Acute selenium toxicosis in a dog

A toxic dose of selenium administered by IM injection to a 3-year-old Chihuahua resulted in pulmonary edema and death. The compound had been dispensed to the owner inadvertently in combination with a vitamin E preparation. Vitamin and mineral products often are considered safe for use in megadoses by the uninformed public. The potential danger of selenium overdosage should not be underestimated.     

Acute thallium toxicosis in a dog.

A Doberman Pinscher was evaluated for acute onset of gastroenteritis, characterized by anorexia, hematemesis, and hematochezia. The dog had ingested mole bait containing thallium 2 days prior to admission. Thallium toxicosis was confirmed by detection of thallium in the urine, using colorimetric analysis. The dog responded well to administration of antibiotics, fluids administered IV, warm-water enemas, and oral administration of activated charcoal slurries.     

Acute monensin toxicosis in broiler breeder chickens

Peracute onset of disease was reported in a 42-wk-old broiler breeder flock that was presented by error with feed containing monensin at approximately seven times the approved level for broiler chickens. Morbidity and mortality were extremely high, and the affected chickens displayed feed refusal, decreased water consumption, and severe paralysis that ranged from abnormal gait to a complete inability to move. During the first 10 days postingestion of the suspect feed, mortality in hens reached 13.7% and 70.9% in the roosters. Hen day production decreased from 67% to 3% in the same period of time. A total of 638 g/ton of monensin was detected in suspect feed samples by one laboratory and 740 g/ton in a second laboratory. Twenty-one days after removal of the suspect feed, the mortality rate returned to normal levels in both hens and roosters, albeit feed consumption and egg production remained extremely low, which prompted the company involved to eliminate the flock.     

Clinical management of potential ibuprofen toxicosis in a South American red-footed tortoise (Geochelone carbonaria).

This article describes the clinical management of potential ibuprofen toxicosis in South American red-footed tortoise (Geochelone carbonaria). A 2.5-year-old, 0.78-kg Geochelone carbonaria tortoise was presented to the emergency clinic after ingesting solubilized ibuprofen (200 mg) in a gelatin capsule. Treatment on initial presentation consisted of esophagostomy tube placement for gastric lavage and activated charcoal administration, intravenous and intraosseous fluid therapy, and administration of gastrointestinal protectants (sucralfate and famotidine). The tortoise was discharged to the owners. Although follow-up diagnostic monitoring was minimal because of owner compliance, the patient was noted to be alive and in reasonable health 1 year after initial presentation. This is the first report on the management of potential nonsteroidal anti-inflammatory drug toxicosis in any chelonian species.     

Acute copper toxicosis in the Canada goose.

Acute copper toxicosis resulted in Canada geese, Branta canadensis, following ingestion of copper sulfate at about 600mg/kg from a small man-made pond on a game farm. The lesions were those associated with copper toxicosis in other avian species. The primary pathologic change was necrosis and sloughing of the proventriculus and gizzard. A greenish discoloration of the lungs also occurred.     

Hyperadrenocorticism in a ferret

A 7-year-old adult male ferret had progressive hair loss that was bilaterally symmetric. Also clinically evident were severe dehydration, polydipsia, muffled heart sounds, weak femoral pulses, hepatomegaly, lethargy, weakness, temporal muscular atrophy, dyspnea, and weakness. The blood profile of the ferret indicated profound leukopenia, eosinopenia, and high phosphorus, BUN, creatinine, and potassium concentrations, as well as high aspartate transaminase activity; the albumin concentration was low. The serum cortisol concentration was 8.1 micrograms/dl. Necropsy and histologic findings confirmed a diagnosis of hyperadrenocorticism, complicated by dilatative cardiomyopathy, chronic active hepatitis, and renal disease.     

Blastomycosis in a ferret

An 18-month-old female ferret with an ulcerated metacarpal pad and signs of respiratory illness was diagnosed as having blastomycosis by visualization of organisms on a tissue imprint, an agarose gel immunodiffusion test, and thoracic radiography. The ferret was treated intravenously with amphotercin B at 0.4 to 0.8 mg/kg and orally with ketoconazole at 8 mg/kg for approximately 1 month, during which time clinical and radiographic improvement was noted. A change to SC amphoterocin B therapy resulted in relapse of clinical signs despite continuation of ketoconazole therapy, and necessitated euthanasia. Necropsy revealed granulomatous lesions typical of Blastomyces dermatitidis infection in the lungs, thoracic pleura, spleen, meninges, and brain. Comparisons between this case and canine blastomycosis cases are made and alternative treatment regimes for mustelid blastomycosis are suggested.     

Insulinoma in a ferret

Insulinoma was diagnosed in a 7-year-old female ferret examined because of generalized seizures, intermittent paraplegia, and abnormal behavior. Low serum glucose, high serum insulin, and infinite amended insulin/glucose ratio values in this ferret supported the clinical diagnosis of insulinoma. Histologic examination of the pancreas confirmed the diagnosis of insulinoma. The clinical signs and laboratory evaluations in this case and in a previously reported case of insulinoma in a ferret were consistent with variations reported in dogs with insulinoma.     

Endrin toxicosis in a cat

Endrin toxicosis was believed responsible for the sudden death of a cat. Stomach contents contained bird remains, and chemical analysis revealed 233 micrograms of endrin/g. The cat's owner had been using an avicide on the premises just before the cat's death. Endrin is an effective pesticide for control of insects, rodents, and birds. It poses a problem with secondary poisoning in other animals.     

Macrozamia toxicosis in a dog

A case of Macrozamia riedlei seed poisoning is described in a young Dachshund. Vomiting and depression commenced within 6 h of ingestion; other signs that developed included severe hepatopathy, jaundice, abdominal pain that was unresponsive to analgesics, severe gastro-intestinal haemorrhage and thrombocytopenia as well as crystalluria and marrow dyserythropoiesis. The dog was euthanased 6 days after ingestion of the seeds.     

Ibuprofen toxicosis in a dog

Acute renal failure, vomiting, and melena developed in a 10-month-old dog after ingestion of ten 600-mg tablets of ibuprofen. After 5 days of IV fluid therapy, clinical signs resolved and azotemia decreased. With increased availability of nonsteroidal anti-inflammatory drugs, similar complications may become more common in veterinary practice. If acute renal failure should develop, the prognosis for recovery is good, with rapid institution of appropriate therapy. However, renal dysfunction may not be completely reversed.     

Lead toxicosis in a puppy

After showing clinical and radiographic signs of a gastrointestinal foreign body, a 5-month-old puppy began head pressing, which progressed to convulsions. Hematological abnormalities suggested lead poisoning; serum lead was 2.61 mumol/L. The puppy made a complete recovery after intensive treatment for lead toxicosis.     

Ivermectin toxicosis in a dog

A 5-year-old male Doberman Pinscher was examined after ingesting an equine paste dewormer containing approximately 115 mg of ivermectin. Clinical signs consisted of profound hypothermia, mild dehydration, dilated unresponsive pupils, localized muscle group fasciculations around the face and hind limbs, and no response to any external stimuli. Twelve days after parenteral administration of isotonic fluids and IV administration of dexamethasone and dimethyl sulfoxide, the dog returned to a clinically normal neurologic state. Ivermectin toxicosis has been reported frequently in Collies; however, other breeds may have idiosyncratic reactions to low doses. Patients with severe toxicosis should eventually recover completely if given appropriate intensive care.     

Arsenic toxicosis and suspected chromium toxicosis in a herd of cattle

Arsenic toxicosis and suspected chromium toxicosis were diagnosed in a herd of cattle that ingested ashes from lumber treated with copper, chromium, and arsenic. Findings included peracute death, depression, ataxia, weakness, recumbency, and watery diarrhea. Chemical analyses of liver, kidney, abomasal contents, rumen contents, and ashes revealed high concentrations of arsenic and chromium. Histologically, specimens of abomasum and duodenum had diffuse mucosal degeneration and engorged capillaries. Epithelial cells of the proximal convoluted tubules and distal collecting tubules of the kidney were swollen and had mild granular cytoplasmic degeneration. Burning lumber treated with copper, chromium, and arsenic does not remove the heavy metals from them, and ingestion of the ashes from the wood constitutes a hazard to livestock health.