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.     

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.     

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.     

Levamisole toxicosis in a dog

A single oral dose of levamisole hydrochloride given at the rate of 12 mg/kg was believed responsible for bradycardia, tachypnea, hypothermia, cerebrocortical depression, and diarrhea in a dog. Supportive treatment and symptomatic treatment for the bradycardia were required for 4 days. In addition to these previously reported abnormalities associated with levamisole toxicosis, cerebrocortical depression and multiple foci of irritation were characterized by electroencephalography.     

Naproxen-induced toxicosis in a dog

Naproxen, a nonsteroidal anti-inflammatory drug, induced gastric ulceration and bleeding in a dog. Clinical signs included vomiting, anemia, melena, and weakness. The dog responded to a blood transfusion and supportive treatment (lactated Ringer's solution with added K+ and B vitamins, an antacid, and cimetidine). Naproxen had been given to the dog by the owner, as treatment for shoulder stiffness.     

Suspected albuterol toxicosis in a dog

CASE DESCRIPTION: A 6-year-old male castrated Shetland Sheepdog was evaluated because of severe hypokalemia and progressive paresis. CLINICAL FINDINGS: Physical examination revealed fever, tachypnea, mydriasis, hyperemic mucous membranes, severe forelimb paresis, and hind limb paraplegia. The dog had superficial and deep pain sensation in all 4 limbs. Forelimb spinal reflexes were considered normal, but hind limb reflexes were normal to slightly hyperreflexive. The panniculus reflex was considered to be normal, and cranial nerve reflexes were intact. A CBC revealed mild leukocytosis and erythrocytosis, and serum biochemical analysis revealed severe hypokalemia. Thoracic and abdominal imaging did not reveal relevant findings. Blood pressure and ECG findings were within reference limits. Questioning of the owner revealed possible exposure to albuterol via ingestion of medication intended for the owner's horse. Results of serum testing via immunoassay were suggestive of albuterol toxicosis. TREATMENT AND OUTCOME: Treatment included IV administration of an electrolyte solution and supplemental potassium chloride. The rate of potassium chloride supplementation was slowly decreased as serum potassium concentration increased. No other medical intervention was required, and the dog made a rapid and complete recovery. CLINICAL RELEVANCE: Ingestion of albuterol can lead to profound physical and serum biochemical abnormalities. Appropriate historical information should be obtained to identify possible sources and routes of exposure to intoxicants. Albuterol-induced hypokalemia can be successfully managed medically.     

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.     

Diagnosis of Amanita toxicosis in a dog with acute hepatic necrosis.

Poisoning with amanitin-containing hepatotoxic mushrooms demands extensive efforts from clinicians, toxicologists, and pathologists. Presumptive diagnoses are established by positive identification of the suspect mushroom along with the occurrence of consistent clinical signs. If the animal dies, hepatic lesions may suggest exposure to amanitin-containing mushrooms; however, lesions are nonspecific. A 15-week-old female Dachshund was presented to the referring veterinarian for acute onset of lethargy that quickly progressed to sternal recumbency. Despite supportive care, the dog remained lethargic and died approximately 12 hours after initial presentation. A pale tan liver was noted at necropsy. Microscopically, the liver showed panlobular coagulative necrosis of hepatocytes. A presumptive diagnosis of amanitin poisoning was based on suspect history of exposure to mushrooms, clinical signs, and pathologic findings. Exposure to amanitin was confirmed through detection of alpha-amanitin in the liver by liquid chromatography/mass spectrometry. The objective of this case report is to illustrate the essential components to a successful diagnostic work-up of a suspect case of hepatotoxic mushroom poisoning. Although hepatotoxic mushroom poisoning has been documented in dogs before, confirmatory techniques for biologic specimens have not been used previously in diagnostic investigations.     

Gossypol toxicosis in a dog consequent to ingestion of cottonseed bedding.

Six dogs died after accidental ingestion of cottonseed bedding. No clinical signs of illness were observed prior to death. A full diagnostic workup was performed on one of these dogs. At necropsy, the lungs were congested and edematous, and the liver was firm, congested, and had a marked reticular pattern. There was also moderate ascites. Histopathologic examination revealed multifocal myocardial degeneration and necrosis, severe pulmonary edema, and chronic passive congestion of the lungs, heart, liver, and kidneys. Transmission electron microscopy of the myocardium revealed disruption of myofibrils, chromatin condensation, and disrupted and swollen mitochondria. The cottonseed bedding contained 1,600 mg/kg of free gossypol, a concentration considered toxic for monogastric animals. The stomach content revealed the presence of gossypol, thus confirming ingestion of cottonseed. Gossypol poisoning in dogs is extremely rare and has not yet been associated with cottonseed bedding. This first documented case of gossypol poisoning in a dog, caused by the ingestion of cottonseed bedding, demonstrates how specific toxicological analysis is crucial in reaching an accurate diagnosis.     

Diagnosis and treatment of thallium toxicosis in a dog

A case of chronic thallium toxicosis in a dog is described. The difficulties in diagnosis in the absence of a history of known ingestion of the agent are discussed and a method of increasing urinary thallium to detectable levels is described.     

Tick toxicosis in a dog bitten by Ornithodoros brasiliensis

Ticks are hematophagous parasites of people and animals and are a public health hazard in several countries. They are vectors of infectious diseases; in addition, the bite of some ticks, mainly from the Ornithodoros genus, may lead to local lesions and systemic illness, referred to as tick toxicosis. In this report, we describe a dog bitten by Ornithodoros brasiliensis, popularly known as the mouro tick. The main clinical findings were disseminated skin rash, pruritus, mucosal hyperemia, lethargy, and fever. Laboratory abnormalities 48 hours after the bites occurred included mild nonregenerative anemia, eosinophilia, basophilia, increased serum creatine kinase activity, increased serum C-reactive protein concentration, and prolonged coagulation times. Tick-borne pathogens were not detected by PCR analysis or serologic testing, supporting the diagnosis of a noninfectious syndrome due to tick bite, compatible with tick toxicosis.     

Pericardial effusion and cardiac tamponade secondary to brodifacoum toxicosis in a dog.

Hemorrhage resulting from ingestion of anticoagulant rodenticides may be evident at any traumatized site or in any body cavity. It is important for clinicians to include coagulopathies among the differential diagnoses for pericardial effusion and to evaluate clotting function before routine pericardiocentesis is performed.