Inorganic arsenic toxicosis in a beef herd

Over a 44-day period, 4 of 5 affected calves in a 170-head herd of beef cattle died after exhibiting clinical signs of lethargy, ataxia, anorexia, and diarrhea. Histopathological examination of tissues and toxicological analysis of a suspicious powder discovered in the pasture confirmed arsenic trioxide toxicosis.     

Fescue toxicosis.

Most of the tall fescue pastures in the United States are infected by an endophyte, N. coenophialum. The fungus derives nutrients from the plant while supplying the plant with toxins for defense. The most detrimental toxins for animals in tall fescue are ergopeptine alkaloids, especially ergovaline. Ergovaline functions as a dopamine D2 agonist and alters prolactin and several other hormones in the body. Pregnant mares are most susceptible during their last month of gestation. Clinical signs include prolonged gestation, dystocia, retained placentas, agalactia, and dysmature foals that are either stillborn or weak.     

Metal toxicosis in horses.

The ubiquity and stability of metals in the environment make them unique as a pollutant or an essential dietary component. Metals are neither created nor destroyed by chemical processes but are redistributed in the environment. In combination with other elements, metal compounds and alloys are essential materials of the contemporary world. Inappropriate use or distribution in the environment leads to adverse health effects on all biologic systems, including horses. Gastrointestinal upset is a common feature of acute toxicosis with metals in general. Among the metals discussed, arsenic and inorganic mercury have a propensity to do severe damage to the gut. Deposition of cadmium on forage is the source most likely to intoxicate horses. This subchronic to chronic problem in horses is manifest as disease of the musculoskeletal system and kidneys. Iron-containing hematinics are widely used in racetrack horses and occasionally result in hepatopathy when excessive doses are administered. Lead continues to be recognized as the most significant environmental metal pollutant. Poisoning is encountered routinely in humans and animals. Of the animal species of veterinary concern, lead-poisoned horses are not a frequent encounter. Lead-intoxicated horses show signs of peripheral neuropathy (laryngeal hemiplegia), intermittent colic, and mild anemia. Acute mercury poisoning sometimes occurs from the common use of mercury-containing blistering agents, with most clinical findings related to acute renal failure. Chronic excessive intake of zinc by horses is uncommon but devastating in rapidly growing foals. The mechanism of chronic zinc toxicosis is coupled to the induced copper deficiency. The condition is a disease of cartilage in the articular and growth physes.     

Ethylene glycol toxicosis in cattle.

A 1-month-old Jersey calf died of oxalate nephropathy. The calf had access to antifreeze (ethylene glycol) 3 days prior to death. Since ethylene glycol toxicosis had not been reported in cattle, the effects or oral administration of ethylene glycol were studied in 7 calves and 3 cows. The toxic dose ranged from 2 to 10 ml of ethylene glycol per kg of body weight. Clinical signs were increased respiration, staggering gait, paraparesis, depression and later, recumbency and death. Hemoglobinuria and epistaxis were seen at doses of 10mg/kg of body weight. Azotemia, hypocalcemia and neutrophilia were constant findings whereas acidosis, plasma hyperosmolality and hemolytic anemia were seen in the animals receiving the higher doses. A diagnosis of ethylene glycol toxicosis must be based upon a history of ingestion and the presence of calcium oxalate crystals in body tissues (especially the kidney and brain).     

Selenium toxicosis in feeder pigs.

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.     

Pesticide toxicosis in the horse.

Toxicosis from pesticides rarely occurs in horses and is usually the result of inappropriate pesticide use or handling by humans. Organophosphorus and carbamate insecticides inhibit acetylcholinesterase and are the insecticide class most frequently associated with toxicosis in domestic animals. Metaldehyde is a molluscicide, and zinc phosphide is a rodenticide, both of which have caused toxicosis in horses. All three of these pesticides affect the nervous system of horses and can be fatal if not treated promptly.     

Pennyroyal oil toxicosis in a dog.

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.     

Experimental T-2 toxicosis in sheep.

Lambs received T-2 toxin at a rate of 0.6 or 0.3 mg/kg body weight per day in a protein reduced diet for 21 days to study the immunological and pathological effects of T-2 toxin in sheep. Blood was collected before T-2 treatment and on days 7, 14 and 21 of the trial for hematological and biochemical examination and for the separation of peripheral blood lymphocytes for the mitogen assay. Myeloid:erythroid ratios were determined from sternal bone marrow samples taken a day before T-2 treatment began, on day 12 and at death (day 22). Lambs treated with 0.6 mg/kg body weight of T-2 toxin daily were leukopenic on day 7 and lymphopenic on days 7 and 14. Also, on day 7, the mitogenic responses of these lambs to the B-cell mitogen, lipopolysaccharide, were significantly depressed and prothrombin times were prolonged. At necropsy, lymphoid atrophy of mesenteric lymph nodes and spleens was most marked in lambs treated with 0.6 mg/kg body weight of T-2 toxin per day. To the authors' knowledge, this is the first report of leukopenia, lymphopenia and lymphoid depletion in ruminants fed T-2 toxin.     

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.     

Ionophore use and toxicosis in cattle.

Ionophores comprise a rapidly expanding class of antibiotics produced by filamentous branching bacteria of the order Actinomycetales. The use of ionophores as coccidiostats and growth promotants has resulted in the occurrence of toxicoses in target and nontarget species. Clinical and pathologic effects of ionophore poisoning are caused by bioactivity and damage to excitable tissues such as cardiac muscle, skeletal muscle, smooth muscle, and the nervous system. Ionophore toxicoses are often related to errors in feed mixing, so the practitioner should give primary importance to the removal of suspect feeds and testing to confirm excessive exposure.