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We report the clinical signs and the effects on leukocyte neurotoxic esterase and red blood cell and plasma acetylcholinesterase (AChE) activities in swine orally administered a single dose of tri-o-cresyl phosphate (TOCP) at 400, 800 or 1000 mg/kg. Swine in all dosage groups exhibited signs consistent with inhibition of nervous tissue cholinesterase 3-48 h after TOCP administration. Onset was dose-related, and 2/3 1000 mg/kg dosed swine died 3 or 35 h postdosing. In surviving swine, significant depressions in plasma AChE activity were apparent at 6 h postdosing, ranging from 16-23% of predosing levels. Similar depressions of red blood cell AChE were not observed until 24 h postdosing. Plasma AChE activities appeared to more accurately reflect the development of acute cholinergic signs observed in the 1000 mg/kg dosed swine at 3 h postdosing while red blood cell AChE activities were more consistent with the delayed cholinergic signs exhibited by the 400 and 800 mg/kg dosed swine at 24 h postdosing. All survivors developed signs of delayed neurotoxicity 10-12 d after TOCP administration, and 70% or greater inhibition of neurotoxic esterase activity in leukocytes was apparent during the first 48 h postdosing.

During 1975 to 1977, serum samples were collected from 101 adult coyotes (Canis latrans) captured in northcentral Kansas. Ten samples were seropositive by microagglutination testing and six of those samples were seropositive for multiple serovars. Titers for Leptospira interrogans serovars grippotyphosa, pyrogenes, djasiman, butembo, and pomona were demonstrated.

Pregnant M. ochrogaster received single intraperitoneal (i.p.) doses of 0.06, 0.125, 0.25, 0.5, 1,2, or 5 mg phenyl mercuric acetate (PMA/kg of body weight on day 8, 9, or 10 of gestation or 0.5 mg PMA/kg on day 7, 8, 9, 10, 11, or 12 of gestation. No toxicity was exhibited, and no abnormal fetuses were observed in any group. An embryocidal effect that depended on dose and stage of development was determined by increased numbers of resorption sites; resorption sites were dose-dependent, and the embryocidal effect decreased as the embryo matured. A dose of 0.06 mg PMA/kg of body weight produced no resorptions when given on day 8 or day 10 of gestation; 0.125 mg/kg produced no resorptions if given on day 10; 0.5 mg/kg resulted in live fetuses and resorptions in the same uterus when given on days 7 through 11; the same dose on day 12 produced all live fetuses; and 1, 2, or 5 mg PMA/kg given on day 8, 9, or 10 of gestation caused total embryo resorption. The i.p. LD50 of PMA in Microtus ochrogaster adult females was 10 mg/kg of body weight.

The acute toxicity of lasalocid and monensin was studied in 36 Holstein steers. The cattle were given (orally) a single dosage of lasalocid (1, 10, 50, or 100 mg/kg of body weight) or monensin (25 mg/kg of body weight) or rice hulls. Animals were observed once a day until they died or were euthanatized at 32 days after the dose was given. All cattle were necropsied. Heart, kidney, adrenal gland, liver, spleen, pancreas, lungs, brain, sciatic nerve, skeletal muscle, small intestine, large intestine, and rumen tissue sections, stained with hematoxylin and eosin, were studied microscopically. Lasalocid was lethal at dosages of 50 and 100 mg/kg, and monensin was lethal at the dosage given (25 mg/kg). Cattle dying of lasalocid and monensin toxicoses had gross and microscopic lesions consistent with cardiomyopathy. Dilated heart or petechial and ecchymotic hemorrhages were observed with both drugs. Microscopically, multifocal areas of myocyte necrosis were observed. Those cattle that died within 3 days of dosing with either drug had a marked degranulation of pancreatic acinar cells. Changes were not observed in any other tissues.