Aldicarb toxicosis in a flock of sheep.

Aldicarb toxicosis was diagnosed in 200 sheep that died suddenly. Carbamate insecticide toxicosis was suspected based on observed clinical signs (hypersalivation, diarrhea, urination, paddling, seizures, miosis, and deaths occurring within 1 hour). Tissue samples were submitted from 4 Columbian ewes for pathologic and analytical evaluation. Severe diffuse pulmonary edema was observed on gross and histologic examination. Inhibition of cholinesterase activity in retina (21.2-68.1% of normal activity, n = 3), brain (40.6-45.6% of normal activity, n = 3), and whole blood (27% of normal activity, n = 1) supported a diagnosis of carbamate toxicosis. Reversal of brain and whole blood cholinesterase activities (reactivation factor greater than 1.4) following an in vitro 1 hour incubation at 37 C was also consistent with carbamate poisoning. Aldicarb toxicosis was confirmed following its detection in rumen contents at 1.5, 5.5, and 334 ppm using both high-pressure liquid chromatography with UV detection and gas chromatography with nitrogen/phosphorus detection.

Fumonisin B1 concentrations in feeds from 45 confirmed equine leukoencephalomalacia cases.

During the fall of 1989 and winter of 1990, numerous reports of equine leukoencephalomalacia (ELEM) occurred from many regions of the United States. Typically, horses were consuming feed partially or entirely composed of corn and/or corn screenings. From October 1989 through May 1990, samples from 55 confirmed or suspected ELEM cases were received at the National Veterinary Services Laboratories, Ames, Iowa, for fumonisin B1 analysis. Samples from 9 cases in 1984-1985 were also obtained. Fumonisin B1, a mycotoxin produced by Fusarium moniliforme, causes ELEM, but little is known of naturally occurring toxic or safe levels in feeds. To determine what levels of fumonisin B1 in feeds are associated with ELEM, 45 selected cases were studied. The fumonisin B1 concentrations ranged from less than 1 ppm to 126 ppm, with the majority of the samples above 10 ppm. All types of feeds were included: corn, screenings, sweet feeds, and commercially pelleted rations. The length of exposure varied from 7 to greater than 35 days. Horse feed samples not associated with ELEM were also collected and analyzed. None of the nonproblem feed samples contained fumonisin B1 levels greater than 8 ppm.

Diagnosis of bromethalin toxicosis in the dog.

Dogs given a single oral dose of bromethalin at 6.25 mg/kg developed a toxic syndrome characterized by hyperexcitability, tremors, seizures, depression, and death within 15-63 hours after bromethalin administration. Gross lesions included mild cerebral edema (2/5) and mild pulmonary congestion (2/5). Histologic lesions included diffuse white matter spongiosis (5/5), mild microgliosis (3/5), optic nerve vacuolization (3/5), mild thickening of Bowman's capsule (2/5), and occasional splenic megakaryocytes (2/5). Ultramicroscopic examination of midbrain stem revealed occasional swollen axons, intramyelinic vacuolization, and myelin splitting at the intraperiod line. Bromethalin was detected in kidney, liver, fat, and brain tissues, using gas chromatography with electron capture detection. Photodegradation of extracted bromethalin may limit accurate quantification of tissue residues.