Dogs Poisoned Research Articles

Nitrite poisoning in cats and dogs fed a commercial pet food

The death of three cats, from two separate households, was linked to toxic concentrations of sodium nitriterused as a preservative, in a commercial pet food. Post-mortem examination of the three cats revealed a brownish discoloration of the blood suggestive of methaemoglobinaemia. Analysis of two samples of the pet food fed to the cats revealed a mean concentration of 2850 mg of total nitrite per kg of food (as fed). In a further incident, ataxia and weakness was noticed in two of four dogs after they were fed the same brand of pet food. One dog was successfully treated for methaemoglobinaemia with intravenous methylene blue.

Safety and efficacy of 4-methylpyrazole for treatment of suspected or confirmed ethylene glycol intoxication in dogs: 107 cases (1983–1995)

Objective— To evaluate safety and efficacy of 4-methylpyrazole (4-MP) treatment in dogs and to determine clinical signs and outcome of, and clinicopathologic abnormalities in, dogs treated in early or late stages of ethylene glycol (EG) intoxication. Design— Retrospective study. Animals— 107 dogs. Procedure— For dogs treated with 4-MP, 1 of 2 dosage regimens was usually used: 20 mg/kg of body weight, IV, initially, 15 mg/kg 17 hours later, and 5 mg/kg 25 and 36 hours after the initial dose, or 20 mg/kg, IV, initially, 15 mg/kg 12 and 24 hours later, and 5 mg/kg 36 hours after the initial dose. Results— Neither adverse clinical signs nor clinicopathologic abnormalities were associated with the administration of 4-MP except in 1 dog, which developed tachypnea, gagging, excess salivation, and trembling after the second dose of 4-MP was given. Ethylene glycol intoxication was confirmed in 37 dogs. Of these, 21 were azotemic or became azotemic within 18 hours after admission, and only 1 of the 21 survived. All 16 dogs that did not become azotemic survived. Median time from EG ingestion to treatment with 4-MP was 5 hours (range, 2 to 8.5 hours) for dogs that were not azotemic at admission and 14.5 hours (range, 8.5 to 38 hours) for dogs that were azotemic at admission. Clinical Implications— 4-MP was a safe and effective treatment for EG intoxication when it was given before sufficient quantities of EG had been metabolized to induce renal failure. Dogs treated within 8 hours of EG ingestion had a good prognosis. (J Am Vet Med Assoc 1996;209:1880–1883)

Protective effect of stroma-free methemoglobin during cyanide poisoning in dogs.

During fire exposure, cyanide toxicity can block aerobic metabolism. Oxygen and sodium thiosulfate are accepted therapy. However, nitrite-induced methemoglobinemia, which avidly binds cyanide, decreases oxygen-carrying capacity that is already reduced by the presence of carboxyhemoglobin (inhalation of carbon monoxide in smoke). This study tested whether exogenous stroma-free methemoglobin (SFmetHb) can prevent depression of hemodynamics and metabolism during canine cyanide poisoning. In 10 dogs (weighing 18.8 +/- 3.5 kg) anesthetized with chloralose-urethane and mechanically ventilated with air, baseline hemodynamic and metabolic measurements were made. Then, 137 +/- 31 ml of 12 g% SFmetHb was infused into five dogs (SFmetHb group). Finally, the SFmetHb group and the control group (n = 5, no SFmetHb) received an intravenous potassium cyanide infusion (0.072 mg.kg-1.min-1) for 20 min. Oxygen consumption (VO2) was measured with a Datex Deltatrac (Datex Instruments, Helsinki, Finland) metabolic monitor and cardiac output (QT) was measured by pulmonary artery thermodilution. From baseline to cyanide infusion in the control group, QT decreased significantly (p < 0.05) from 2.9 +/- 0.8 to 1.5 +/- 0.4 l/min, mixed venous PCO2 (PvCO2) tended to decrease from 35 +/- 4 to 23 +/- 2 mmHg, PvO2 increased from 43 +/- 4 to 62 +/- 8 mmHg, VO2 decreased from 93 +/- 8 to 64 +/- 19 ml/min, and lactate increased from 2.3 +/- 0.5 to 7.1 +/- 0.7 mM. In the SFmetHb group, cyanide infusion did not significantly change these variables. From baseline to infused cyanide, the increases in blood cyanide (4.8 +/- 1.0 to 452 +/- 97 microM) and plasma thiocyanate cyanide (18 +/- 5 to 65 +/- 22 microM) in the SFmetHb group were significantly greater than those increases in the control group. SFmetHb itself caused no physiologic changes, except small decreases in heart rate and PvO2. Peak SFmetHb reached 7.7 +/- 1.0% of total hemoglobin. Prophylactic intravenous SFmetHb preserved cardiovascular and metabolic function in dogs exposed to significant intravenous cyanide. Blood concentrations of cyanide, and its metabolite, thiocyanate, revealed that SFmetHb trapped significant cyanide in blood before tissue penetration.

Abstract

Treatment of lead poisoning in dogs; Ramsey, D. T., Casteel, S. W., Faggella, A. M., Chastasin, C. B., Nunn, J. W. &amp; Schaeffer, D. J. (1996) Journal of the American Veterinary Medical Association 208, 371

Prairie dog poisoning in northern Great Plains: An analysis of programs and policies

This paper describes the programs and policies regarding prairie dog control in the northern Great Plains states of Montana, South Dakota, and Wyoming. The poisoning programs of federal and state agencies are described, along with the statutes and legal mandates that shape agency management of prairie dogs. Current policies on National Grasslands and other federal lands typically limit prairie dogs to small percentages of available potential habitat, to the detriment of prairie dogs and associated species. State programs to assist landowners in prairie dog control differ greatly, employing cost-share incentives (Wyoming) and regulatory fines (South Dakota) to encourage the poisoning of prairie dogs. Prairie dog control is not actively funded or practiced by state or county agencies in Montana. We document federal and state involvement in more than 1 million acres of prairie dog poisoning in the study area during 1978-1992. In combination with undocumented poisoning by private landowners, plague, and shooting, prairie dogs may be experiencing net regional declines, contributing to the disintegration of the prairie dog ecosystem. We recommend that Animal Damage Control operations concerning prairie dogs be terminated, on the basis that they duplicate state programs and are at cross purposes with federal wildlife management programs that seek to perpetuate and/or recover wildlife species that depend on the prairie dog ecosystem. We further recommend that federal range improvement funds be offered as subsidies for the integration of prairie dogs in range management, as opposed to funding prairie dog eradication programs.

Use of orally administered succimer (meso-2,3-dimercaptosuccinic acid) for treatment of lead poisoning in dogs

Objective— To determine whether succimer (meso-2,3-dimercaptosuccinic acid) would be effective in reducing blood lead concentration in dogs with naturally acquired lead poisoning and whether treated dogs would develop clinically important adverse effects. Design— Prospective case series. Animals— 13 dogs with moderate-to-high blood lead concentrations (39 to 120 μg/dl) and clinical signs of lead poisoning. Procedure— Dogs were treated with succimer (10 mg/ kg of body weight, PO, q 8 h) for 10 days. Blood and urine samples were analyzed for lead concentration before, during, and after treatment with succimer. Results— Mean blood lead concentrations on days 0, 3, 7, and 20 were 70.6, 32.7, 16.8, and 27.6 μg/dl, respectively. Mean blood lead concentrations decreased 53.6, 76.2, and 60.9% from pretreatment value on days 3, 7, and 20, respectively. Mean urine lead concentrations on days 0, 3, 7, and 20 were 70.0, 485.4, 254.3, and 28.3 μg/dl, respectively. Clinical Implications— In dogs with naturally acquired lead poisoning, succimer administered orally for 10 days effectively reduced blood lead concentrations and eliminated clinical signs of lead poisoning. (J Am Vet Med Assoc 1996;208:371-375)

Efficacy of 4-methylpyrazole for treatment of ethylene glycol intoxication in dogs

Summary 4-Methylpyrazole (4-mp), an alcohol dehydrogenase inhibitor, was administered to dogs to treat ethylene glycol (eg) intoxication. Eleven dogs were given 10.6 g of eg/kg of body weight; 5 dogs were treated with 4-mp 5 hours after eg ingestion and 6 dogs were treated with 4-mp 8 hours after eg ingestion. 4-Methylpyrazole was administered iv as a 50-mg/dl solution in 50% polyethylene glycol: initial dose, 20 mg/kg; at 12 hours after initial dose, 15 mg/kg; at 24 hours after initial dose, 10 mg/kg; and at 30 hours after initial dose, 5 mg/kg. Physical, biochemical, hematologic, blood gas, serum and urine eg concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, 72 hours, and at 1 week and 2 weeks after eg ingestion. Dogs of both groups developed clinicopathologic signs associated with eg intoxication, including cns depression, hyperosmolality, high anion gap metabolic acidosis, polydipsia, polyuria, calcium oxalate monohydrate and dihydrate crystalluria, and isosthenuria. Fractional excretion of sodium was increased in all dogs between 1 and 9 hours after eg ingestion, but remained increased beyond 24 hours only in the 2 dogs treated at 8 hours after eg ingestion that developed acute renal failure. All dogs treated 5 hours after eg ingestion recovered without morphologic, biochemical, or clinical evidence of renal impairment. Of the 6 dogs treated 8 hours after eg ingestion, 2 developed acute renal failure. One of the dogs treated 8 hours after eg ingestion remained isosthenuric for 2 months, but did not manifest any other signs of renal impairment. Of the dogs treated 8 hours after eg ingestion, 3 recovered without morphologic, biochemical, or clinical evidence of renal impairment. Serum half-life of eg was prolonged in the dogs treated 8 hours after eg ingestion. Percentage of eg excreted unchanged was 84 ± 2% in the dogs treated 5 hours after eg ingestion, and was 40 ± 10% in the dogs treated 8 hours after eg ingestion. 4-Methylpyrazole was effective in preventing renal failure in all dogs given 10.6 g of eg/kg when treatment was initiated by 5 hours after eg ingestion, and in 4 of 6 dogs when treatment was initiated by 8 hours after eg ingestion.

Theobromine poisoning in dogs

Theobromine poisoning in dogs

Identification of anatoxin-A in benthic cyanobacteria (blue-green algae) and in associated dog poisonings at Loch Insh, Scotland

Dog deaths occurred in 1990 and 1991 after the animals drank water containing blooms of benthic cyanobacteria along the shoreline of Loch Insh, Scotland. Signs of poisoning in the affected animals and the high neurotoxicity of bloom extracts in laboratory bioassays indicated acute poisoning due to cyanobacterial neurotoxin(s). The neurotoxic blooms consisted largely of benthic Oscillatoria species which were also observed in the stomach contents of the poisoned dogs. Stomach contents were also neurotoxic in bioassays with the same signs of poisoning as the Oscillatoria blooms. The cyanobacterial alkaloid neurotoxin anatoxin-a was identified in bloom extracts and poisoned dog stomach contents by high-performance liquid chromatography and gas chromatography-mass spectrometry. A species of benthic Oscillatoria has been isolated from the neurotoxic bloom material and shown to produce anatoxin-a in laboratory culture. These findings are the first to associate anatoxin-a toxicoses with benthic, rather than planktonic, cyanobacteria. Procedures for anatoxin-a extraction and identification from the blooms and animal material are also detailed.

Depletion of essential elements by calcium disodium EDTA treatment in the dog

The effect(s) of calcium disodium ethylenediaminetetraacetate (CaNa 2EDTA) on the metabolism of Zn, Cu and Mn was investigated in mongrel female dogs. Dogs received either CaNa 2EDTA (0.75 mmol/kg subcutaneously) or 0.9% NaCl (controls). Urine was collected every 6 h. Tissue samples were obtained from liver, kidney, duodenum, muscle, hair, skin and bone post exsanguination. CaNa 2EDTA treatment increased urinary excretion of Zn, Cu and Mn, significantly when compared to controls ( P < 0.05, n = 5). Furthermore, CaNa 2EDTA either decreased Zn levels (hair, duodenum, skin) and Mn levels (hair) or increased Cu levels in kidneys ( P < 0.05). These data suggest that the sustained urinary loss of Zn, Cu and Mn was probably associated, in part, with mobilization and redistribution of these essential elements from storage tissues as well as soft tissues. It was concluded that the use of calcium disodium EDTA for the management of heavy metal poisoning in dogs could adversely affect the metabolism of essential elements, particularly Zn, Cu and Mn.

Suspected cycad (Cycas revoluta) intoxication in dogs

Three dogs which ingested part of the stem of a Japanese cycad (Cycas revoluta) vomited repeatedly within hours after ingestion, showed marked depression, severely congested mucous membranes, increased thirst and profuse salivation. Subsequent hematological and blood chemical investigation revealed elevated serum concentrations of alanine transaminase, an initial mild lymphocytopenia, thrombocytopenia and a leucocytosis. The dogs recovered uneventfully.

Efficacy of ?-ketoglutaric acid as an effective antidote in cyanide poisoning in dogs

Efficacy of ?-ketoglutaric acid as an effective antidote in cyanide poisoning in dogs

A surprising case of endrin poisoning in dogs

A case of possible malicious poisoning of dogs by endrin was investigated. A variety of tissues were analysed. The stomach contents of one dog contained 5 g/kg endrin. The results are compared with recorded data from feeding studies pursued elsewhere to aid the diagnosis of dieldrin and endrin intoxication. A number of organochlorine compounds closely related chemically to endrin were tentatively identified.

Liver Necrosis Caused by Mushroom Poisoning in Dogs

Mushrooms in Category A cause hepatic and renal damage after a prolonged latent period and are the most common cause of fatal mushroom poisonings in human beings. Category A is subdivided into 2 groups on the basis of the type of toxin produced. The genera Amanita and Galerina produce cyclopeptide toxins (Group I), and Gyromitra produces monomethylhydrazine toxins (Group II). Several Amanita species contain 3 kinds of cyclopeptide toxins: phallolysin, phallotoxins, and amanitins. 9 Of these toxins, only the amanitins play a significant role in poisonings. Mushrooms in categories B, C, and D have a rapid onset of clinical signs and effect the autonomic nervous system, central nervous system, and gastrointestinal tracts, respectively. Only one of the reported cases of mushroom poisoning in the dog was associated with a mushroom in Category A in which several animals were poisoned by ingesting Amanita phalloides. 6 Other mushrooms in this genus and category that have either been associated with human poisonings or contain amanitins are Amanita verna, Amanita virosa, Amanita bisporigera, and Amanita ocreata. 8 The purpose of this report is to describe the clinical and laboratory findings in 2 cases of canine mushroom poisoning. A 7-week-old male golden retriever had a sudden onset of extreme listlessness, ataxia, and petit mal seizures. The owner had observed the animal eating mushrooms on the day prior to onset of clinical signs. The puppy did not respond to intravenous Lactated Ringer’s solution and Valium and died within 6 hr of onset of clinical signs. Fresh and formalinfixed tissue, stomach contents, urine, clotted blood, and a mushroom were submitted to the diagnostic laboratory for evaluation. Strychnine was not detected in urine or stomach contents. The mushroom was identified as A. verna by a mycologist. The owner of the second case owned a small kennel and observed a sudden onset of yelping and a tense abdomen in a 12-week-old female Labrador retriever. The puppy became

Brodifacoum poisoning in a dog

A case of brodifacoum poisoning is described in a six-year-old male Kelpie cross working dog. The clinical features were severe exercise intolerance, haemorrhage from the oral and nasal cavities, dyspnoea and pale mucous membranes. Diagnosis was confirmed by demonstrating an abnormally long whole blood clotting time. The dog was treated successfully by administering 1 litre of whole blood intravenously, intramuscular vitamin K1 and a three week course of oral vitamin K3. Experience at the Massey University Small Animal Clinic and Hospital has indicated that poisoning of dogs with the newer long acting anticoagulant rodenticides is becoming more common.

The efficacy of hemoperfusion for ediphenphos poisoning in dogs : Takeda M, Yoshino K, Yamashita M, et al. Jpn J Acute Med 1987;11(8):1007–1012

The efficacy of hemoperfusion for ediphenphos poisoning in dogs : Takeda M, Yoshino K, Yamashita M, et al. Jpn J Acute Med 1987;11(8):1007–1012

A comparison of calcium disodium ethylene diamine tetra‐acetate (CaEDTA) by oral and subcutaneous routes as a treatment of lead poisoning in dogs

ABSTRACTFour dogs accidentally poisoned by lead on a farm were used in a study to compare the efficacy of oral and injectable CaEDTA as chelating agent. Blood lead concentrations indicated that though both routes of administration were effective in reducing the lead levels, the injectable route appeared to reduce the lead level to within the normal range in a shorter period. The oral route, however, has the advantage that hospitalization is not required and it avoids the discomfort of numerous injections of the chelating agent.

Diagnosis of lead poisoning in dogs.

Australian Veterinary JournalVolume 62, Issue 12 p. 434-435 Diagnosis of lead poisoning in dogs T-S KOH, T-S KOH Central Veterinary Laboratories, Department of Agriculture, Institute of Medical and Veterinary Science, Frome Road, Adelaide, South Australia 5000Search for more papers by this author T-S KOH, T-S KOH Central Veterinary Laboratories, Department of Agriculture, Institute of Medical and Veterinary Science, Frome Road, Adelaide, South Australia 5000Search for more papers by this author First published: December 1985 https://doi.org/10.1111/j.1751-0813.1985.tb14139.xCitations: 4AboutRelatedInformationPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessClose modalShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume62, Issue12December 1985Pages 434-435 RelatedInformation RecommendedDogsBreed Predispositions to Disease in Dogs and Cats, [1]Paralytic shellfish poisoning and palytoxin poisoning in dogsNicola Bates, Cassandra Morrison, Leah Flaig, Andrew D Turner, Veterinary RecordSalmon Poisoning Disease in Dogs: 29 CasesJ.E. Sykes, S.L. Marks, S. Mapes, R.M. Schultz, R.E. Pollard, D. Tokarz, P.P. Pesavento, L.L. Lindsay, J.E. Foley, Journal of Veterinary Internal MedicineDiagnosis of rickettsial diseases in dogs and catsRobin W. Allison, Susan E. Little, Veterinary Clinical PathologyPrevalence of the breed‐related glaucomas in pure‐bred dogs in North AmericaKirk N. Gelatt, Edward O. MacKay, Veterinary Ophthalmology

Diagnosis of lead poisoning in dogs.

Diagnosis of lead poisoning in dogs.

Identification of calcium oxalate monohydrate crystals by X-ray diffraction in urine of ethylene glycol-intoxicated dogs.

Urine sediments of dogs with experimentally induced ethylene glycol poisoning were examined by light microscopy and X-ray diffraction. Massive calcium oxalate crystalluria was observed in all poisoned dogs. By light microscopy, the frequency with which six-sided hippurate-like prisms and envelope forms of calcium oxalate dihydrate occurred was approximately equal. The hippurate-like crystals were shown to be calcium oxalate monohydrate by X-ray diffractometry.