Rabbits were given T-2 mycotoxin orally at 0, 0.25, 0.5, and 0.75 mg/kg of body weight/day for 21 days. Only rabbits in the 0.75 mg/kg/day group (4 of 5 rabbits) died. Alveolar macrophages were harvested on day 22 and used for in vitro phagocytosis of killed Aspergillus fumigatus conidia. Cultures included sera from untreated rabbits or rabbits treated with T-2. Phagocytosis was significantly (P < 0.01) reduced in cultures that used serum from rabbits treated with 0.5 mg of T-2kg/day and alveolar macrophages from untreated rabbits or rabbits treated with T-2. There was little reduction in phagocytosis when alveolar macrophages from rabbits treated with T-2 and normal serum were used. Ingestion of 0.5 mg of T-2 toxin/kg/day significantly (P < 0.05) reduced weight gain, serum alkaline phosphatase activity, serum sorbitol dehydrogenase activity, and serum bacteriostasis. Similar changes were found in the 0.75 mg/kg/day group, as well as a significant (P < 0.05) reduction in PCV, total WBC, and differential leukocyte counts. Neutrophil counts decreased, but not significantly (0.05 < P < 0.10). Significant changes were not detected in alanine transaminase activity, aspartate transaminase activity, blood urea nitrogen concentration, or complement hemolytic activity. Histopathologic changes consisting of centrilobular hepatocellular swelling, mild portal and periportal fibrosis and lymphocyte necrosis within secondary lymphoid tissues developed in most rabbits treated with T-2. Thymic atrophy, bile duct reduplication, and lymphocyte depletion of secondary lymphoid tissues developed in the group given 0.75 mg/kg/day. Severity of lymphoid depletion in secondary lymphoid tissues was greatest in the appendix and decreased in the following order: appendix > sacculus rotundus > ileal Peyer patches > lymph nodes and spleen. In this study, we provide additional data showing that, at these oral doses of T-2 toxin, rabbits could be immunosuppressed, as evidenced by reduced alveolar macrophage phagocytosis and histopathologic changes in lymphoid tissues. Also, these doses caused reductions in weight gain, certain hematologic factors, and serum alkaline phosphatase and sorbitol dehydrogenase activities.

We determined the vasoconstrictive effects of selected ergot alkaloids, and a sample containing loline and its derivative alkaloids, on the isolated dorsal pedal vein of cattle, as a model system to study one of the toxic effects that result from cattle ingesting fescue forage infected with the endophytic fungus Acremonium coenophialum. The ergot compounds ergotamine, ergosine, and agroclavine constricted this peripheral vein of cattle, but much less so than did the alpha-adrenergic agonist norepinephrine, which supports the ergots acting as partial agonists for these receptors. However, the sample of loline and loline-derivative alkaloids did not affect the dorsal pedal vein when given at concentrations similar to those of the ergot compounds. Loline and loline-derivative alkaloid sample at high concentrations partially inhibited norepinephrine-elicited vascular contraction, an effect that appeared to be unrelated to alpha-adrenoceptor activity. Thus, in the dorsal pedal vein model in cattle, the ergopeptide alkaloids were more venoconstrictive than were loline and its derivative alkaloids.

In addition to the 3-striped blister beetles (Epicauta temexa and E occidentalis), other sources of equine cantharidin toxicosis were identified at the Texas Veterinary Medical Diagnostic Laboratory and included E albida and E attrivittata and the previously incriminated E pardalis and E pennsylvanica. Improved methods for diagnosing cantharidin or blister beetle toxicosis involve partial purification of urine and gastric content extracts, using silica cartridges, followed by analysis, using capillary gas chromatography/mass spectrometry. During a 26-month period, 53 episodes of cantharidin toxicosis in horses were confirmed at our diagnostic laboratory. Concentrations of cantharidin in urine and gastric contents ranged from 0.0003 to 3.50 microgram/g. Peak incidences were observed in late summer and early fall.

Five Collies sensitive to toxic effects of ivermectin and 7 nonsensitive Collies were given 100 microgram of ivermectin/kg of body weight, PO. Blood samples were collected from each dog before treatment; at posttreatment hours 1, 2, 3.5, 5, and 8; and at posttreatment days 1, 2, 4, 7, 14, and 21. Each sample was assayed for ivermectin concentration, and statistical analyses were performed on the resulting plasma concentration data to determine differences in absorption and clearance of drugs between the 2 groups. Variables measured were area under the curve (using the trapezoidal rule), peak plasma concentration, and the time to peak concentration. Differences between sensitive and nonsensitive Collies for variables analyzed were not significant (P greater than 0.05).

Studying of toxicity of enterosorbent produced the basis of mixture of filtering pulvis of perlite, kizelgur and activated carbon was realized in the conditions of the Republic of Belarus by the example of healthy white mice of both sexes with body weight of 18-25 grams. Animals were divided in three groups. The tested substance was entered insitu to ventricle on an empty stomach after 12-hours of absolute diet. The first group animals were administrated the enterosorbent in doze of 5 g/1 kg, the second group animals - 2,5 g/1 kg. Glucose content increased from 3,8 +/- 0,47 to 4,3 +/- 0,17 mmol/l on the 30-th experimental day and decreased on 8,2 % on the 60-th experimental day. Cholesterin and triglyceride content lowered on 9,5 % and 11,1 %,respectively. Enzymes concentration of aspartate transaminase and alkaline phosphatase decreased from 120,0 +/- 3,87 up to 117,0 +/- 2,58 units/l and from 396,3 +/- 3,78 to 345,3 +/- 2,97 units/l, respectively. Urea increased from 3,7 +/- 0,16 to 3,9 +/- 0,17 mmol/l on the 30-th experimental day. Research results showed that mixture of filtering pulvis after the single oral administration in dose of 2,5-5 g/1 kg did not cause mice death. The analyzed mixture could be referred to the class of low-toxic substances. The mixture did not have irritation action and did not render chronic toxic action on the experimental mice