatening toxicoses can be a very real concern.     

Toxicology of nonsteroidal antiinflammatory drugs

Nonsteroidal antiinflammatory drugs (NSAIDs) constitute a class of pharmacologically active agents with similar therapeutic actions and side effects, despite diverse chemical structures. NSAIDs inhibit the enzyme cyclo-oxygenase and, thus, decrease inflammation mediated by prostaglandins. Toxicoses due to NSAIDs are manifested primarily by gastrointestinal upset and hemorrhage and by renal damage. Management consists of detoxification measures, in addition to supportive and symptomatic care. The article outlines the incidence, clinical toxicity, mode of action, and pharmacokinetics of nonsteroidal antiinflammatory drugs. The toxic effects of NSAIDs on individual organ systems are described, and general management recommendations for the treatment of NSAID toxicoses are presented.     

Toxicology of ferrets.

Because of their curious nature and small size, ferrets are at risk for various toxicoses. At present, there is not a great deal of information on specific toxicants in ferrets. This article initially reviews general consideration in treating poisoning in ferrets, such as obtaining history and decontamination. It then discusses some specific agents that appear to be common causes of poisoning in ferrets based on the experience of the ASPCA Animal Poison Control Center.     

Toxicology of aquarium fish.

Most aquarium fish live in a closed system, so the effects of toxins can be cumulative and devastating. Most cases of toxicity are due to deficiencies in husbandry and tank maintenance. Poor water quality kills more fish than infectious agents, making client education a very important preventive tool for aquatic practitioners. This article includes a discussion of toxicities related to water quality, chemotherapeutics, pesticides, and household substances.     

Determination of sensitivity of Mycoplasma hyosynoviae to tylosin and selected antibacterial drugs by a microtiter technique.

A microtiter technique was used for determination of the sensitivity of Mycoplasma hyosynoviae to antibiotics and other drugs. Use of a biphasic agar-broth medium in microtiter plates allowed direct visualization of growth. Results were more reproducible with this system than when broth alone was used and evaluation based on color change was required. Attempts to adapt the test for use with Mycoplasma hyorhinis were not successful. Minimal inhibitory concentrations of 12 drugs and drug combinations for 12 strains of M. hyosynoviae are presented. Drugs with the lowest minimal inhibitory concentrations were tylosin (0.37 mcg/ml)and lincomycin (0.88 mcg/ml), both of which have been used for treatment and control of M. hyosynoviae arthritis. Comparison of the minimal inhibitory concentrations of tylosin for 43 isolates of M. hyosynoviae obtained in 1959 and 1960 and from 1966 through 1971 indicated the possibilty of decreasing sensitivity to the drug although differences between recent isolates and earlier ones were not statistically significant.     

Assessment of ruminal degradation, oral bioavailability, and toxic effects of anticoagulant rodenticides in sheep

OBJECTIVE: To assess the rate and extent of ruminal degradation of warfarin, chlorophacinone, and bromadiolone in vitro and determine the oral availability and clinical and hemostatic effects of each anticoagulant rodenticide in adult sheep. ANIMALS: 3 Texel sheep. PROCEDURE: Samples of ruminal fluid were incubated with each of the anticoagulants to assess the kinetics of ruminal degradation over 24 hours. To determine the plasma kinetics of the anticoagulants, each sheep received each of the anticoagulants IV or via a rumenimplanted cannula at 2-month intervals (3 rodenticide exposures/sheep). At intervals during a 240- to 360- hour period after treatment, prothrombin time (PT) was measured, plasma anticoagulant concentration was assessed, and clinical signs of rodenticide poisoning were monitored. In plasma and rumen extracts, anticoagulant concentrations were determined via high-performance liquid chromatography. RESULTS: In the rumen extracts, anticoagulants were slightly degraded (< 15%) over 24 hours. In vivo, oral availability of warfarin, chlorophacinone, and bromadiolone was estimated at 79%, 92%, and 88%, respectively. Although maximum PT was 80 seconds after chlorophacinone and bromadiolone treatments, no clinical signs of toxicosis were detected; PT returned to baseline values within 2 weeks. CONCLUSIONS AND CLINICAL RELEVANCE: In sheep, warfarin, chlorophacinone, and bromadiolone were not degraded in the rumen but their bioavailabilities were high after oral administration; the kinetics of these compounds in sheep and other mammals are quite similar. These data suggest that the lack of susceptibility of ruminants to these anticoagulant rodenticides cannot be explained by either ruminal degradation or the specific toxicokinetics of these anticoagulants.     

Industrial chemicals and the horse.

Poisoning resulting from exposure to a wide variety of industrial chemicals is not a common occurrence in horses, but it does happen on occasion. A wide range of toxicosis can occur from a wide range of industrial pollutants, such as dioxin, carbon tetrachloride, and tetrachloroethylene, to heavy metals, such as cadmium and zinc. The equine practitioner must consider industrial chemical toxicosis in differential diagnoses and work with a reputable veterinary diagnostic laboratory to confirm or rule out industrial chemical poisoning.