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.     

Tricyclic antidepressant toxicosis

Accidental ingestions of TCAs by companion animals often occur. During the past 4 years, over 450 cases have been reported to the IAPIC. At least 7% of the animals that displayed clinical signs of toxicosis eventually died. Overdoses of TCAs adversely affect the cardiovascular, parasympathetic, and central nervous systems. The cardiovascular system is involved most seriously and ventricular arrhythmias with severe hypotension are believed to be the primary cause of death. Animals that ingest a potentially lethal dose (over 15 mg/kg) may die within 1 to 2 hours if appropriate treatment is not administered. Treatment involves the use of initial life-supportive measures (control of seizures, maintenance of an airway, ventilation, and so on), detoxification of the animal (enterogastric lavage, activated charcoal, etc.), and the intravenous use of sodium bicarbonate (2-3 mEq/kg) to control signs of acidosis, hypotension, tachycardia, bradycardia, and other cardiac conduction abnormalities. The animal must then be monitored closely for the return of the clinical signs and sodium bicarbonate therapy should be repeated as needed. In addition, to enhance removal of the TCAs from the gastrointestinal tract and, ultimately, from the body, activated charcoal should be repeated at 3-hour intervals until the animal is asymptomatic.     

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.     

Methionine toxicosis in cats

Cats given DL-methionine (1 g/kg of body weight/day) developed severe hemolytic anemia with marked increase of methemoglobin (MetHb) concentration and Heinz-body formation at treatment-day 6 to 10. Cats fed 0.5 g of methionine/kg for 52 days had a moderate Heinz-body hemolytic anemia with methemoglobinemia at treatment days 17 to 31, but thereafter recovered from the anemia despite continuation of methionine feeding, indicating an adaptation of the cats. In vitro, significant (P less than 0.01) increases of MetHb concentration and Heinz-body formation were observed when RBC were incubated with plasma from cats fed (1 g of methionine/kg) or with 10 mM 3-methylthiopropionate, a product of methionine catabolism. However, these increases were not observed when RBC were incubated with 10 mM methionine. Seemingly, excessive methionine intake leads to production of an intermediate of the methionine catabolism that may affect RBC directly as an intensive oxidizing agent, resulting in an excessive oxidation of hemoglobin to MetHb and Heinz-body formation.