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OBJECTIVE To establish the minimum toxic dose of isoniazid in dogs, characterize the clinical signs and outcomes for dogs following isoniazid ingestion, and determine whether IV administration of pyridoxine to dogs with isoniazid toxicosis is protective against death. DESIGN Retrospective case series. ANIMALS 137 dogs with isoniazid toxicosis. PROCEDURES The electronic database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center was reviewed from January 2004 through December 2014 to identify dogs with isoniazid toxicosis. For each dog identified, information extracted from the medical record included signalment, estimated dose of isoniazid ingested, clinical signs, treatment, and outcome. Follow-up communication with pet owners or primary care veterinarians was performed when necessary to obtain missing information. RESULTS Clinical signs of isoniazid toxicosis were observed in 134 of 137 (98%) dogs and included seizures (n = 104), CNS signs without seizures (94), and gastrointestinal (41), cardiovascular (19), urogenital (4), and respiratory (1) abnormalities. Of the 87 dogs for which the outcome was available, 61 survived, 18 died, and 8 were euthanized. Probability of survival was positively associated with body weight and IV administration of pyridoxine and negatively associated with dose of isoniazid ingested and presence of seizures. Dogs that received pyridoxine IV were 29 times as likely to survive as dogs that did not receive pyridoxine IV. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated rapid diagnosis of isoniazid toxicosis and prompt treatment of affected dogs with pyridoxine and other supportive care were imperative for achieving a successful outcome.

Objective: To evaluate records of dogs exposed to zinc phosphide rodenticides and characterize the patient population, including breed, sex, age, body weight, time since exposure, development of clinical signs, clinical signs observed, treatments performed, veterinary care received, outcome, and overall prognosis., Design: Retrospective case series., Animals: 362 dogs with presumed zinc phosphide exposure., Procedures: An electronic computer database from an animal poison control center was searched to identify dogs that ingested zinc phosphide between November 2004 and July 2009., Results: Accurate information regarding development of clinical signs was available in 94.5% (342/362) of cases. Over half the dogs (58.8% [201/342]) did not develop clinical signs, and specific clinical signs were reported for the remaining 41.2% (141/342) of dogs. There were 180 total clinical signs recorded for these 141 dogs, with some dogs having developed > 1 category of clinical signs. Clinical signs involving the gastrointestinal tract were the most commonly reported type of clinical sign (66.7% [n = 120/180 reported signs]), followed by generalized malaise (17.8% [32/180]), CNS signs (8.9% [16/180]), respiratory signs (3.3% [6/180]), and cardiovascular signs (1.7% [3/180]). Approximately 65% (234/362) of patients received veterinary care (including decontamination via induction of emesis, gastric lavage, or activated charcoal administration), and of these dogs, 51.3% (120/234) were hospitalized. For the 296 dogs for which survival data were available, the survival rate was 98.3% (291/296)., Conclusions and Clinical Relevance: Overall, the prognosis for zinc phosphide toxicosis was good. Zinc phosphide rodenticide toxicosis is a potential public health concern, and veterinary staff should be aware of this commonly used rodenticide.

A 20-month-old 1.44-kg (3.2-lb) castrated male ferret was examined because of vomiting, defecating in an abnormal location, dyspnea, and signs of depression. Within 5 minutes of initial evaluation, the ferret became nonresponsive to all stimuli except deep pain. Despite intensive supportive treatment, the ferret died. Toxicologic analyses for ibuprofen were performed on serum, urine, and liver, using gas chromatography and mass spectrophotometry. Serum ibuprofen concentrations were 245 micrograms/g before and 269 micrograms/g after death. Acute ibuprofen toxicosis may cause severe lethargy progressing to coma, apnea, and death in ferrets. Ibuprofen toxicosis should be considered in differential diagnoses for ferrets with signs of depression, with or without clinical signs of gastrointestinal tract dysfunction.

Objective: To document clinical signs and gross pathologic changes associated with naturally acquired cantharidiasis (blister beetle poisoning) in equids., Design: Retrospective study., Animals: 70 equids with laboratory-confirmed blister beetle poisoning., Procedure: Medical records were reviewed to obtain history, physical examination findings, feeding practices, and diagnostic test and necropsy results., Results: 32 horses and 2 donkeys died from exposure to cantharidin, whereas 36 horses survived. Diet content varied, but alfalfa hay was the common component. Onset of signs of disease was rapid. Most equids had signs of gastrointestinal tract distress. Six horses had nonspecific neurologic signs. All equids dying from cantharidiasis were in shock terminally, with duration of clinical signs ranging from 3 to 18 hours. Six horses that died had no gross lesions, whereas 14 had mild to moderate erythema of gastric, small intestinal, or colonic mucosa. Only 2 horses had gastric or duodenal ulceration, and 2 had hemorrhage of the urinary bladder mucosa. One horse had cardiac muscle necrosis. Clinicopathologic data available on 10 horses included hypocalcemia, hypomagnesemia, and azotemia. Cantharidin concentrations in urine or pooled gastric-cecal contents did not always correlate with severity of disease., Clinical Implications: Blister beetle poisoning is not universally fatal in equids. Clinical signs are related to the amount of cantharidin ingested. Every horse that survived was treated aggressively. In fatal poisonings, gross lesions may be minimal or inapparent, and diagnosis must be confirmed by chemical detection of cantharidin in urine, blood, or stomach or cecal contents.

Two sexually intact female silver-shaded domestic ferret siblings from different litters were examined because of CNS depression and lethargy. Ferret 1 was dehydrated and hypothermic, whereas ferret 2 was icteric and febrile and had serum bilirubin concentration > 12.0 mg/dl and BUN of 59 mg/dl. Despite supportive treatment, the ferrets died within days of evaluation. On necropsy, ferret 1 had chronic hepatopathy, with diffuse vacuolation of hepatocytes. In ferret 2, the liver had centrilobular degeneration and necrosis, and hemoglobinuric nephrosis was evident, with hemoglobin in the renal tubules. In both ferrets, Kupffer's cells and macrophages contained eosinophilic material in the cytoplasm. Special staining revealed copper pigment in hepatocytes and phagocytic cells in both livers. Analysis of liver specimens revealed 850 and 700 ppm of copper in ferrets 1 and 2, respectively. Copper values > 200 ppm in liver are considered evidence of toxicosis in most animal species. Copper toxicosis was diagnosed on the basis of the findings from histologic examination of the liver and high hepatic copper values. Lack of related illness in 11 other ferrets in the same environment and fed the same diet, plus sibling relationship and same phenotypic coat color in the affected ferrets, suggested that these ferrets had an inherited defect in their ability to metabolize normal amounts of ingested copper.

Selenium toxicosis was diagnosed in feeder pigs on a central Michigan farm. Use of a commercial supplement, found to contain approximately 20 times the intended Se concentration, resulted in a Se concentration of 8.1 mg/kg of the complete feed. This was fed for 34 days during which daily feed consumption decreased approximately 35%, several pigs developed weakness and forelimb paresis, and 1 pig died. The highest serum Se concentration measured was 1,550 ng/ml (normal range, 140 to 190 ng/ml). Normal feed consumption returned when an alternative feed was provided. Mean serum Se concentrations of representative pigs, monitored over the subsequent 26 days, decreased from 905 to 258 ng/ml. Histologic examination of a recovering pig revealed skeletal and cardiac myopathy and bilaterally symmetric malacia of the gray matter of the ventral horns of the spinal cord. During the developing toxicosis, the pigs consumed an estimated 11.4 mg of Se/pig/d.

Each week over a 6-week period, 80 adult cockatiels (Nymphicus hollandicus) of either gender were dosed orally with fine particles of pure zinc or galvanized coating removed from welded wire mesh. At dosage of 32 mg/wk, all birds became severely ill and either died or were euthanatized within 2 weeks. Dosage of 2 mg/wk induced chronic illness marked by dullness, weight loss, and intermittent excretion of greenish droppings. Necropsy findings were unremarkable, except for signs suggestive of impaired gastrointestinal tract motility and histologic degenerative changes associated with focal mononuclear infiltration in the liver, kidneys, and pancreas. Tissue, especially pancreatic, contents of zinc were markedly high. Pure zinc was as toxic as galvanizing zinc. White rust, an oxidation product, also was toxic. The galvanized coating on cages and flights must be carefully wirebrushed and examined before housing psittacine birds.

A dog was treated for fleas with the application of pennyroyal oil obtained by the owner at a health food store. Vomiting ensued within 2 hours, and despite emergency treatment, the dog died within 48 hours. At necropsy, pennyroyal oil was determined to be the cause of death.

Clinical and pathologic alterations during the development of furazolidone-induced toxicosis were investigated in a group of 35 newly hatched male Pekin ducklings fed a ration containing 700 mg of furazolidone/kg of feed for 27 days. A control group (n = 25) was fed the same ration without added furazolidone. Every 3 days, ducklings were weighted and palpated for ascites and 3 were chosen at random for euthanasia to determine the severity of lesions and to obtain hearts for gross measurements and ultrastructural study. Clinical alterations in treated ducklings consisted of decreased feed consumption with lower weight gain and nervous signs. Gross pathologic alterations included cardiomegaly with dilatation of all chambers and thinning of the myocardium, pericardial effusion, pulmonary edema and congestion, ascites, and testicular enlargement. Gross lesions were not observed before day 8. The earliest lesion (day 9) was cardiac chamber dilatation, with the left ventricle and left atrium most commonly and most severely dilated. Hearts from ducklings euthanatized on days 6, 12, 18, 24, and 27 were examined ultrastructurally. Myofibrillar lysis was first observed on day 12 in 1 duckling (of 3) and in at least 1 duckling from subsequent euthanasia periods. Myofibrillar lysis did not appear to be uniform among the cardiac chambers.

Case records of 21 horses with acute illness following ingestion of hay containing dead striped blister beetles (Epicauta spp) were selected for review. Abdominal pain, fever, depression, frequent urination, shock, and, occasionally, synchronous diaphragmatic flutter characterized clinical illness. Hematologic findings included hemoconcentration, neutrophilic leukocytosis, and hypocalcemia. Hematuria and low urine specific gravity were abnormal urinalysis results. Sloughing of the epithelium of the esophageal part of the stomach, hemorrhagic and ulcerative cystitis, enterocolitis, and myocardial necrosis were important post-mortem findings. Signs and lesions in 5 horses experimentally poisoned were similar to those of the natural disease. The findings were regarded as sufficiently characteristic of blister beetle poisoning to be useful in differential diagnosis but were not constant in all cases. Therefore, when blister beetle poisoning is suspected, access of affected horses to hay containing striped blister beetles should be demonstrated.